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45 minutes | Mar 10, 2020
Eukaryotes – Pick your Poison
Heeeey! I’m going to start this episode with a little story. When I decided I was going to be crazy and start this podcast, I was trying to think of a name for it, and I came up with the name Cellfie Life. I was running it by my best friend who is a social media manager. She does social media for a living, and she wasn’t exactly a fan of the name because she thought it sounded like a prison podcast, which is not at all what I was going for, but I was excited and proceeded to tell her all about Robert Hooke. Robert Hooke was looking through a microscope at a desiccated cork, and he thought that it looked like the little cells that the monks slept in, and so he used the word “cells” for what he saw through the microscope. I was thrilled to be able to share the connection between the two types of cells with my bestie. My friend wasn’t particularly entertained, but, nonetheless, welcome to the Cellfie Life! I am very excited this episode is on cells—kinda its namesake. Robert Hooke – Biography, Facts and Pictures Before we jump in, I want to thank you for listening. Please subscribe, and if you’re going to find the script notes, you can find them on the website at cellfielife.com. I also want to give a special thanks to Emily, and Abby, they messaged me on insta earlier this week about the podcast. It honestly meant so much that you guys contacted me. I told Emily that I usually just feel like a crazy person sitting in my closet talking to myself, so it’s really nice when people reach out and give me feedback. So thanks, ladies. Okay, let’s just dig in today. Eukaryotes We will specifically be reviewing eukaryotes today. So, we, as humans, have a lot of cells, so it makes sense that we have an understanding of how they are organized and how they communicate and react. Pop quiz from the last episode: Q: What is the main difference between prokaryotes and eukaryotes? A: Prokaryotes don’t have membrane-bound organelles, and eukaryotes have membrane-bound organelles. Another difference between the two is that prokaryotes are always going to be single-celled organisms where eukaryotes can be unicellular or multicellular with multicellular organisms, such as ourselves. Eukaryotes can form tissues and have a division of labor between the cells. This means that cells will be specialized with form following function. Some cells might need more mitochondria or have more of a rough ER, depending on what type of work they are specialized in performing. I want to mention here that there are four types of tissue: nervous, muscle, connective, and epithelial. We won’t be covering tissue in this episode, but I wanted to mention the types since we talked about eukaryotes being multicellular organisms and forming tissues. When I was first learning all the science stuff, I really had a hard time keeping the cell types associated with the right name. I switched majors from creative writing to biology, so the change was a big one. Anyway, I was having a hard time keeping prokaryotes and eukaryotes associated with the correct types of cells. I knew that one was the cell with membrane-bound organelles, and the other was the one that didn’t have membrane-bound organelles. So, of course, I turned to my root words. So “karyon” is essentially the Greek word for “nut” and “eu” is the word for “well.” So, Eukaryotes are well-nutted. I know, I know. I’ll let you insert the dirty joke. But, it makes sense the old school scientists were looking at these cells for the first time, and they see that they have well-formed kernels, (as in the nucleus) so that’s what they called them. Eukaryotes have membrane-bound organelles. I’m going to say that again. Eukaryotes, well-nutted, have membrane-bound organelles and contain a true nucleus. Let’s start from the outside of the cell and work our way in; Starting with the membrane. Membranes Membranes are responsible for some crucial things. They define cellular boundaries; provide intracellular boundaries like the mitochondria and the nucleus. Remember, we are talking about eukaryotes that have membrane-bound organelles, so these lipid membranes can be found around the nucleus and lysosomes and other organelles. These membranes organize the cell and contain chemicals. They also regulate the flow of information and transport things into the cell. One more time. They: Define cellular boundaries Provide intracellular boundaries like the mitochondria and the nucleus. Organize complex reactions, receptors, ion channels, for example. Regulate the flow of information [Have] dynamic structures. Components of Cell Membrane Starting with the components of the cell membrane. Pop quiz Q: What are the 3 main components that make up the cell membrane? (this is a quiz question) A: Phospholipid bilayer Cholesterol Proteins Let’s review each starting with the phospholipid bilayer, which also has three parts: Phosphate head Glycerol backbone Fatty acid tails I’m sure you have seen the phospholipids sketched-out. They look like a stick figure that is only a head with two legs sticking out. I always kinda envisioned it like a jellyfish with only two tentacles hanging down, or, it could be a balloon with two streamers. Pick your phospholipid poison. So, the head is the phosphate head. It literally is called a head, so this should be easy to remember. And, [the head] is hydrophilic. It loves water and, remember, water is polar, and the phosphate heads can carry a charge, so it makes sense. What does a phosphate head look like? What is its chemical structure? It is a phosphate surrounded by four oxygens. And, what do you know about oxygen and water? Oxygen and hydrogen are what make up water and that oxygen is 1 of 3 elements that can form hydrogen bonds. So, these phosphate heads LOVE WATER! https://courses.lumenlearning.com/introchem/chapter/phospholipids/ So, you have the hydrophilic phosphate head, and then you have the glycerol backbone, which attaches the fatty acid tails to the phosphate head. I like that they appropriately named the glycerol “the backbone.” It’s the backbone: it holds it all together. It connects the head to the rest of the body. Attached to the backbone are the fatty acid tails. The tails are hydrophobic—”phobic” as in fear—like arachnophobia, fear of spiders. Or, this one is one of my favorites, arachibutyrophobia, which is the fear of peanut butter sticking to the roof of your mouth. I Googled that one. You’re welcome. Back to plasma membranes. So, we have two layers of these phospholipids with the hydrophobic tails facing in towards one another with the phosphate heads facing the water (A.K.A. the extracellular and intracellular fluids). https://courses.lumenlearning.com/introchem/chapter/phospholipids/ If you forget which is hydrophobic and which is hydrophilic, think about the cell being a water-filled bubble in a pool of water. The part that likes water would be on the outside, interacting with the water, and on the inside. The phospholipids have a hydrophobic portion and a hydrophilic portion which makes them, what is called, “amphipathic.” What would be able to pass through the phospholipid bilayer? It is semipermeable. As a rule of thumb, small and nonpolar molecules will be able to pass through. Quick note: Do you all remember cis and trans bonds from O-Chem? Quick reminder: A cis is a double bond with the attached carbons coming off the same side. So, if it were a scale of some sort, it wouldn’t be balanced. Trans is when the carbons coming off the double bond are on the opposite sides. Keep this in mind when we talk about membrane dynamics. But, first, we are going to talk about the other two main components of cell membranes: cholesterol and proteins. And, there are actually carbohydrates or glyco’s that attach to proteins (e.g. “glycoproteins”) or lipids (e.g. “glycolipids”), and, these play a huge role in communication. Cholesterol Okay, so, cholesterol in the membrane helps to maintain fluidity. It really works to keep the cell in a happy, chill state. So, what keeps you in your chill state? Is it by chance a food, a food that is high in cholesterol? For me, it’s sweet potato fries. Proteins Two groups of proteins are in the cell membrane: Integral proteins and peripheral proteins. Integral proteins, or, transmembrane proteins, go throughout the membrane. They’re integrated into the membrane. Peripheral proteins sit on the periphery. So, they are on top, or just slightly into the membrane. Integral proteins are often used to transport things in and out of the cells. They are integrated into the membrane. There are two types of transport proteins: Channel Carrier These transport proteins are very selective of what is permitted to pass through into the cell. Channel proteins are exactly what they sound like; they are proteins with holes that go through them, so that things can move into and out of the cell. They are hydrophilic tunnels through which hydrophilic ions and molecules can pass. Carrier proteins hold on to molecules and change shape in such a way that molecules are shuttled across the membrane. So, carrier proteins are transforming to move things into the cell. What kind of molecules will be transported through these proteins? So, to review, our membranes are made of: Phospholipid bilayer Cholesterol Proteins Now that we have talked about what the outside of the cell membrane has on its surface, let’s try to imagine how it might look. To do this, think back to when you were a kid
36 minutes | Feb 25, 2020
Pathogens(Bacteria & Viruses) – Meet the Pro’s
Pathogens!! In this episode, we will be talking about fungus, archaea, bacteria, virus, and prions specifically as they relate to the human condition. ____________ So, two bacteria walk into a grungy bar. The bartender says, “We don’t serve bacteria here!” And, the bacteria says, “But, we work here. We’re staph.” “Why did the mushroom get invited to the party?” “Because he’s a fungi.” LOL, I didn’t have a good bacteria song, so I Googled jokes about bacteria. So, you’re welcome for the dad jokes to start this episode. If you haven’t figured it out, we’re going to be talking about bacteria, archaea, fungi, viruses, and prions in this episode. Welcome to the Cellfie life. This is Nikaela, and I wanted to thank all of you for listening, and rating, and reviewing, and subscribing. If you are enjoying the podcast and want to help support the production of it, I have set up a Patreon page where you can support the podcast for as little as 25-cents an episode! Which is $1 a month. Your contribution helps me pay hosting sites and my editors and really allows me to keep putting this content out there. So, check out Patreon if you want to help me keep making these podcasts. You can also support the podcasts by just subscribing, rating, reviewing, [and] telling your friends about it. If you have questions, comments, corrections, please let me know. The best way to reach me is on Instagram @t-h-i-s- c-e-l-l-f-i-e life or the website cellfielife.com. I post the script notes on the site, and I post MCAT review questions on my story just about every day. Now, let’s talk about those tiny little prokaryotes. Question (Q): Do you remember the difference between prokaryotes and eukaryotes? Simple Answer (A): Prokaryotes do not have membrane-bound organelles; eukaryotes do have membrane-bound organelles. Okay, let’s meet the pro’s, and by the pro’s I mean those amazing prokaryotes that can: Survive in extreme environments, form symbiotic environments, replicate in many different ways… Some can survive with oxygen and without, meaning they can adjust their metabolism to meet the demands of their environment. They are pretty cool! And, eukaryotes are the true nucleus, so are membrane-bound organelles—which is what our cells are—but we will talk about that next episode when we go into cells, specifically our cells. So, prokaryotes are super simple: they don’t have membrane-bound organelles, and their DNA is usually concentrated in an area called the nucleoid region. We’re going to talk about the pro’s (the prokaryotes) but, first, let’s do a quick rundown of taxonomic ranks. So there are eight basic taxonomic categories; this doesn’t include subspecies. Taxonomic ranks are just a way of classifying things in a step-down method where organisms are split into more specific groups. The order from broadest to narrowest categorization Domain Kingdom, Phylum, Class, Order, Family, Genus, Species How are we going to keep these taxonomic ranks in the correct order? Obviously, we’re gonna use a mnemonic device. Dumb Kids Playing Cards On Freeway Get Smashed—I like this one because it sounds like a news headline. There is also King Philip Came Over For Ginger Snaps! But, this one leaves out the domain. Prokaryotes make up two of the three domains—and, remember, that domain is the first one listed on the taxonomic ranks. “Dumb kids playing cards on freeway get smashed…” Domain, kingdom, phylum, class, order, family, genus, species. Q: Can you name the three different domains? A: Eukarya, Archaea, and Bacteria. So, let’s take a closer look at Archaea and Bacteria, both of which contain prokaryotes. Actually, fun fact, there used to be only two domains: monera and eukarya. But, based on genetics, they separated into three domains. Scientists looked at the 16s rRNA region, which is the region that I work with a lot for my research, so that’s kinda cool. I’ll go into more depth when we talk about genetics. Archaea So, archaea are similar to bacteria, but they are that badass aunt that rides a motorcycle, and travels the world, and makes friends wherever she goes. She helicopter-skis and swims with sharks. Some might even say she’s a little extreme. Archaea are archaic; they are ancient, and very well adapted, and can survive and thrive in extreme environments. They are extremophiles, thermophiles, [and] halophiles. Some are photosynthetic, but others can survive on things like methane gas and sulfur. Archaea are in super harsh environments, high temps, cold temps, high salt, [and] low light. So, those hot springs in Yellowstone, and the Great Salt Lake in Salt Lake, and probably in the south pole—all these locations have archaea and have extreme environments. /https://gypsyguide.com/tour/yellowstone-grand-teton/ https://oceanwide-expeditions.com/blog/the-first-race-to-the-south-pole-in-50-years Archaea are resistant to a lot of antibiotics and can be hard to target because of the similarities they have with eukarya. Both archaea and eukarya start the translation with methionine and have similar RNA polymerases. But, archaea have circular DNA like bacteria and reproduce via budding or binary fission. Both archaea and bacteria have flagella and come in different shapes and sizes. Basically, archaea and bacteria look similar which is why they have grouped the same origin and called archaebacteria. Bacteria Let us talk about bacteria. I will try not to get too excited or nerdy about it, but I really love the little guys. What do you think of when you hear bacteria? Do you think germs and disease, antibacterial hand soap and gels? Maybe you’re up on the current research that has really surged in the past ten years and think “microbiomes”? Specifically, [microbiomes] in your body. There are tons of bacteria in our bodies: about 10 times as many microbes in our bodies than human cells. And, the great thing about them is how helpful they actually are. Thus, all the studies on microbiomes. The MCAT mostly focuses on human biology as opposed to microbiology, but there are some things we should be familiar with since they pertain to human health, disease, and treatment. The first thing we brushed by is that bacterial DNA is circular and not membrane-bound; it just hangs out in a specific region. It can also have extra tiny circular non-chromosomal DNA called plasmids. We will talk more about that. But, with bacteria, the basics are really with the shape. We still group bacteria based on shape. There are 3 categories to be familiar with: Cocci are round. I think of this as a single grape. Bacilli are rod-shaped like a baguette. And, spirilla are spiraled like a corkscrew. It sounds like the makings of a lovely picnic. Pop quiz time Q: What was the spirochete that—we talked about in the Embryogenesis II episode—that can cross the placenta and hurt a fetus? Hint: Remember the T-O-R-C-H-E-S! A: Here, we are talking about the S in the TORCHES acronym which is syphilis: Treponema pallidum. And, while we’re talking about spiral bacteria, I want to mention the big three spirochete bacteria are pathogenic. Borrelia burgdorferi is Lyme disease. Treponema pallidum—which is syphilis. Leptospira interrogans: In humans, this bacteria is more of [an] accidental infection. It causes what is known as Weil’s disease. It is contracted from coming in contact with infected animals, specifically their urine and blood, among other things. How are we going to remember these…? BLT? BLT is not only for bacon, lettuce, and tomato sandwiches. It’s also for the spirochetes that are pathogenic in humans. B: Borrelia burgdorferi – I remember this one because I think of the store Burgdorf’s in NYC. Not that the two are not exactly related. But, Burgdorf’s is in NYC, and Lyme disease is prevalent on the east coast, including New York. Lyme Disease Maps: Historical Data | Lyme Disease L: Leptospira interrogans. So, this spirochete looks like a question mark when viewed under the microscope. And, when you are interrogating someone, what are you doing—asking them a lot of questions? So, this interrogans looks like a question mark. [T]: Treponema pallidum: I don’t have a great one for remembering this one… I did some Googling and did not come up with anything significant. The best I have is that treponema sounds like a worm to me. I have no idea why, at some point, I decided that treponema sounds like a worm, and, a worm relates to syphilis. I don’t know why my brain makes that connection. If you have a great way to remember that treponema pallidum is syphilis, please let me know, so I can share it. So, there we have our spirochete BLT. LOL, I hope you’re hungry! Along with the shape of the bacteria, we look at how they cluster or group together. Strepto means they are in a line or a twisted chain. Staphylo is bunched up in a group like a bunch of grapes. Diplo means they are partnered up. Diplo. So, now we know that bacteria are prokaryotes that don’t have complex membrane-bound organelles—but, rather, have circular DNA chromosomes—and are named after their shape and how they group. Now, let’s talk about bacterial cell walls. Bacterial Cell Walls There are two types of bacterial cell walls: One has two membranes with a thin cell wall in-between them Two has a thick cell wall and then a membrane. Cell walls are made of peptidoglycan; basically, a sugar and an amino acid that cross-bind together to form the cell wall. It’s actually really cool, but I won’t get into the details here because you don’t need them for the MCAT. Just know that bacteria cell walls are made of peptidoglycan, and since humans don’t have cell walls, this is a site for antibiotics to target. The cell wall is responsible for the movement of solutes in and out of the bacteria. It also provides structure. Let’s start with the cell wall that is thick (and then has a membrane) since it’s a bit simpler in that it doesn’t have as many layers to its envelope. For clarification, the envelope is the cell wall and the membrane. This type of cellular envelope is gram-positive. We will go into the gram test in just a minute. Gram-positive has two main layers in their envelopes with a space called the periplasmic space in between. So, starting on the outside, working our way into the cytoplasm region of the bacteria, we have a very thick cell wall of peptidoglycans. Then, [there is a] periplasmic space and then a cellular membrane that is similar to our cell membranes. Gram Positive vs Gram Negative The other type of cell wall is called gram-negative. This is the envelope that has a membrane, then a thin cell wall, then a periplasmic space, and then another membrane. Another difference in this bacterial envelope structure is that the outer membrane has lipopolysaccharides sticking out of it. One more time: gram-negative bacteria have an outer membrane that has lipopolysaccharides sticking out of them. I think of the lipopolysaccharides like those air dancers; the tall, skinny, tube-like structures people put in front of stores to get people’s attention. They dance and move around because of the fan. Air Dancers | Image Rights These lipopolysaccharides stick out of the outer membrane on gram-negative bacteria and are part of the reason gram-negative bacteria are so pathogenic in humans: the lipopolysaccharides can trigger an immune response. Another reason gram-negative bacteria can be tricky to target with antibiotics is because they have that additional outer membrane—which makes it harder for antibiotics that target the cell wall to reach the wall and break it down—so that the bacteria can undergo osmotic rupture. Now, let’s talk about the gram-positive and -negative, specifically, where that name comes from. Basically, back in the day, a guy named Hans Christian Gram noticed when we were trying to satin some bacteria that some stained blue-purple while others stained red-pink. This difference in staining color came from the physiological differences in the bacteria we just discussed. The gram-negative absorbed the safranin counterstain which makes the cell appear red-pink. The gram-positive absorbs the crystal blue and appears a blue-purple. I remember the difference in this by saying: red is dead. Red is dead: Gram-negative bacteria are usually much more worrisome and hard to kill. Gram-negative bacteria are harder to kill because they have three layers of defense. Gram-negative stain[s] red-pink—red is dead. I also used to swear there was an Elvis Presley song that sang about being ‘positively blue.’ But, when I Googled that, nothing came up. But, it still sounds like a song Elvis would sing, right? “I’m positively blue over you.” Gram-positive—stain[s] blue-purple. Before genetic identification was so prevalent, gram staining was used to help determine the type of antibiotics that would work on someone with a bacterial infection. Red is dead—AKA—danger. When you think dangerous bacteria think gram-negative [bacteria] have an extra layer, so it makes them harder to kill with things like antibiotics. Positively blue—gram-positive stain blue. They have a thicker cell wall with an inner membrane. Gram Positive vs Gram Negative I have linked some images and additional articles about gram staining if you’re interested. They are in the script notes on the website. Bacterial Environments & Characteristics Just like humans like to live in different areas, I prefer dry heat, some people like snow, and some like humidity. I don’t know why. Humidity and I aren’t on the best of terms. Actually, I think bacteria are more like sea life. Some require coming up to the surface for air, some don’t need to surface. Bacteria have specific environments where they thrive. Anaerobes don’t require oxygen. Obligate aerobes require oxygen for survival; they need oxygen to metabolize. Facultative anaerobes are real little badasses because they can survive with oxygen or without oxygen. Aerotolerant anaerobes are unable to use oxygen for metabolism, but the presence of oxygen doesn’t harm them. Bacteria get around by using flagella—which are basically long tails that they use to propel themselves around. Think propellers on a boat. They can use these flagella to move them towards or away from something. An important vocab word to know is chemotaxis. You might have heard chemotaxis when you talked about the immune system in school. Your body uses chemotaxis for an immune response. Bacteria can also use chemotaxis. Chemotaxis is simply the ability to detect chemicals and move towards or away from them—which bacteria do by way of flagella or cilia. You can also think of humans doing chemotaxis by smell. When you smell fresh bread, you might wander into the kitchen to see what’s baking. If you smell something terrible coming from the bathroom, you’ll probably walk the other way. Okay, so bacteria have cytoplasm, and cell walls, and membranes. They have DNA in the nucleoid region and they don’t have membrane-bound organelles, but what organelles do they have? Some of the prep books mentioned that some bacteria have histone-like structures, but I think the most important thing to note is that the ribosomes are different in prokaryotes and eukaryotes. The reason [for] noting the differences between prokaryotes and eukaryotes is it gives us a place to target destruction via drugs. So, we mentioned that some drugs target the cell wall, particularly the peptidoglycan links. Another set of drugs target the ribosomes. Bacterial ribosomes contain the 30s and 50s subunits, while eukaryotes contain 40 and 60s. Now, how do I keep these sizes straight? So, my friend really likes a Korean singer named CL, and a few years ago, she was like, “Hey, want to go see her in concert in LA?” And, I was like, “Sure.” At the time, I didn’t know who CL was, so on the way to LA, I learned one song, and it goes: “I got myself a forty; I got myself a shorty.” https://www.youtube.com/watch?v=Mr29X77OA5g Bacteria can’t get themselves a 40. Only we (humans) can pick up a 40, and then, I just remember for eukaryotes or prokaryotes, it’s 20+ in size. So, eukaryotes have the 40s and 60s: prokaryotes have the 30s and 50s. Prokaryotes also don’t have mitochondria: they use their cell membrane for the electron transport chain, which, if you think about, makes so much sense. You’ve probably heard of the endosymbiotic hypothesis which suggests that our modern-day mitochondria are descendants of a specialized bacteria that survived endocytosis by another species, and, eventually, lead to them being incorporated into our cytoplasm. So, if we believe that our mitochondria are the descendants of a bacteria being endocytosed, it makes sense that bacteria wouldn’t have mitochondria and, instead, electron transport chain as part of their membrane. Mitochondria Another interesting thing about bacteria is how they share their DNA and how they replicate. At the beginning of this episode, we talked about how bacteria don’t have membrane-bound organelles: they simply have an area called the nucleoid region where their circular DNA resides. But, what is really cool is that bacteria don’t have to have all their DNA contained in this region or one circle of DNA. There are these little sections of DNA that are smaller circles that are called plasmids. Now, bacteria can take in plasmids from other bacteria. Plasmid DNA is not necessary for survival. The bacteria can get on fine without it, but the plasmid can carry extra genetic information, like antibiotic resistance. Plasmids are not required, so they are considered extrachromosomal DNA. So, how do bacteria share genetic information and reproduce? Bacteria do not undergo mitosis or meiosis, but they still have ways of increasing their genetic variability. Distribution of extrasomal DNA is random, and daughter cells may or may not get a copy. So, genetic variability can be increased one of three ways: conjugation, transformation, and transduction. Conjugation: Conjugation is basically bacteria sex. One bacteria must have an F + plasmid. If it has the F+ plasmid, it is considered F+ if the bacteria is F+. It has the gene for a sex pilus, or a conjugation bridge, which is a one-way transfer of genetic material from the male F+ bacteria to the F- bacteria. Transformation is pretty straight-forward. Transformation is when bacteria pick up DNA from the environment. Transduction is when they incorporate genetic material via a vector, such as a virus, like a bacteriophage. Bacteriophages are fascinating—they are viruses that infect bacteria. They look like weird, little spaceships that inject their genetic material. Bacteriophages can carry genetic material from one bacterium to another. A bacteriophage can accidentally incorporate DNA from one bacteria, and then, when it goes and infects another bacteria, [it] can transfer this captured DNA. So, these three methods are how bacteria can increase their genetic variability, but how do they reproduce? It’s not via mitosis or meiosis: it’s by binary fission. Bacteria reproduce via binary fission, which is asexual reproduction. The circular DNA replicates while the cell grows until it’s large enough that it will pinch inward in the middle and produce two roughly identical daughter cells—I say “roughly” because remember that the plasmids are divided between the daughter cells randomly. As you can see, binary fission is a lot less involved than mitosis, which means that it can happen a lot faster and can cause bacteria to grow exponentially, doubling each generation. The limiting factor for colonies is resources and waste accumulation. Yay!! That wraps up our bacterial discussion. Fungi We are only going to cover a few things with fungus. Fungi isn’t huge on the MCAT. We are just going to mention the barebones here. I do think that it will be more prevalent in medicine and on the MCAT as research advances into autoimmune disorders. Fungi have cell walls made of chitin, which is the same thing lobster exoskeletons are made of… I always found that kinda freaky. Fungi are also heterotrophs meaning, they have to take in nutrition from their environment. Fungi can reproduce either sexually or asexually. Fungi spend the majority of their lives as haploid and grow these long intertwining branches called hyphae. Current research suggests that MS has a fungal component. I am going to link a few articles in the script notes if anyone is interested. The Role of Fungi in the Etiology of Multiple Sclerosis Viruses Now, we are going to move on to viruses. But, first, what is a virus, and is it alive? If you want, you can go Google this very thing and see the different factions defending different positions. I don’t have a super-strong opinion, so I’m just going to outline what I was taught. Viruses have a lot of variabilities, as far as pathogenicity, but are pretty physiologically basic. They have a protein coat, called a capsid, and genetic material, which can be DNA or RNA. And, a few [viruses] have an envelope of proteins and lipids. One more time. If a virus was a person, they would have on their coat, which is called a capsid, but some viruses are extra and like to layer, so on top of that capsid layer, they might have a massive fur coat. Think Macklemore here. Now, the extra envelope, or fur coat, if you will. Actually, we’re gonna go with a faux fur coat here. The faux fur is very sensitive; you can’t just throw it in the washing machine with detergent and then move it to the dryer. No, the viral envelope is heat-sensitive and sensitive to detergents. So, if you’re wearing the beautiful faux fur coat that is super sensitive, you’re gonna be easier to take-out—same with these viruses. The ones that have envelopes are easier to kill. The viruses that don’t have the envelope are harder to kill because they aren’t as sensitive. https://www.youtube.com/watch?v=4aik4-Zty1Q&list=RD4aik4-Zty1Q&start_radio=1 Also, this is one of my favorite Macklemore green room songs. I have listened to it so many times. I’m slightly obsessed. Donna Missal is so raw -listen to it. Back to viruses. Viruses are tiny—smaller than bacteria. Viruses have to infect a host cell and hijack the host cell’s machinery in order to reproduce, which is the main argument for why viruses aren’t considered living. Viruses can’t replicate by themselves. They are deemed obligate intracellular parasites, which I think is just rather fantastic! Viruses lack the ribosomes to carry out protein synthesis, which is why they need a host! So, once the alien invader has hijacked a cell—I think of viruses as alien invaders, I mean they even look alien, have you seen the structure of bacteriophages? If that is not an alien spaceship I don’t know what is—anyway, once the virus has got into a host cell and taken over their computers and machines, it starts pumping out viral progeny, which are called virions. The little baby viruses, virions can now go forth and infect other cells. Speaking of the bacteriophage spaceship, bacteriophages are viruses that target bacteria. I think this is a fascinating area of research. Bacteriophages that are targeted for specific pathogenic bacteria can be the next vast area of medicine. Instead of prescribing your patients an antibiotic, you could send a specimen to a lab that would program a targeted virus for that bacteria which would be sent back and injected into your patient. The research I conduct hasn’t been on viruses, but I do work with bacteria, and I would love to get into bacteriophages a little bit. Something I think is pretty cool about viruses is that they can have RNA or DNA; single-stranded [or] double-stranded. They can have a lot of genes or only a few. So, humans and other animals have stringent regulations on what information we need in our genomes. Viruses are just like, “Hey, I’ll take anything.” Important terms for viral genetic material include: positive sense, negative sense, and retroviruses. Positive sense: If a virus has RNA that can be directly translated to functional proteins it is said to be positive sense. Negative sense means that the RNA strand is the template for a complementary strand. Once the complementary strand is made, the new strand can be used for protein synthesis. Negative sense RNA viruses must also carry an RNA replicase to help with this creation of the complementary strand. So, to remember these, I just think, if someone is an optimist, they are positive, and they just go for it—like positive-sense RNA viruses can be directly translated. If people are a little negative about a project, they may need to talk themselves into it before they get to work. It’s more of a two-step process. Same with negative-sense RNA: it takes the two steps to get where it needs to go. Retroviruses: Retroviruses work backward. They have an enzyme called reverse transcriptase, which takes the single strand of RNA and makes DNA. This DNA is then incorporated into the host’s genome, and, then, the DNA is transcribed as if it was the host’s own DNA. See how tricky these obligate intracellular parasites are? The only way to kill the virus once it’s in the host is to kill the cell. Note: This is a bacteriophage shape, just fyi. Retrovirus by Velica Q: What is the most infamous retrovirus? A: Human immunodeficiency virus (HIV) So, this is old science news like 2011—so, more than a little old, but when this came out, I was slightly obsessed. The headline in my brain was those who had family in Europe that lived through the plague have a 10% chance they are immune to HIV. So, basically, viruses can only infect a specific set of cells, which is dictated by the receptors on the host’s cells. HIV can only infect if the host has receptors called CCR5. The paper released talked about how the black death sweeping across the continent was a reason that Europeans, or those [of] European descent, have a higher chance of being immune to HIV. The frequent plague outbreaks occurred in tandem with the mutation frequency of CCR5. Others think that smallpox is the reason that Europeans have higher immunity to HIV. I’ll link an article. Did Black Death boost HIV immunity in Europe? I mean, it’s just cool. I love the idea of that hypothesis. Also, I’m linking episodes of the podcast This Podcast Will Kill You not because this is an ad, but I love this podcast and their review of infectious agents. They have episodes on smallpox and the plague, so listen and enjoy. Ep 3 Gnarlypox – This Podcast Will Kill You | Podcast Ep 5 Plague Part 1: The GMOAT – This Podcast Will Kill You Ep 6 Plague Part 2: TGFA – This Podcast Will Kill You Just as viruses have different genomes, viruses have different ways of getting into the cells. Some are endocytosed. Others inject their DNA like a needle. Others bind and become part of the cells membrane. Okay, so the virus gets into the host, takes over, makes a bunch of baby viruses that now need to be released to the world. So, the cell could just rupture and release the virions like a baby spiders hatching of my nightmares. But, if you kill the thing that you are using to reproduce, that is not the best life choice, because, then, you can’t use the cell that you have taken over and already put in the energy to hijack. Another way virions can escape is by doing a viral version of exocytosis called extrusion, which is where the virus binds to the plasma membrane and escapes in a membrane bubble. Escaping this way keeps the host cells alive and lets the virus keep using the cell as its puppet. When the virus is keeping the cell alive, the virus is said to be in the productive cycle. Again, there are basically two phases of progeny release: lytic and productive. Lytic: The cell lyses and releases all the progeny. In the productive phase, the cell is kept alive, and the virions escape via extrusion. Bacteriophages also have two cycles called lytic and lysogenic cycles. The lytic phase is basically the same. The virus hijacks the machinery, makes a bunch on viorins, and then ruptures the cell and releases the virions. If a virus is in the lytic phase, it’s called virulent. The lysogenic phase is when the virus integrates itself into the bacterial genome. The virus integrates as a provirus or prophage. The virus integrating into the bacterial genome is what initiates the lysogenic phase. The virus will be replicated along with the bacteria. However, if the bacteria are exposed to environmental factors, the virus can come out of the genome and enter a lytic phase. As the virus leaves the bacterial genome, it can take part of the bacteria’s DNA with it, which is what allows transduction between bacteria using a viral vector. Prions The last thing we are going to talk about in this episode is prions. Prions are like proteins from hell. They are not alive. They are simply a protein that causes other proteins to misfold. They go from alpha-helical to a beta-pleated structure. Mad cow disease, Creutzfeldt Jakob disease, and fatal familial insomnia are all examples of prion disease, which sounds like one of the most terrible ways to die. In fact, I’m going to start making a list of ways I don’t want to die, and prions are going to be near the very top. If you want to read a book about prion disease, check out The Family That Couldn’t Sleep: Medical Mystery. (The Family That Couldn’t Sleep: A Medical Mystery) Final Thoughts And, on that happy note, we are done! Thanks for listening. Ask me questions on Insta @THISCELLFIELIFE. Subscribe, rate, review. Study hard, friends!
35 minutes | Jan 28, 2020
Embryogenesis II- ‘Magic School Bus’ style.
Embryogenesis II- we finish up the embryology review by going over gastrulation, neurulation, and getting into a discussion on the germ layers, teratogens, stem cells, and fetal circulation. Hey, hey, hey – It’s Nikaela, and this is Cellfie Life. Where we talk about complex science principles by relating them to, I love lucy episodes and bunnies. If you have no idea what I’m talking about listen to the Early Embryogenesis episode, it was the episode right before this one. Also, For those of you questioning my three heys, I heard someone say it in the library when I was writing this episode and thought I would try it on. I’m not sure how I feel about it. Hi, I’m Nikaela welcome to the Cellfie Life. This subject is a two-parter because it was getting a little longer than I wanted. I want to keep these episodes around 30 minutes-ish. So, I decided to chop the Embryogenesis review in half. But first housekeeping! I have set up a Patreon page; If you are enjoying the show and want to share the love, you can head over to pateron.com. With Patreon, you can pay a small amount of money each month to help me cover production costs. It will help me pay for hosting and pay my amazing editors that help me get these episodes out every week. You can support the podcast for as little as .25 cents an episode, a dollar a month. Or if you are just such a broke student and you need that dollar for ramen, I get it, share the love by telling your friends about this podcast, and rating and reviewing. https://www.patreon.com/cellfielife You can follow me on Instagram. I post review questions on my stories just about every day or check out the website at cellfielife.com, where you can find the script notes and the gifs and memes and youtube links I talk about in the show. Now, let’s jump right in- Okay, so the last episode we talked about fertilization and implantation, and cleavage and morulas, and blastocysts and the trophoblasts and the inner cell mass. And how the inner cell mass gives rise to the bilaminar disk, which ultimately gives rise to the germ layers. I know we covered a lot. And this is where we are going to pick up on this episode. We are going to pick up right after implantation. The embryo is just heading into gastrulation at this point, which we have already talked about a little in the previous episode, but we’re going to talk about it more in detail here. Gastrulation is the formation of the three germ layers. It also happens about the 3rd week of development, so it happens pretty early. We haven’t gone over these germ layers, but do you remember them from school…? Q: What are the three layers of the trilaminar disk called? A: Ectoderm, Mesoderm, Endoderm. If you got that one give yourself a high five- Follow up: Where do these three layers develop from? A: the inner cell mass that forms the bilaminar disk, which is made up of the epiblast and hypoblast. The epiblast layer will become the trilaminar disk, which is made up of ectoderm, mesoderm, and endoderm. Let’s talk about how these three layers form. We will start by taking another look at the bilaminar disk just to remind us where we’re at; the bilaminar disk has formed and is the two pancakes, remember? The top layer is the epiblast, and the bottom layer is the hypoblast. Cells of the epiblast migrate inward, downward, and then differentiate. Picture the migration of the epiblast cells like two waterfalls facing each other. These waterfalls are long and on the epiblast layer. These waterfalls are happening where the primitive streak formed. Remember, the primitive streak is a grooved structure along the caudal midline of the bilaminar disk. In the last episode, we talked about it being that one line of syrup on our pancakes. From either side, this continuous passage begins down the center of the top pancake, like symmetrical waterfalls facing each other. If you were standing in the middle of a canyon and water was coming in from both sides, creating symmetrical waterfalls, this is what the epiblast layer does. The spot where you are standing would be on top of the hypoblast layers. So these moving cells of the epiblast are what macroscopically create the primitive streak. So the epiblast cell that just went down the waterfall, that is the primitive groove, the cells that fall down the waterfall go down and start mixing with the layer that is the hypoblast. The hypoblast layer starts deteriorating, and the new differentiated epiblast layer has now completely replaced the hypoblasts. So now we have a new bottom layer of cells, called the endoderm. The endoderm is derived from the epiblast. The epiblast cells don’t stop there; they continue down the waterfall and stat making a middle layer of cells in between the newly formed endoderm layer, and that top epiblast layer. The mesoderm, the middle layer of cells, is derived from the epiblast layer; it sandwiches itself below the epiblast and, above the endoderm, is now called the mesoderm. Meso, as in middle So now we know that the endoderm and mesoderm are both derived from the epiblast. So now the remaining part of the epiblast is like, no, I’ve changed. I need a new name too! The remaining portion is now called the ectoderm. So the epiblast layer is super talented. It has now created the endoderm, mesoderm, and epiderm along with the notochord. In the last episode, we mentioned the notochord starts in the middle of the middle, so the notochord is a knot of cells that forms in the middle of the mesoderm. https://embryology.med.unsw.edu.au/embryology/index.php/Notochord But these three layers, the endo, meso, and ecto-derms, are also known as the germ layers. Neurulation – this is the process where the neural tube forms. Later it will form the spinal brain cord and meninges. We enter the neurulation phase with the three primary germ layers, and this is where they start differentiating further to become different types of tissues. Another flashback to school days question. Do you remember what the germ layers, gives rise to in developed bodies? Lets review that really quick Q: What does the ectoderm give rise to? A: remember the ectoderm is the “attract-o- derm,” so it gives rise to things we might think of as attractive about a person. Their (big doctor) brain, skin, hair, the lens of the eye. The tricky one to remember is the adrenal medulla, Q: how about the mesoderm, what does the mesoderm develop into? A: the mesoderm is the means-o-derm, so the means of how you get around. Think skeletal muscles, circulatory system, most of the excretory systems, the gonads are also from the mesoderm germ layer, cause you’re getting around 😉 as well as the adrenal cortex. So because the adrenals are composed of 2 different germ layers, make sure you pay attention to that. The adrenal medulla is from the ectoderm, and the adrenal cortex is from the mesoderm. I actually think this makes a lot of sense if you think about it. So, the adrenal glands are these small glands that basically are just sitting on top of your kidneys. But they produce hormones. When I think about who the big player in hormone production is, I’m thinking of the brain. Which we know is from the ectoderm layer. The adrenal medulla is the inside of the adrenal glands, and the adrenal cortex is the outside. Remember, we talked about cortex, meaning bark or shell in Latin. So the cortex is the outside of the adrenal gland. The hormones get made inside, in the medulla, the adrenal medulla is from the ectoderm. The exterior of these glands is from the mesoderm layer. Mesoderm like the layer that makes the kidneys that these things are hanging out on top of. Does that help a little? I find if I get a better picture, I don’t have to memorize everything because I understand it. The last gem layer, the endoderm. A: the endoderm forms the pancreas, thyroid, bladder, parts of the liver, the epithelial linings of the digestive, and respiratory tracts. Humans are basically complicated origami. https://www.youtube.com/watch?v=fmiNk5An00k So the short version of neurulation is that folding of the three germ layers, specifically the ectoderm, results in the formation of the neural tube. Different parts break off of the ectoderm; these are called neural crest cells, and these travel throughout the forming body, to make things like the adrenal medulla, and autonomic ganglia, and those other parts of your nervous system that aren’t housed in the brain or spinal cord. Obviously, it’s more complicated than origami. In med school, you’ll need to know all the details but honestly of all the things as long as you understand that neurulation is the folding of the germ layers, that starts the differentiating, and results in the formation of the neural tube which ultimately forms the brain and spinal cord, I think we will be okay. Nurulatioin = human origami Also, I don’t think this will be on the test, but remember how folic acid deficiency can result in spina bifida; that’s one reason why a lot of female multivitamins contain folic acid, and if you are trying to get pregnant you should definitely be taking this vitamin. https://en.wikipedia.org/wiki/Spina_bifida While we are speaking about things that can harm the fetus, let’s chat about teratogens. Teratogens are things that interfere with development and cause defects or death. However, not every teratogen has the same effect. Teratogens range from alcohol to environmental chemicals, bacteria, viruses, drugs, so really anything that can hurt development can be called a teratogen. I just looked up Teratogen in my little root word book, which I love and use al the time its called “Dictionary of root words and combining forms” by Donald J Borror. It was recommended to me the first time I took anatomy, and now it has a perma place in my heart. Also, that’s not an add, I just talk about root words a lot, and this is where I’m looking most of them up. I’ll like it in the script notes. Any way, Terato means monster in greek and gen means to bare or produce. This is kinda terrible, but now you should never, ever, forget what a teratogen is or does. Who came up with that word!? I think that it is rather torrible. (torrible is a combination of terrible and horrible). Teratogens are torrible. While we are talking about the few things that can be harmful to a growing embryo, then a fetus, let’s talk about TORCHES. T-O-R-C-H-E-S is an acronym for things that can cross the placenta and cause harm to the baby. TORCHES stands for TO – Toxoplasma gondii R – rubella C-cytomegalovirus HE-herpes and HIV S-syphilis. Toxoplasma gondii is a parasite that you can get from cats. So like changing the kitty litter, if the cat is infected, you can also get it from eating undercooked meat or from mother to child, like what we’re talking about. Rubella – which is a virus and preventable because there is a vaccine Cytomegalovirus – is a virus, as the name says, and actually, most people that are infected are asymptomatic. This virus usually only causes problems in pregnancy or those with weakened immune systems. Herpes- is a super common sexually transmitted infection. The highest risk of transmission to the fetus and the newborn occurs in case of an initial maternal infection contracted in the second half of pregnancy. But doctors can treat with antivirals, and in some cases, c sections are recommended. HIV – human immunodeficiency virus (HIV) and I googled HIV and passing it on to the baby and read an article that said if you work with your doctors and follow guidelines, 99% of HIV-infected women will not pass HIV to their babies. I had no idea it was that is 99% preventable of passing it on to your child if you worked with your doctor and, of course, have access to the drugs. Syphilis – is caused by a spirochete bacteria called Treponema pallidum, which is a spirochete. Which means it is corkscrewy. Syphilis is treatable with the right drugs, but left untreated can cause problems, like neurosyphilis. Now let’s talk a little bit about stem cells. I know awkward segway, but we were going over neurulation, and then we took a sidetrack into bad things for the fetus, let’s circle back around and finish up the neurulation talk with some details about stem cells, which are frekin cool. Like how!? How!? How do they know they are supposed to do that and not do that other thing. There are chemical messengers, and only specific genes are turned on, but still, science is pure magic, and I freakin love it. SO let’s talk about stem cells. When talking about stem cells, you might hear terms such as specification and determination, and in the past, I have heard these explained in a slightly confusing manner, but it’s really not confusing at all. Specification is reversible Determination is not reversible. This is not the best metaphor, but what popped it to my head immediately is dating and marriage. We’re just going to pretend like divorce isn’t a thing for this metaphor. A lot of people like to date around before they get married, and once they find someone, they want they might be like, ‘okay, you aren’t entirely terrible are then make them their significant other, boyfriend, girlfriend, whatever have you. Now, this is still a reversible action, so in terms of stem cells, this would be considered specification. The cell is reversibly designated as a specific cell type. Now, if things are working out well, you might move on to marriage. Marriage is a more serious commitment. Some might even say irreversible. Marriage is determination in stem cell talk. Before determination, the cell can become any cell type. After determination, the cell is in it for life. Now how a cell knows to become a specific type of cell is what I think is a cool area of research. Determination is, forgive me, determined by a lot of different things like how much cytoplasm is in the cell, RNA distribution, one of my favorites is when the neighbor tells it what to do. “On Wednesdays, we wear pink.” So the neighbor cell that tells the cell what to become secretes morphogens. Like its the queen bee telling everyone else what to do, by messenger. These messages are telling the person what to morph into. Basically, the perfect human morphogen example is Regina George. Quite frequently, morphogens work by gradient, so the closer the cell is to the morphogen point of release, the higher exposure it will be subjected to. Some of the prep books name some common morphogens, but I’m not going to lie here. The only one I remember is Sonic hedgehog (Shh), which is the best nerdy name for anything in science. Question for you. If you do research and discover a little protein, like a morphogen, what would you name it? I would definitely name it after some small creature. What would you call it? What would I call it.? I could just call it creature… or Doby? I asked my brother, and he suggested Karl Malone, the mailman. He’s been a lifelong jazz fan. Or Navi from Zelda. I might call one avo toast. Cause I could. If anyone has some great names, I want to hear them. Send them to me on Insta: @thiscellfielife. Really I want to see them. Show me your nerdy creativity. Okay, back on track. So we have specification, determination, and then we have differentiation. If we are sticking with the marriage analogy, this is like maturing in the relationship. Stem cell differentiation may include changing the structure and biochemistry. Like when you get into medical school, and now your person moves across the country with you. specification – Determination- Differentiation – So Stem cells are essentially cells that can differentiate into lots of different types of cells. Two main types of cells are talked about: embryonic stem cells and adult stem cells (aka somatic stem cell) Embryonic stem cells are pluripotent stem cells that are taken from the inner cell mass. Q: what stage of embryology are there inner cell mass cells? A: Remember, the inner cell mass was that group of cells that huddled together in the blastocyst that later differentiated into the germ layers. Refresher that pluripotent basically means that these cells can form any cell in the body. And there are different levels of potency. O – that’s potent. What do you mean? So let’s go down the line from the greatest level of potency to the least amount of potency. Totipotent means that the cells can differentiate into any cell type. So the morula’s cells would be totipotent because these cells can differentiate into any cell type, either the placenta structure or the fetus. The next is pluripotent Pluripotent stem cells are master stem cells that can potentially create any cell within the human body. So the inner cell mass cells are pluripotent. The next level of potency is multipotent Multipotent stem cells can differentiate into multiple types of cells within a particular group. This is what most somatic stem cells are. A typical example of a multipotent cell is the Hematopoietic stem cell, which is capable of making red blood cells and platelets and all the different types of white blood cells. A lot of differentiation depends on the neighbors of the cell, just like morphogens influenced determination. Differentiation can be determined or influenced by inducers. It’s like when someone wants you to do something, so they induce you with pizza. So if someone is trying to get you to do something (with pizza or pancakes. I’m in a mood for pancakes), they would be the inducer. The person responding to the bribe is the responder, and the responder is considered competent if they can respond to the inducing signal. https://media.giphy.com/media/7Wst0EswP4C665l8sA/giphy.gif This stuff is essential and can be confusing, so let us review that one more time. Here we go. Specification determination then differentiation. Morphogens can influence determination. After determination, cells can differentiate. Cells that have not yet differentiated or can give rise to other cells are stem cells, and their potency groups these. Cell potency refers to the varying ability of stem cells to differentiate into different specialized cell types. The hierarchy of potency is TPM. Totipotent, pluripotent, multipotent. I’ve never heard a great way to remember this TPM -idk toilet paper man.. Lol I don’t know, but their level of potency is also contained in their name. Totally, plural and multiple Determination and Differentiation can be determined or influenced by inducers. If a cell is open to inducing, it is called competent. I have a khan academy video link in my notes if you need an extra visual. https://www.youtube.com/watch?v=uUH5YI5dTOg So inducers help cells to differentiate. Inducers act through autocrine, paracrine, juxtacrine signals. Do you remember what these crine words mean? Autocrine: is when the signal acts on the same cell. So the cell sends a signal to itself. Like when you leave yourself a post-it on the door so you won’t forget to grab your lunch out of the fridge as you’re rushing to the lab. Paracrine: the signal is for the general area. So you send out a message to the people in the general area you are in. Juxtacrine: this is for the person right next to you, so if you pass a note to the person sitting right next to you. One thing that I think is really cool is that induction is not always a one-way path. Cells can induce each other to become certain cell types. When this happens, it is called reciprocal development. Kaplan had a neat example in their book, the lens of the eye and the optic cup induce each other, which is called… reciprocal development. O my gosh, we’re getting so close We are getting close, I promise, really close. I know that embryogenesis is very dense, but the last item I want to cover is fetal circulation. https://tvtropes.org/pmwiki/pmwiki.php/Recap/TheMagicSchoolBusS1E3InsideRalphie We need to know the fetal circulation specifically because fetal circulation works quite a bit differently than adult circulation. After all, the fetus isn’t using its lungs to take in oxygen. It’s getting its oxygen from mom, through the placenta. Remember that mom and baby’s blood is not mixing. We talked about the beginning formation of the placenta in the last episode if you need a quick review. But in the meantime, let’s do a little pop quiz on the topic… Q: Can you remember what extraembryonic structure will form the baby’s portion of the placenta? A: the chorion. Follow up Q: what cells give rise to the chorion? A: trophoblasts. Here’s another question from the last podcast. Q: what extraembryonic membrane surrounds the fetus? A: the amniotic sac, which is full of amniotic fluid. When people say their water broke, its this amniotic sac and the fluid that they are talking about. So the fetus is surrounded by this fluid that acts as an extra protective layer surrounding the fetus. This also means that the fetus isn’t using its lungs to get oxygen. So how is the fetus getting oxygen? From the placenta, from the mom. But how does this work as far as circulation? So you probably remember that your arteries carry oxygenated blood away from your heart and lungs, and veins carry deoxygenated blood back to your heart and lungs. In the fetus, the arteries still carry blood away from the heart, but the blood is not oxygenated because the baby is getting its oxygen from the placenta. So the fetus is getting its oxygen from the fetal vein. okay Oxygenation happens through diffusion. The little oxygen molecules that are on mom’s red blood cells jump ship and hitch a ride on the babies’ red blood cells. This switching from mom’s RBC’s to fetus RBC’s is accomplished with the help of fetal hemoglobin. Fetal hemoglobin has a higher affinity for oxygen. The waste products from baby, such as c02 are diffused the opposite way from fetus to mom. Just to be clear, mom and fetus’s blood does not mix. Diffusion is happening across the placenta. Let’s follow the oxygenated blood from the placenta, and let’s do it magic school bus style. So we are a little red blood cell, and we just picked up some oxygen in the placenta, and we are now catching the umbilical vein and traveling through the umbilical cord. Pop quiz. Q: what two extraembryonic structures form the umbilical cord? A: the yolk sac and allantois From the umbilical cord, we travel towards the liver where some of the oxygenated blood is going to go to the liver to feed it oxygen. Still, we go through a shut called the ductus venus into a large vessel called the inferior vena cava, when we enter the Vena Cava, we bump into some deoxygenated blood returning from delivering blood to the kidney and the legs and get all mixed. We enter into the right atrium of the heart. Remember that blood doesn’t need to go to the lungs for oxygen, so the blood doesn’t need to go to the right ventricle to be pumped into the lungs. To get around this, our red blood cell goes through a shunt called the foramen ovale. The foramen ovale is a short cut from the right atrium to the left atrium. It’s like a secret door that only the people in the know get to use. And by people in the know, I mean the fetuses. This foramen ovale works because of pressure differentials. In the fetus, the right side of the heart has higher pressure; this will change after birth. And the pressure causes a healthy heart to slam that trap door shut, and make it impossible to pull open against the pressure. From the left atrium, we go into the left ventricle and are pumped out through the aorta and dispersed throughout the body. But some of the blood that was in the right atrium went down into the right ventricle, and when the heart pumps, we know that it will send that blood to the lungs. But it doesn’t need to go there to get oxygenated. So the blood that was in the pulmonary arteries can get back on track b going through the ductus arteriosus into the aorta, where it et back on track. It’s like when you take a wrong turn and then take a side road to get back on track. There is also a lot of pressure in the lungs right now, which helps keep blood from flowing there. They are basically squeezed shut. Now we dropped our oxygen off our oxygen and need to make our way back to pick up some more oxygen and get rid of the co2 we picked up, We make our way to the internal iliac arteries and take a right at the Ulta and hop on the umbilical artery expressway headed right towards the placenta. Another thing to note here is that the placenta isn’t resistant at all. The placenta wants the blood to come there and get more oxygen. Overall essential things to remember about fetal circulation: Fetal circulation is not as clean-cut as our circulation, oxygenated, and deoxygenated blood is getting mixed together. Fetal circulation works because of the different pressures. -right atrium high pressure -lungs high pressure -placenta low pressure For pressures, you can substitute in the word resistant. So the lugs are highly resistant to blood flow, and the placenta isn’t resistant to blood flow. The other reason fetal circulation works is because of adaptations Adaptations Umbilical vein – blood from the placenta to liver and ductus venosus. Ductus venosus. – allows blood to go from the vein to the inferior vena cava. Foramen ovale. – blood from the right atrium to the left atrium. Ductus arteriosus. Allows blood to go from the pulmonary artery to the aorta Internal iliac artery – umbilical artery – low resistance. Khan Academy has a great video on fetal circulation is linked in the notes. https://www.youtube.com/watch?v=-IRkisEtzsk Last thing humans are pregnant for 38.5 weeks!!! And then events are further separated into trimesters, which are approx 13 weeks. Vaginal birth is also called parturition and happens because of the hormone oxytocin, which creates uterine smooth muscle contractions. OMG, we are done!!!!! I feel like the last three episodes, female reproduction and embryogenesis episodes are some of the heaviest in the biology section of the MCAT review. Pat your self on the back, We MADE it!! Study hard friends!
32 minutes | Jan 21, 2020
Early Embryogenesis and ‘I Love Lucy’
Let’s talk about fertilization and implantation, and cleavage and morulas, and blastocysts and the trophoblasts and the inner cell mass. And how the inner cell mass gives rise to the bilaminar disk which ultimately gives rise to the germ layers. This episode is dense but has so much good info! buckle up and get ready for embryogenesis!! Early Embryogenesis “Come on, baby. Baby baby baby…” Can anyone name that movie line? It’s Reese Witherspoon in Walk the Line. I really love that movie, and I know you’re all surprised I’m not singing at you. https://www.youtube.com/watch?v=6bR-BPDwdXo I considered doing a rendition of Britney Spears “Hit Me Baby One More Time.” But when I’m animating the word “baby” in my mind, Reese beats Britney to the punch. Hello, everyone, welcome to the Cell-fie Life! Where we are reviewing topics that are covered by the MCAT. My name is Nikaela, and today I’m going to be reviewing embryogenesis. And I’m not going to lie to you; It is complicated. Probably as complex, if not more so, than the female reproductive system But, I mean, come on, does anyone out there expect growing babies to be easy!? But I am going to do my best to break it down and tie it all together. Growing human babies blows my mind. I mean, growing any type of a baby is crazy, but human babies are next level. How cells are this smart to pull off this sorcery (like witch fingers and bunny ears) is just another reason that I love science. Science is so cool. Let’s jump in and start with the basics. What is embryogenesis!? Embryogenesis is the formation and development of the embryo in the first eight weeks after fertilization. And it is kind of a whirlwind of mitotic activity and cell differentiation, which makes sense because you are taking a single-celled organism and turning it into an organism that is developing brains and intestines and limbs and eyelashes. Okay, let’s be honest: At the end of embryogenesis, it’s basically a ball of cells with tubes, but they will develop into the guts and brains and limbs and all that stuff. So, without further ado, let’s get into embryogenesis. Actually, there is some more ado…. This episode may contain some sexual health material. But it’s really more of a review of embryogenesis, but there might be some flashback material. Okay, pop quiz time. You didn’t know that you would be starting this episode with a pop quiz, did you!? It’s okay; this is one pop quiz you’re gonna ace because I’m grading, and I make the rules. Question 1: Q: A spike in what hormones causes ovulation? A: LH and FSH. Follow up: Q: Which surge point, LH and FSH, was highest, and why? A: The LH surge was higher because the inhibin being produced is already inhibiting FSH. Okay, so ovulation of a secondary oocyte has occurred. Like just occurred… Q: …and the egg is arrested right now in what phase? A: Metaphase II. If you’re having any trouble with these concepts, just use it as an informative experience that is showing you where you can improve. You can just go back and give the last few episodes a listen for a helpful review. Okay, back to the egg. The egg has been swept up by the fimbriae. It is now in the fallopian tube, minding its own business, hanging out in the ampulla, which is the widest part of the fallopian tube, and a common spot for fertilization. And along comes this sperm. Now egg cells are about 10,000 times larger than the sperm. So there is a considerable size difference. And this is where the real magic happens. And by “real” magic, I mean science. Do you remember that part of the sperm that I called the beanie? It’s on the top of the sperm head? The acrosome. When the acrosome binds to the oocyte, it releases some special enzymes that allow it to penetrate the corona radiata and zona pellucida. This first sperm to the egg creates a specialized tube, called the acrosomal apparatus, which penetrates the cell membrane so that the pronucleus can enter the oocyte once the oocyte has completed meiosis II. So basically, it needs a tunnel, to deliver its unique genetic material. Let’s be honest, right here I imagine the sperm is basically using its penis to put its genetic material into the egg. After you have sex, the egg and sperm basically have to do the same song and dance. So, the penis, in this case, is this acrosomal apparatus. After the sperm has penetrated the membrane, something called a cortical reaction happens. Now, a few more root words for you here because you know that I love root words. Anyway! Corico- actually means “bark,” like the bark of a tree, or shell, in Latin. So, the cortical reaction is what happens when the sperm gets through the shell of the egg. Q: Which would be what two layers from the external to the internal? A: Corona Radiata, zona pellucida. There are other layers, but these seem to be the ones we need to be familiar with for the general anatomy and physiology on the MCAT. I don’t know if you’ve seen the illustrated images of the egg cell, but, to me, the egg cell always kinda looked like the sun drawings I did in elementary school with all the rays coming off and wearing the sunglasses and smiling. The rays that are sticking out are the corona radiata. Radiata means “spoke” and/or “ray” in Latin. And it is just the cell’s crown; the name paints an image in my brain. So when you hear “corona radiata,” think of those elementary-school-kid drawings of suns. This image will also help you keep the layers straight since those rays are on the outside. And the corona radiata is the outside layer. Back to the cortical reaction: the cortical reaction is pretty cool. A bunch of calcium is released, which depolarizes the membrane of the ovum. A quick reminder that depolarization is when there is an electrical shift within the cell. So basically, all of this calcium, which has a positive charge, is released from pockets, and the cell becomes less negative because all of this positive calcium was released. This reaction prevents polyspermy, which just means fertilization by multiple sperm. The increased calcium also increases the metabolic rate of this new little zygote. And now this zygote needs to implant in the uterus; or baby box, if you will. But, there are a few things that happen to the zygote as it travels from the ampulla to the uterus. The zygote will start undergoing rapid mitotic division, without growth, which is known as cleavage. Once this cleavage starts, the zygote can now officially be called an embryo! Cleavage is splitting without growth. Cleavage happens in the embryo because it has to divide so fast, it doesn’t have time to grow. So the embryo is doing all of these quick cleavages. There are two types of cleavage: indeterminate cleavage and determinate cleavage. This difference is completely contained in the names. Determinate cleavage means, essentially, that the cells’ fates are set. These cells differentiate into already determined types of cells. Indeterminate cleavage means that the cells can still develop into complete organisms. In fact, this is how you can get monozygotic twins. Monozygotic meaning one zygote is formed, and then it is split, so there are going to be identical twins. So monozygotic twins are one egg fertilized by one sperm that then splits and implants. Get it? Monozygotic—one zygote. Does anyone know another type of twins? I know a smart alek out there said non-identical twins, which is correct, but doctors call this dizygotic or fraternal twins. Dizygotic because two different eggs are fertilized by two different sperm, thus two zygotes. So if you are a dizygotic twin, you share no more genetic information than regular siblings share. Back to the embryo… Once the embryo has divided 16 times, it really starts to look like a mulberry, and it’s called a morula; I’m gonna be honest here, I know that this stage is called a morula because it looks like a mulberry, but I didn’t know what a mulberry looked like, so I googled it. A mulberry seems like a mix between a raspberry and blackberry. It was kind of freakishly long. But even with these pinky-length berries, I now want to try something with mulberry in it. So if any of you have a good mulberry recommendation, shoot it my way. But really. Send me some recipes. Pic taken from https://www.froghollow.com/products/2020-mulberry-madness-organic-fruit-club-4-shipments After a morula forms, the little berry now goes through what is called blastulation to form a blastula. For me, I think of a blastula like one of those old school gumballs that are hollow on the inside. So a blastula is a hollow ball of cells with fluid on the inside. The inner cavity is called a blastocoel. Coel—C-O-E-L—means “hollow” in Greek. So a blastocoel means “hollow bud.” Which is precisely what this little guy is: a hollow bud. Also, you could just think of it as a blasted out cell. Really quick, we’re going to run down the list of stages and names, from zygote to blastula. Zygote. Embryo. Morula. Blastula. And after blastula, we have the blastocyst. The blastula is the hollow ball, and the blastocyst is what it’s called once a few different layers have formed: trophoblasts and inner cell mass. The trophoblasts are on the outside, and the cluster of cells on the inside are the inner cell mass. One more time, the cells that make up the outside, or the gum part, if we are sticking with the gumball analogy, are the outside layer, which is called the trophoblast. The trophoblast is the outer layer that surrounds the blastocoel. Tropho means “nourish,” like with food, in Greek, which makes sense because this outer layer will become part of the placenta, which is needed to nourish the growing fetus. Also, tropho kinda sounds like a “trough,” the things that you use to feed the animals. That should help you remember this outer layer. There is another important small clump of cells on the inside called the inner cell mass. The inner cell mass cells have clustered so tight together that they leave a cavity on the other end. It’s like when you are trying to catch baby animals, and they all cluster away from you. We’re going to use puppies in this scenario. Actually, puppies might not be a good example. My dog Banana Joe always wants to be touched and held and just walked right up to us as a puppy… ummmm…let’s go with bunnies! Imagine this: You walk into a circular enclosure, the fence on the outside is the trophoblasts, and the bunnies that are huddling on the other side, cowering from you, are the inner cell mass and you are hanging out in the hollow area which is called the blastocoel. So now, this is no longer looking like a mulberry and is no longer just a hollow shell of cells. It has graduated from a blastula to a blastocyst. I put a stick figure drawing of this in the notes, if you need an extra visual and/or want to see how terrible my stick figure drawings are. I forgot to mention at the beginning that the script notes can be found on the website: CellfieLife.com. So, as you walk towards the bunnies, they fan out, and now there’s a layer of bunnies in front of you, to the sides of you, and behind you. They have formed a new cavity with you in the middle of this new cavity. This new cavity is called the amniotic cavity. Does this make sense? I might have run this bunny scenario into the ground. Okay. Imagine this: You have a circle, there is a line that cuts halfway across the circle and lines the inside of half this circle. The inner cell mass has hollowed out, so now there are two hollow areas. The one that is lined by the inner cell mass is now called the amniotic cavity, and the other cavity is still called the blastocoel. The inner cell mass differentiates even more, and the cells closest to the blastocoel side are called hypoblasts, and the cells right above it are called epiblasts. That’s kind of a lot, so let’s run through that one more time. You have a ball of cells, and we are going to look at a cross-section of it. So we are looking at a circle. Let’s draw this circle in black. You split the circle in half with a red line and outline the inside of the top half of that circle in pink. Underneath your pink line that divides the diameter of the circle is that red line you drew. The red line is called the hypoblast, and the pink line on top of the redline is called the epiblast. So we have two hollow areas inside our circle. The hollow bottom area that is cut in half by a red line is the blastocoel, with that red line being the hypoblast layer. The other hollow space is on top, and is outlined in pink. This is the amniotic cavity. You guys, super boiled down, it’s a circle that has two layers down the middle — the hypoblast and epiblast. The hypoblast and epiblast layers came from the inner cell mass. The hypoblast and epiblast layers are the bilaminar disk because this is what will give rise to the three germ layers, which will form the entire tiny human. The top layer, epiblast. Epi, over. The bottom layer, hypoblast. Hypo, under. This is the bilaminar disk. The bilaminar disk is like a stack of two pancakes that are perma-stuck together, and then you pour one line of maple syrup on the top pancake. You start just before the midpoint and draw the line to the edge so that the line is not quite half the diameter of your pancakes. This weird little streak thing happens along the middle of the epiblast layer. This is called the primitive streak. Which, come on, is kind of a great name. A primitive streak. It’s not in Latin or Greek. It’s basic and one of the primary steps in development. This primitive streak marks the beginning of gastrulation. Image from: https://www.researchgate.net/figure/Cell-migration-over-the-primitive-streak-during-gastrulation-in-higher-vertebrates_fig1_257852243 Okay, here’s what I’m going to do, I’m going to do a quick outline of gastrulation and neurulation so that you can get a big picture. Don’t worry; I will go into more depth. But I think a general outline here is helpful because embryogenesis can be a little dense. The primitive streak marks the area where the epiblast cells start moving. The cells along the primitive streak burrow down in between the epiblast and hypoblast layers, differentiating until there are three layers. This formation of three layers is called gastrulation. Now there are three layers, and these three layers are called “germ layers.” Okay, we had two layers that were the bilaminar disk, and now we have three layers, the trilaminar disk, the germ layers, the top is the ectoderm, the middle is the mesoderm, and the bottom is the endoderm. Knowing these three layers is essential. They always seem to pop up on the practice MCAT questions. And doctors need to know this, so these will be important to know. Again, right now, we are just doing a general overview. After gastrulation, we have neurulation. We are going to start with our three layers: What are the three layers? Do you remember? I know I said them, like, four seconds ago, but let’s name them from top to bottom, just for the review. Ectoderm is the top. Mesoderm is the middle. Endoderm is the bottom layer. To me, they always looked like a hamburger when the professors were drawing them out. The top bun is the ectoderm, the mesoderm is the patty, and the endoderm is the bottom bun. Neurulation starts in the middle of the hamburger patty. So in the middle of the middle, a.k.a. the middle of the mesoderm. There starts to be some differentiation of these cells; this little knot of cells is called the notochord. So let’s remember that the notochord happens in the very middle of the middle — the notochord forms in the center of the mesoderm. The formation of the notochord is vital because it causes a change in the ectoderm, which ultimately results in the neural tube. In the notes, I have a link for a YouTube video I found helpful. https://www.youtube.com/watch?v=dAOWQC-OBv0 I wanted to introduce you to neurulation, but we are going to pause there. We will come back to, though. Because all of this is great, but none of these layer differentiations can happen if the embryo doesn’t implant into the endometrial lining of the uterus. Q: Do you know at what stage the embryo is in when implantation occurs? A: A blastocyst is implanted into the endometrial lining. Let’s go into some detail about this. The endometrial lining is proliferating and building up in preparation for the implantation of an embryo. So the embryo is bouncing around and ends up in a valley in the endometrial lining, where it burrows in; kinda like at the end of a really long day (a.k.a. my yesterday), and you climb in bed and burrow into the blankets, and it is just the best feeling. Ever. This is how I picture the little blastocyst; just really trying to burrow in and find the comfiest spot. Q: Now, do you remember what was the outermost layer of the blastocyst is called? A: The trophoblast. The blastocyst has shed the zona pellucida before it implants. The trophoblast cells give rise to the chorion, which develops into the placenta. Now, this next part I’ve always thought is really cool: The trophoblasts form these finger-like projections called the chorionic villi. These chorionic villi are projections into the endometrium. I always think of it as clawing with like really long crooked witches fingers. The chronic villi aren’t witches fingers, but they’re really digging into the endometrium, and these microscopic projections are what will support the maternal-fetal gas exchange. So these fingers are in the endometrial lining, and they are finding uterine blood and are joining up with them. There is no direct exchange; a thin layer of trophoblasts will separate the fetal blood from maternal blood. The trophoblast implants and sends out these finger-like projections that will support the maternal-fetal gas exchange. It will continue to grow until it takes up most of the uterus, and it is called the placenta. While the placenta is still growing, the embryo is supported by the yolk sac. But let’s rewind a little and talk about Mama. What’s going on with Mama right now? What are her hormones up to? Now, maybe you’ll remember that in the female reproductive episode, we talked about the corpus luteum, which is what the ova’s house is called after the ova has been ovulated. It’s what’s left behind after the egg has left the ovary. Remember, the corpus luteum releases a bunch of hormones. I was going to tell you what these hormones are, but I feel like this is a great pop quiz question. Q: What are the three hormones the corpus luteum releases? A: Progesterone, inhibin, and estrogen. Follow up question: What does each of these hormones do? I know one of you is like, they do a plethora of things, but what do these hormones do concerning the uterus? Progesterone. Progesterone is the pro-gestation hormone, so it is maintaining the uterus for implantation. Progesterone is hoping for a little embryo. The high levels of progesterone also cause a negative feedback loop with the brain’s hormones. Inhibin. Inhibin inhibits FSH so that the body is investing in the egg it has in production and not getting ahead of itself and working on multiple eggs at once. It’s not like a factory conveyor belt. I think of that I Love Lucy episode, the one where she is shoving the chocolate in her face and can’t keep up with the conveyor belt. No, this system is quality over quantity. It wants to give all the attention to one egg at a time. (There are exceptions, a.k.a. multiple births, but you get what I’m saying.) Basically, what I’m getting at is that inhibin is one of the hormones that make this possible. If inhibin were to talk, it would say, “Hey, let’s focus on finishing this one project before we move on to another project.” https://www.youtube.com/watch?v=_y0nsN4px10 Finally, estrogen. Estrogen helps regenerate the uterus after menses. But, in this case, the egg was fertilized, and the blastocyst is going to implant into the uterus. So, what needs to happen with mom’s hormones? The blastocyst will implant and secrete human chorionic gonadotropin (hCG); that chorionic sound a little familiar? It should remember how the chorionic villi stretch out their fingers and weave their way in to set up the placenta? This chorionic development is one of the first things that the newly implanted embryo does, so it makes sense that it also releases human chorionic gonadotropin, hCG. See, it’s not too bad! It all fits together! hCG is very chemically, similar to LH. It’s so similar that it can actually stimulate the LH receptors, and the corpus luteum is maintained. Instead of the corpus luteum dying off, and the levels of hormones decreasing, until the GnRH once again starts the FSH and LH cycle over, the corpus luteum is maintained by the hCG. So once you get pregnant, the corpus luteum hangs out for a little bit because the embryo is like, “Hey, hey you. You should stick around for a minute. I’ll give you this hCG,” and the corpus luteum is like, “Might as well.” And since the corpus luteum is sticking around, it does its thing, the “thing” being releasing hormones. The corpus luteum keeps releasing estrogen and progesterone. So the hCG is critical because it keeps the corpus luteum around, and the corpus luteum releases progesterone and estrogen, which maintain the uterine lining so that it is not sloughed off, a.k.a. no period. By the second trimester, the placenta is large enough that it can take over the progesterone and estrogen, so the hCG levels decline. These high levels of estrogen and progesterone that are being secreted by the placenta now are high enough to take care of the negative feedback loop so that gonadotropin-releasing hormone (GnRH) is still inhibited. Also, please note that the placenta is releasing hormones, which makes it an endocrine organ. Side note: Have you guys heard of the hCG diet? People take hCG and then are on a super low-calorie diet. I’ve heard that if they take a pregnancy test while on the diet, the pregnancy test will come back positive because a lot of pregnancy tests are looking for the presence of hCG. Quiz question: By the time that the blastocyst is ready to implant, the endometrial lining will be under the influence of what hormone? A: Progesterone. Follow up question: What is producing the progesterone? A: The corpus luteum. Q: What phase is the endometrium in? Remember, the endometrium has those three stages? A: If progesterone is the primary hormone, we know that we are in the secretory phase. You guys are freaking brilliant! If you were stuck, it’s all good. Go give the female reproductive podcast another listen for a refresher. Okay, now let’s go back to the embryo before I took us down that hormonal memory lane. We were talking about how, until the placenta is up and producing enough estrogen and progesterone, that the yolk sac is what supports the embryo. The placenta is the most important extraembryonic structure, but there are other important structures, especially in the early phases, when the placenta has not yet fully developed. So what are these extraembryonic membranes? And what do they do? Also, they are called “extra”-embryonic membranes, so other than the embryo, what else is there? Let’s put our embryo in the middle. The first layer that surrounds it is called the amnion, and it contains the amniotic fluid. Amnion is the extraembryonic membrane that surrounds the developing embryo. The amnion is filled with fluid, and its main job is to serve as a shock absorber. It also helps regulate temperature. It is just a protective layer—think bubble boy. The baby can inhale and exhale this fluid, but it does not get any oxygen from it. Here’s a thought for you: The waste products from the little embryo are also excreted into the fluid. So the fluid is just circulating… So this amnion layer starts in early development surrounding the embryo. The embryo right now is more of a bean shape with the indent being about at the embryo’s belly button. Okay so picture this: You have a bean. From the bean’s belly button, there is a sac that completely surrounds and envelops the embryo. But there are also two other structures that stick out, and at this early stage in the drawings, they kind of look like bunny ears. These are the yolk sac and the allantois. A-lan-to-is. One more time: You have a bean that is surrounded by a bubble that meets at the bean’s belly button. At the belly button, you also have two bunny ears sticking out. These “bunny ears” are the yolk sac and the allantois. The yolk sac doesn’t have a huge role, but a really cool fact about the yolk sac (that I don’t think we need to know for the MCAT, but you’ll need in med school) is the fact that the yolk sac will form the embryos first red blood cells. It’s the yolk sac, then the liver, then the bone marrow. The other structure is the allantois. The allantois and yolk sac will form the umbilical cord. The allantois is involved in the early fluid exchange between the yolk sac and the embryo. The fourth and final of the extraembryonic membrane is the chorion, which surrounds the entire system and has some folds, or villi, which result in extra surface area. These villi ultimately absorb nutrients from the endometrium. Can you guys remember what villi we mentioned earlier? So on one side, we have the chorionic villi, which are going to be the embryonic portion of the placenta, and the other side is just called the chorion. Okay, let’s go over that one more time, from the embryo out. Surrounding the embryo is the amnion. Then we have the yolk sac and allantois. Ultimately, remnants of the yolk sac and allantois will form the umbilical cord, but mostly the allantois. Then surrounding the entire thing is the chorion. The chorionic villi form the embryonic portion of the placenta. So how do I remember the allantois? It kind of sounds like Atlantis. You know, Plato’s lost island, the one that sank in a-day-and-a-night around 9,600 BCE and nobody knows if it was real or a metaphor? Anyway, that island, Atlantis, is wasted. The allantois will remove waste from the embryo—waste like CO2—and it does this through the umbilical cord, which was formed by the allantois. Okay, this episode is getting longer than I wanted, so I’m going to split this episode into two. I’ll call this episode early embryogenesis, and in the next episode, we will finish up the embryogenesis review. In this episode, we talked about fertilization and the cortical reaction, types of twins, the zygote, morula, blastula, and blastocoel. We also reviewed the development of the bilaminar disk and outlined what will be covered in gastrulation and neurulation. Friends, thanks for listening! Please rate, review, subscribe, and tell your fellow want-to-be doctor friends about this podcast. You can follow me on Instagram @thiscellfielife and check out the script notes on the website, CellfieLife.com. Do me a favor and practice some self-love and schedule a nap in your near future. And when you are getting all snuggled in, just be like, “I am a blastocyst getting all sorts of cozy.” Study hard, friends! Byeeeeee! Hit me, baby, one more time https://www.youtube.com/watch?v=C-u5WLJ9Yk4
40 minutes | Jan 14, 2020
Female Reproductive System – Let’s talk about sex
**This episode contains sexual health material** https://www.youtube.com/watch?v=3KL9mRus19o Let’s Talk About Sex: Female Reproductive System Okay, hold up—I know the perfect song for this episode. Awkwafina’s “My Vag”. I like the way you work it…no diggity, got to bag it up. “My vag like an operatic ballad Yo vag like Grandpa’s cabbage” Let’s be perfectly honest about a few things: One, I can’t sing, and two, there is no way I could do this song justice, so do me a favor. Pause this podcast, go and listen to Awkwafina’s song “My Vag”, then hit play on this podcast. And if that song doesn’t get you seriously excited to learn about the female reproductive system, then listen to it again. And don’t “at” me about a vag song because there are so many songs about penises. https://www.youtube.com/watch?v=z726OPwCnjE Maybe I should mention that this episode does have sexual health material—so this is your warning. We’re gonna be talking about vagina’s and periods and all of those hormones that make it all happen. Welcome to the Cell-fie Life. This is Nikaela and I wanted to thank you, so much, for listening. If you have questions or comments or corrections, please let me know. The best way to reach me is either the website CellfieLife.com or on Insta @thiscellfielife. You guys subscribe to this podcast. Just hit that little button and then you will get the latest episode automatically. There really is no downside to subscribing. Seriously. Are you guys ready for this? You all know that females have a complicated reproductive system and it’s cause we can grow new humans. New humans. That is just crazy to me. So take a deep breath and dive in. Last note before we begin in earnest. This episode is about biological sex and not gender expression. Okay, now, let’s talk about the ladies, which are hella-complicated, but we can get this all sorted. The major reproductive organs for females include the ovaries, which are homologous to the testes, meaning they came from the same precursor during development. The ovaries are where the ova, a.k.a. the gametes are produced. Then there’s the uterus. Or, as I like to call it sometimes, the baby box. But we’re being science-y here, so it’s “the uterus”. The uterus is where a viable progeny develops. I say “viable” because ectopic pregnancies are pregnancies where implantation happens outside the uterus. This is super dangerous for mothers if not caught in time. And finally, breasts are also included in reproductive organs; breasts because of lactation. So these are all included in the reproductive system along with the brain. Because as we learned from the last episode, sex starts in the brain. Q: Do you remember what part of the brain releases gonadotropin-releasing hormone? A: The hypothalamus. Do you remember where the GnRH travels to and acts upon? A: The anterior pituitary. Nice job, you guys are so smart, you should all be doctors! If you missed those questions, no worries. We will review them in, like, 30 seconds; you could also review the last episode which goes over the male reproductive system. The ovaries produce some major female hormones, like estrogen and progesterone. Estrogen is also responsible for the secondary sex characteristics, such as breast development and the widening of the hips. But just as in males, it all starts in the brain. The hypothalamus regulates the hormones released by the anterior pituitary through the portal blood that travels from the hypothalamus to the anterior pituitary. Just like in males, the hormones that are released from the hypothalamus is gonadotropin-releasing hormone, GnRH. The GnRH runs up to the anterior pituitary and tells it to release the luteinizing hormones, LH, and follicle-stimulating hormone, FSH. Hell, yes! Those are the exact same hormones that are released in male brains. I love it when I go to learn something and I’m like, “Wait a second. I already know and understand that because I learned all about it, over there!” (“Over there” is the podcast that talked about the male reproductive system.) The hormones FSH and LH travel through the blood to the ovaries. We are going to pause there for a minute with the hormones, and we are going to do a broad overview of meiosis in females to really get a general idea about the different aspects of meiosis, a.k.a. ova development and the ovarian cycle. Let’s start with the specifics of female meiosis. There are some very big differences between males and females. (I can hear all of you that just said, “Duh…”) First, females do not have the same unending supply of stem cells as men do in spermatogonia. Females have ALL their eggs, at birth. The ovaries created the eggs during Baby Girl’s gestation, and the eggs just remain in an inactive state until puberty. The production of female gametes, eggs, is called oogenesis. Q: Do you remember what the production of males gametes was called? A: Spermatogenesis. The double “oo-” thing you will see is because “oo-”…I don’t know how to pronounce it, but the “oo-” means “egg” in Greek. So the word oogenesis literally means “egg birth”. Early in uterine development, the precursor germ cell is called an oogonium. (Sound familiar? Remember, the male germ cell is spermatogonium.) Anyway! The oogonia undergo a ton of mitotic division to make loads of themselves. At around seven months, the division stops, and this is the egg supply that the baby girl will have for the rest of her life. But there are actually a ton of them, anywhere from two to four million. Which would be a ton of babies. So females have all their eggs at birth, and all the eggs have already gone through interphase and replicated their DNA and entered meiosis I. The eggs are really just hanging out as primary oocytes. They have started meiosis but have stopped immediately in the first stage of meiosis I. Q: What is the first stage of meiosis I? A: prophase I. So these cells are in meiotic arrest. Meiosis has been stopped—arrested. So when a baby girl is born, her eggs will be in meiotic arrest in prophase I until she enters puberty and has her first period, which is called menarche (men-arch-EI). I actually didn’t know that was the name of your first period until I started fact-checking this episode. I didn’t mention this in the last episode, but biological sex is determined by the 23rd pair of chromosomes. Males have XY chromosomes and females have the XX chromosomes. So ova only carry the X chromosome and sperm can carry the X or Y. Which I find slightly vindictive because back in the day women were blamed for having girls and then—BAM!—science is like, “Yeah, no, that’s on you sperm donors…” And I’m pretty sure all the ladies that were ever harassed for having daughters just felt so vindicated when they got to heaven and were like, “Ya, no dudes, that’s on you!” So every month, one primary oocyte will complete meiosis I and become a secondary oocyte. This is what gets ovulated. (This is a side note that I googled to learn: Meiosis I isn’t completed until the day before ovulation.) Now you have listened to episode 1 and have meiosis down and you are like, hold up: One 2n cell splits into two n cells with meiosis I. Which is true. But in females, one of the cells gets all the cytoplasm and the other is called a polar body. The polar bodies just wither up and die because they didn’t get any of that cytoplasm. We are basically putting all of our eggs in one basket, or all of our cytoplasm in one ova. So every month, one primary oocyte will complete meiosis I and become a secondary oocyte. This is what gets ovulated. Along with the secondary oocyte, a polar body is produced. With each round of meiosis, one polar body is produced. Which leaves our end count at one ova and two polar bodies discarded. Q: Were you paying attention? What stage is the egg in when it gets ovulated? A: A secondary oocyte is ovulated. The secondary oocyte then pauses in metaphase II and will not complete meiosis II unless fertilized. So, the egg is just hanging out, in the fallopian tubes and—for kicks and giggles—let’s say that the egg is fertilized. Sperm has managed to penetrate the zona pellucida and corona radiata, which are layers that surround the egg. This triggers meiosis II to proceed forward to an ovum and a polar body. The ovum is successfully fertilized and is now a zygote. I know that was kinda thick so let’s do a review/questions. Q: What phase is are all oocytes arrested in until they are chosen to mature during an ovarian cycle? A: prophase I. Q: What specific phase is an ovulated egg arrested in? A: metaphase II. Q: When will an oocyte undergo meiosis II? A: not until a sperm cell penetrates the zona pellucida and corona radiata. You guys might be thinking, “The zona whats’a and a beer?” So the corona radiata and zona pellucida are just layers that surround the egg, and the acrosome fusing sets off enzymatic reactions that help the nucleus of the sperm get through the layers to the nucleus of the cell. This reaction is what signals meiosis II to finish. How are we gonna remember what phase the ova get arrested in? Okay. Arrested in meiosis I in prophase I; arrested in meiosis II in metaphase II. I remember this because prophase is the FIRST phase so meiosis I; so, the primary oocyte is arrested in the primary phase of meiosis. And in meiosis II it is hanging out in metaphase II which is the second phase of meiosis. If you don’t remember this, give episode 1 another listen. ***insert oogenesis flow chart Now let’s talk about the path the egg takes from the ovary to the uterus. In my opinion, the egg’s path is a simpler path than the sperm takes in males. So we don’t really need a terribly awesome roller coaster analogy to remember this pathway. The ovary actually releases the egg into the abdominal cavity and the oocyte will get pulled in by the fimbriae, which are just beating cilia, and travel through the fallopian tube. The fallopian tubes are where eggs often get fertilized. Then the egg continues to the uterus. This is where the fertilized egg should implant. From the uterus, there is the cervix, that separates the uterus from the vagina. Then the vagina is where the sperm are often deposited. Phew, you guys got that!? You’re doing great. Now let’s take a look inside the ovaries. Remember, the oocytes are hanging out as primary oocytes, arrested in prophase I of meiosis. Actually, before we start that, let’s do a broad overview of an ovarian cycle. Each month an egg goes through a maturation process. This cycle creates the secondary oocyte that can then be fertilized by a sperm, and if all of these exact processes happen—ta da!—BABY! This ovarian cycle is responsible for the menstrual cycle. So we will look at them in tandem. It is also important to remember that fluctuations in female sex hormones, released from the ovaries, control the development of the egg and the menstrual cycle. The main sex hormones released from the ovaries are estrogen, progesterone, and inhibin. Q: Do you remember what major sex hormones the testes make? A: Testosterone. Q: Do you remember what cells make testosterone? A: Interstitial cells of Leydig, which creates secondary sex characteristics like bigger muscles, which is why they are so good at digging holes. Okay, let’s start with a broad overview of the ovarian cycle. Cycles are approximately 28 days long, and day one is the first day of menstruation. Day one through day 14 is called the follicular phase. Ovulation happens on day 14. So, halfway through the cycle, ovulation occurs. Day 15 through 28 is the luteal phase. We will be going into more detail, but I think that having a broad picture going in is helpful. It’s a basic bell curve, going up its the follicular phase. At the top in the middle is day 14—ovulation—and going down the other side of the curve is the luteal phase. ** inset bell curve pic So first I need you to picture an American football or rugby ball. They are round but have those pointy-ish ends. You are holding this ball out in front of you with the pointy ends out horizontally so they are lining up with the earth. The pointy ends run left to right in front of your face. Or a lemon—you know, for those of you that are totally like, “That’s the sport that has a ball, right?” Now, this is the shape of an ovary (roughly). Starting with the point on the right as day one and tracing the outside of the ball, going counter-clockwise, over the top to the other point. This other point is day 14. Now continue around the ball going counterclockwise, along the bottom, back to the point on the right. Back to day one. In a full circle. Or, you know, a cycle! Having this imagery really helps me in understanding where we are at in the ovary, on each day, which translates to having an understanding of what hormones are increasing, decreasing, spiking, etc. *insert pic of football/lemon cycle Now let’s follow one of these eggs through to ovulation and see what happens. In the ovaries, females have a ton of these primordial follicles, and primordial follicles are the most immature stage of an ovarian follicle’s development. It’s the oocyte that is surrounded by a single layer of cells. And for me, when I hear primordial follicle, I’m thinking old-school Jurassic Park. Like the first Jurassic Park, with Jeff Goldbloom, here they watch the egg hatch at the beginning. “Life, uh, finds a way” All of this imagery really helps me remember that the most basic stage of egg development is called a primordial follicle. Come on, they named it primordial, which, yes, makes sense since it means giving origin to something. But all I can think of is dinos. “Clever girl.” Okay, I’ll stop. But I’m gonna watch that movie tonight and I’m gonna link the egg hatching scene in the script notes. You’re welcome. https://www.youtube.com/watch?v=zP2m95JAD4g Inside the ovaries, eggs develop in follicles. (Follicular phase is starting to make sense, huh?) So, day one, we are looking at the ball in front of us. We are focusing on the pointy end on our right. We are calling this “day one”. Day one, a follicle is one egg surrounded by a layer of granulosa cells. Remember granulosa cells. They are very important and we will talk about them more, but the granulosa cells become more and more numerous as the follicle matures. I like to think of this follicle starting out on the right side and moving slowly counterclockwise to the other point. During this time, the granulosa cells increase and get larger. The granulosa cells are responsible for some of the sex hormones, specifically estrogen (which we will go into the detail of). So thinking of the number of cells increasing over the next 13 days, what would you expect to happen? You would expect the hormones that the granulosa cells make to increase, more cells equal more hormones. So while the oocyte is progressing towards day 14 and getting more granulosa cells and growing in size, it’s making more and more estrogen. During this progression of the follicular phase, there is a layer that develops between the granulosa cells and the oocyte. This layer is the zona pellucida. (Wait a second, that sounds familiar!? Remember the zona pellucida is one of the layers that surround the cell that the sperm has to penetrate.) I say that, and then I hear Fat Amy say, “Not a good enough reason to use the word penetrate.” Even though there is now this wall—the zona pellucida—that separates the egg from the granulosa cells, the granulosa cells can still nourish the egg through gap junctions. So it’s a wall that has all these gateways that are open. The egg at this point is still stuck in meiotic arrest; it hasn’t completed meiosis I yet. Q: Do you remember what phase of meiosis the egg is stuck in right now? A: Prophase I! You all got that right, didn’t you!! If not, don’t worry about it. You will pick that detail up on your next listen of this episode. Q: For those of you that have already listened to episode 1 on meiosis, how many chromosomes does the egg have at this phase? The egg is in meiotic arrest (kinda like house arrest) in prophase I, so how many chromosomes? A: 46 chromosomes. Q: How many sister chromatids? A: 92!!! If you just got that without even stressing a hair, I am legit proud of you, and you should probably buy yourself a cookie. If you didn’t get it, or if it took you a little longer than it should, don’t sweat it. Buy yourself a cookie and listen to episode 1 to freshen up on the details of meiosis. If you guys haven’t noticed by now, I am really going to try and build and pull information from previous episodes into the new episodes so that we are repeating everything and really building those connections. Okay, back to the ovary. We are in the follicle and we have granulosa cells that all around and increasing in number, and we also have a layer separating the granulosa cells from the egg, but it has gap junctions so that the egg and the granulosa cells can still chat through hormones, and the egg is still stuck it prophase I of meiosis I. Now, another layer starts to form around the outside of the granulosa cells. These cells are called theca cells. Theca cells are important because they have receptors for luteinizing hormone, which is the hormone that is released from the anterior pituitary. Starting from the outside of this follicle, working our way in, let’s go over the layers, as of right now. The outermost layer is the theca cells, then the granulosa cells, then the zona pellucida, then the egg. Once the luteinizing hormone from the anterior pituitary binds the theca cells, the theca cells produce a hormone called androstenedione. Once the theca cells make the androstenedione, they hand it to the granulosa cells who convert the androstenedione into estrogen. Legit what came to my mind when I was researching this: Have you seen that otter meme? It’s super old. But it’s an otter holding up a baby otter and there are the words, “I MAED DIS”. This is how I aced my classes, converting complex science principles to memes and gifs. And I kinda picture the theca cells holding out the androstenedione to the granulosa cells being like, “I MAED DIS”. And, obviously, in my mind, the granulosa cells reply, and they pat the little otter on the head like you would a child, and they say, “Oh, that’s so nice, I love it.” And then they take the androstenedione and make it into something usable—estrogen. Then they release the estrogen levels into the blood. So the blood estrogen levels start to go up; estrogen will increase until ovulation and then drop slightly. Eventually, at around day 14 the follicle is so large that it presses up against the edge of the ovary and the egg ruptures out with the help of some enzymes, leaving behind its house of granulosa cells. Now, normally only one egg develops to the point of rupturing out of the ovary, even though several start along the path. The one that makes it and is ovulated is called the dominant follicle. If you have a few eggs that all make it and are ovulated, you have one way to get twins or multiple births. So the egg has left the follicle and ovary behind and is getting swept up by the fibrae and taking its own journey. But what happens to the house that was left behind? All those granulosa cells? Just really quick, for reference, we just passed day 14, so if we are looking at that football (or lemon), we went from the point on the right, counter-clockwise, to the point on the left (day 14) and the egg was expelled from the ovary. Now we are continuing our cycle, counter-clockwise, back to day one. The follicle that expelled the egg now transforms itself into a structure called the corpus luteum. Which is basically a dead follicle. I mean it’s called a “corpus”. The corpus luteum secretes three hormones: estrogen, inhibin, and progesterone. Let’s delve in! The corpus luteum is like when you move out of your parents’ house and your entire life they went to bed at 10. And you go home for a surprise visit and arrive at 11 thinking they are going to be asleep, but instead they are having a pool party with all the neighbors and your house is really just not the same. This is basically what happens. The egg is out and the follicle becomes the corpus luteum. (Luteum, as in luteal phase—sound familiar?) In this new house, the granulosa cells actually get a lot bigger and continue producing estrogen, but the corpus luteum really starts pumping out progesterone and some inhibin. Some progesterone and inhibin is produced during the follicular phase, but a lot is produced in the luteal. Estrogen will increase until ovulation and then drop slightly. Inhibin is present after ovulation and will increase after ovulation because of the corpus luteum. Progesterone levels were low until after the ovulation and will continue to increase after ovulation, during the luteal phase. So on day 21 of the female reproductive cycle, progesterone is increasing, inhibin is increasing. Inhibin inhibits, so it will inhibit the secretion of FSH. We are in the luteal phase; we don’t need any more follicles stimulated. We don’t need any more eggs to mature just yet. Inhibin lowers the amount of FSH—follicle-stimulating hormone—that is released from the anterior pituitary. Which, if think about the words, is literally telling you what it does, and it makes sense. Follicle-stimulating hormone stimulates the follicles to develop and mature. But when we are in the second phase of the cycle, the luteal phase, we don’t want follicles stimulated. We don’t want eggs to keep developing. So when the follicle becomes the corpus luteum, it starts producing inhibin to inhibit the FSH so that follicle growth isn’t stimulated. Nifty little system, right? Women’s hormones and cycles can look like a lot at first glance, but I have found if I really understand what is at play, they aren’t as terrible as that graph you are shown in physiology, here you are like, “Holy shit. Women are so freakin’ complicated!” And not to say that we aren’t complicated. But if you break down the cycles and hormones, it’s not so bad. Taken from clue, the app that helps you track your cycle. Find the article here: https://helloclue.com/articles/cycle-a-z/the-menstrual-cycle-more-than-just-the-period Progesterone is the most important hormone in the luteal phase Progesterone stimulates endometrial growth. Which is great because the name, “progesterone”, is telling you what it does. Pro-, as in “in favor of”; gest-, as in “gestation”. Actually, “gest” is Latin for carried (as in carrying a baby). “Progesterone” the word basically means “in favor of carrying a child”. It makes sense that your endometrial lining will grow to get ready for implantation to occur. And the lining would need to be ready for this implantation after ovulation. So progesterone levels go up drastically after ovulation. If you ever get stuck on a hormone question go back, in your brain, to the thing that you absolutely know. And now you know that progesterone is pro-baby. To get ready for baby the uterus walls need to be ready. When do the uterus walls need to be ready? They need to be ready after ovulation when there is a chance for pregnancy. And you won’t ever forget that is what progesterone does because the word tells you what it does. Progesterone also has a negative feedback loop with the hypothalamus and inhibits GnRH. At the end of the cycle, the corpus luteum is going to degenerate, so all those hormones will decrease. The progesterone and the estrogen and the inhibin will start to decrease because the corpus luteum is degrading, so it can’t produce those hormones at the same level. Makes sense, huh? The decrease in progesterone means that progesterone is no longer at a high enough level to inhibit the GnRH. and inhibin isn’t inhibiting, so a new cycle will be able to start. It also means that these hormones cannot maintain the endometrial lining of the uterus so it will shed, a.k.a. the period. ***feedback loop pic So if the egg doesn’t get fertilized, the corpus luteum reaches its max size, and the corpus luteum undergoes apoptosis. This is around day 25 in the 28-day cycle. But if the egg does get fertilized, the corpus luteum hangs out. And by hanging out, I mean it keeps living and producing estrogen and progesterone. This is really important because it is this estrogen and progesterone that take care of the endometrium where the egg will be implanted. Wow, that was a lot. To reward you I will ask you a question. Q: What are the two phases of the ovarian cycle called? A: One to 14 is the follicular phase, and 15-28 is the luteal phase. Boom aced it. There are some really great graphs that give good visuals of the hormones. If you have a second, google that. But we are still going to create a really good understanding, so that you can picture this in your head, so that when it pops up on the MCAT, you will be like, “Oh yeah, I have that filed right here in my mind palace.” Now let’s talk about the uterus and do a little review at the same time. Did you guys ever see the movie with Ashton Kutcher and Natalie Portman…I can’t think of what it’s called… I googled it. It’s No Strings Attached. I still get a kick when Ashton brings cupcakes to the apartment full of doctors all on their period and recites what is happening to their bodies from an excerpt he found on google. https://www.youtube.com/watch?v=pJFZLCoqB9w Anyway, the uterus is that organ that is kinda a pain in the ass, as it causes periods. I mentioned earlier that day one is the first day of the period, medically called menses. This is when the uterine lining sloughs off. Menses is considered to be days one to seven, but it usually doesn’t last a full seven days. Then, after the endometrial lining is gone, there is what is called the proliferative phase, where the lining starts to build back up in hopes that an embryo will be implanted. After day 14, it is what is called the secretory phase. So the endometrium has three phases: one, menses, days one to seven; two, proliferative, days eight to 14; and three, secretory, days 15-28. After the end of menses, roughly days five to seven, the endometrium will grow increasingly thick in preparation for the implantation of a zygote. If implantation does not occur, the uterine lining will slough off and start over. Point of clarification: You will hear or see day zero sometimes. Day zero is day 28 of the previous cycle. So there isn’t ever space where you would see day 28, then day zero, then day one. It’s either 28 or zero, then one. So from the anterior pituitary, we have FSH and LH being released. The FSH is stimulating the growth of the follicle. I mean, come on. It’s called follicle-stimulating hormones. So down in the ovary, the follicle will start to develop and get surrounded by those granulosa cells. As it gets bigger, the number of granulosa cells are increasing. The more granulosa cells there are, the more estrogen they will secrete so the estrogen levels start to go up in the blood. Remember the LH cells cause the theca cells to make androstenedione, which it hands over to the granulosa cells, which converts it into estrogen. So as the follicles grow, the estrogen really starts to go up. These estrogen levels really start to rise around days seven to nine, which means that the uterus is in the proliferative phase. The uterus is proliferating because the estrogen levels are telling the endometrium, “Hey, it’s that time again. Let start building up in hopes of a baby.” Let’s check back in with the brain. The hypothalamus in the brain is really responsible for homeostasis, which means it is always keeping track of what’s going on in the body, what’s going on in the blood. So the brain senses that the estrogen levels are getting high so the levels of FSH and LH decrease slightly. The granulosa cells are still producing estrogen, but they also start to produce more inhibin and progesterone. Q: Do you remember what inhibin does? A: Inhibin inhibits FSH release. Q: Where is FSH released from? A: The anterior pituitary. This inhibin causes a drop in the FSH. So at this point, you can see that there is a type of negative feedback loop. Where the estrogen levels signal the brain to decrease FSH and LH. ***hormone loop But at this point, the granulosa cells are like, “No, we got this.” They are a runaway train. So what happens is that the level of estrogen gets so high that it actually triggers a spike in the FSH and LH. But remember the granulosa cells have also been spitting out inhibin so the spike in FSH is not as high as the spike in LH. This huge rush of LH from the anterior pituitary is called a luteal surge. In my head, I think of it as a hallway that is getting flooded. It’s violent, there’s a surge coming at you. And this LH surge is what pushes the follicle to ovulation. After this spike, the FSH and LH slowly decline due to all of the progesterone and inhibin being pumped out by the corpus luteum. https://makeagif.com/gif/titanic-hallway-flood-CnW6db Let’s think: On day 14 we are at the left point on the lemon/football. So we are at ovulation and the follicle is about to turn that corner and become a luteal body. In the uterus, we are on the last day of the proliferative stage and moving into the secretory phase. Yas, we are champions. I know we just covered a lot in this episode. It was a lot. I really hope that this podcast helped you get a solid review in while driving or working, or hitting the gym, or wherever. If you are listening, I tremendously appreciate it. Study hard friends, and do me a favor: Compliment a stranger today. P.S. I am a fan of the podcast Ologies and today I actually listened to the episode on gynecology, and I found it so serendipitous that I listened to that episode at work earlier today, and now I’m recording this episode. If you want to listen to a really great interview with a gynecologist, check out the gynecology episode on Ologies. I will also put a link in the script notes on the website, Cellfielife.com https://www.alieward.com/ologies/gynecology?rq=gyno Study hard friends.
37 minutes | Jan 13, 2020
Male Reproductive System-Let’s talk about sex
**This episode contains sexual health material** Let’s talk about sex, baby! Let’s talk about you and me…or let’s talk about reproductive systems, and hormones, and the anterior pituitary, and the endometrium, and the epididymis. Welcome to the Cellfie Life. Thank you so much for listening. If you have questions or comments, or corrections, please let me know. The best way to reach me is either the website CellfieLife.com or on Insta at @thiscellfielife. On the website, I have the script notes from all the episodes. So if you want to print out and use them to aid in your studying, the transcripts are available under the episodes. And follow me on Insta! I post MCAT prep questions on my story every morning, and I will let you know when a new episode drops, but if you subscribe, they will be automatically downloaded for your listening pleasure. And tell your friends about this podcast. As a non-traditional premed, I decided to make this podcast because I couldn’t find an MCAT review podcast, and I really wanted one. So now that I am making it, I want other premed students that are out there hustling and busy—like you all are—to have this as an added resource for your test prep. This episode does have sexual health material—so this is your warning: We’re gonna be talking about penises and vaginas. And one last note before we jump in: This episode is about biological sex, not necessarily gender expression or gender identity. Anyway, let’s get down…to business, that is, and the reproductive system. You guys, I’m gonna try not to do a ton of sex puns, but as I was writing this episode, everything sounded like a sexual innuendo. Sorry, not sorry Okay! The reproductive system includes sex organs and parts of our brains. We are going to start with males because they are easy. In my opinion, male reproductive systems and hormones are pretty straightforward, so we are going to start with males and then graduate up to females. Along with what we usually think of as reproduction duties—creating sperm and eggs—the reproductive system is also responsible for producing hormones. Because these hormones come from our reproductive system, they are dubbed our “sex” hormones. Sex starts in the brain. The sex organs are controlled by the brain, specifically the hypothalamus and anterior pituitary. The hypothalamus is really important. I think of the hypothalamus as an air traffic controller. The air traffic controller sits up in the tower and watches everything that is going on. If a plane is taking a long time on the landing strip, the air traffic controller tells the incoming plane to hang on before it lands so that there is not a crash. The hypothalamus does the same thing. It sits up in the brain and monitors what is going on in the body and gives directions if it sees that something is straying too far from homeostasis. The hypothalamus regulates body temperature, appetite, physiological cycles, and sexual behavior, to name a few. We will talk more in detail about the hypothalamus later, but I wanted to introduce it because it has a really important role in homeostasis and, thus, health. But right now, we’ll just talk about the hypothalamus’s role in regards to the reproductive system. The hypothalamus is bossy, just like a good air traffic controller. You don’t want an air traffic controller that waffles back and forth about whether a runway is clear for a plane to land. The hypothalamus bosses the body around by releasing hormones. In the reproductive system, the hypothalamus releases gonadotropin-releasing hormone a.k.a. GnRH. GnRH goes to the anterior pituitary through the blood vessels, and these guys are neighbors, so it really doesn’t have a long way to travel. You know when you were a kid, and your mom sent you next door for something? Like you had to go borrow an egg, or take the neighbors a plate of cookies? This is what GnRH does. It is sent to its neighbor, the anterior pituitary, to deliver a message. Physiologically the anterior pituitary sits right below the hypothalamus, and they have blood vessels connecting them. The anterior pituitary, in response to the GnRH, releases luteinizing hormone—a.k.a. LH—and follicle-stimulating hormone, FSH. It is these two hormones from the anterior pituitary, LH, and FSH that affect the male and female sex organs. MALES: The male reproductive system “in a nut-shell.” So male sex organs include the testes and the penis. The testes are super important because the testes are where the sperm form and the penis is used to deliver the sperm. Those are the major male reproductive organs. In the testes, two major things need to occur: Sperm needs to be made, and the testosterone needs to be secreted. Let’s take a closer look at the testes and spermatogenesis. This will be a bit of a review. If you haven’t listened to the cell cycle, mitosis, and meiosis episode, you might want to check out that episode first. It goes deeper into meiosis and the formation of haploid cells, which, in males, are sperm. Did you guys know that the technical plural name for sperm is spermatozoon? So singular is spermatozoa, and the plural is spermatozoon. In males, sperm are made through a process called spermatogenesis. You guys: genesis. Anytime you hear or see “genesis,” think the origin or formation of something. So Genesis in the Bible talks about the forming of the Earth. Sidenote: I’m not saying that is how the Earth was formed, I am saying that the Book of Genesis in the Bible talks about the formation of something, so they called it “Genesis.” So, spermatogenesis will be the formation of sperm, and this occurs in the testes, specifically in the seminiferous tubules. We pronounce the word like “semi-niferous,” but it’s spelled S-E-M-I-N, which is the Latin word for semen. You guys, it’s literally one letter off from how we spell semen today. The great thing about a lot of medicine is they literally name it after what it does, just in Latin. So learning your Latin root words and/or really looking at the word and breaking it down will tell you the answer a lot of the time. Okay, in the testes, in the seminiferous tubules—which are super convoluted—is where the formation of haploid sperm takes place. Quiz, from Episode 1: How are haploid sex cells created? Answer: through meiosis. Let’s start with the exterior sex organs and zoom in: So we have the scrotum, which is where the testes are located. The testes have the seminiferous tubules where haploid sperm are made. Along with seminiferous tubules, we also have interstitial cells of Leydig. These cells are where testosterone is made. The cells of Leydig are just on the outside of the seminiferous tubules. Whoa—scrotum, where did that come from? You haven’t mentioned the scrotum yet. If you’re studying for the MCAT, I’m gonna assume you’re an adult, and, as an adult, I’m pretty sure that every one of you knows what the scrotum is. The scrotum is the external pouch that’s hanging out, literally. It houses the testes where sperm production occurs. Sperm production has to happen at certain temperatures, which just so happens to be a little cooler than body temperature, about two to four degrees cooler, so they literally hang outside the body so as to not get too hot. I’m not gonna lie, the first time I heard the physiological reason why testes were outside the body, my mind was kinda blown, and I was like, finally, it makes sense, why that thing is hanging there. What happens when it’s cold out? I’m pretty sure I heard you all say shrinkage. But why is this happening? How is this happening? The body always wants to maintain that homeostasis. So if it’s too cold, the muscles will contract to raise the testes to maintain the proper temperature for sperm development. So, in addition to the spermatogenesis, what is another important function of the testes? Answer: the creation of the major male hormone, testosterone. Males’ major sex hormone, which is produced in the testes, is testosterone. Testosterone is the most important male androgen. Testosterone has a lot of responsibilities: It helps men maintain libido, it helps in muscle and bone growth, and it is responsible for secondary sex characteristics, like facial hair and deep voices. Testosterone is produced by the interstitial cells of Leydig. How are we going to remember that? (Men, forgive me for this one) Men lie and dig themselves into holes with those lies. (I know, I know, not all men lie and dig themselves into holes, but come on, that’s pretty low hanging fruit…and when I wrote that, it was not supposed to be a sexual reference to the scrotum, but everything can have a dirty meaning if you try hard enough). So, the LH from the anterior pituitary travels through the blood to the testes and enters the interstitial space and hooks up with the Leydig cells, and the Leydig cells secrete testosterone. The testosterone enters the blood and influences the “masculine” traits we have already mentioned. It also has some influence on the production of sperm in the seminiferous tubules. If testosterone levels get too high, there is a negative feedback loop with the anterior pituitary. So the anterior pituitary senses the high levels and stops producing LH, which is what stimulated testosterone production in the first place. Side note: Its testosterone, in the womb, that pushes the reproductive organs to turn into masculine organs, which will be important when we talk about embryogenesis. So the LH and FSH from the anterior pituitary travel to the testes, through the blood. In the testes, LH will enter the interstitial space. Here the LH will target the Leydig cells, which secrete testosterone. The FSH will act on Sertoli cells in the seminiferous tubules. I want to go into a little more detail about the spermatogenesis process and make sure that you understand how sperm-specific vocab lines up with what you already understand about meiosis. But I find it helpful if you get a visual of where the spermatogenesis is taking place—think of a wheel, like an old-school wagon wheel. It has the rim and the spokes and the center. (If you don’t know what a wagon wheel is, imagine a bike wheel, enlarged and made of wood.) Back to the wheel. This wagon wheel is a really loose interpretation of what a cross-section of the seminiferous tubules look like. On the outside of the wheel, the rim, there is a smooth layer of muscle that will help move sperm along through peristalsis into the epididymis. The wedges that make up the wheel’s negative space are the Sertoli cells. Now the spokes that go into the center, these are where the sperm actually develop, on these spokes between the two Sertoli cells. So the sperm start development at the rim and move down the spokes, getting taken care of by the Sertoli cells as they move towards the center of the wheel. The center of the wheel is the lumen, which will carry them onto their next stop in their journey. Just a reminder that peristalsis is a type of coordinated contraction, with a wave-like movement that pushes the contents forward. Remember how the FSH acts on the Sertoli cells? The FSH stimulates androgen-binding protein (ABP), and ABP is released from the Sertoli cells. In order for the Sertoli cells to make androgen-binding proteins, the Sertoli cells must have FSH and testosterone present. This ABP is what promotes the synthesis of spermatozoa. Sertoli cells also produce inhibin which, as the name says, inhibits something. Inhibin travels up to the brain and tells it to stop releasing so much FSH, which then decreases sperm development. Okay, you guys don’t judge me too much, but how are we going to remember Sertoli cells? Sertoli, that just sounds Italian, doesn’t it? It’s because it is. Enrico Sertoli discovered the cells in the 1800’s while studying medicine, and the line that came to mind was “at least buy me dinner first, possibly Italian”…’cause his name is Italian, and we are talking about the reproductive organs. Come on, you will be able to pick the Italian name out of the lineup if it’s an option on the MCAT, and you can’t remember the title outright, right? Sertoli, at least buy me dinner first! In spermatogenesis, the diploid 2n cells are called spermatogonia, so these are the starting stem cells in sperm formation. The spermatogonia cells are the cells that will produce the haploid sperm. The spermatogonia cells also need to make sure that there are always spermatogonia cells to make more sperm. Males make several million sperm a day for most of their lives, so having spermatogonia cells is important. So what these cells do is they undergo mitosis. One of the daughter cells will become another spermatogonium cell, and the other will move down the meiosis pathway. But let’s stop and think about this: If the seminiferous tubules are roughly shaped like a wheel, and the process of maturation starts at the rim and as it matures it works its way into the center of the wheel, where will the spermatogonia cells be located? Answer: That’s right! They are located near the rim. Spermatogonia are just hanging out in interphase, and then they start going through the stages of interphase: G1 and S. S is where they replicate their genetic material and become primary spermatocytes, then G2, and finally enter meiosis. A quick note here: At first, I was like, why would they change the name of the cell after the DNA has replicated, but before it has done any sort of division? Like, this is cheating. It’s because the primary spermatocyte goes through a physical barrier, a tight junction. So once it has its DNA replicated, it now has a ticket and can pass through the security gate (like at the airport). Understanding the anatomy here helped me to visualize and understand the difference in names. The primary spermatocytes then undergo meiosis I and become secondary spermatocytes—so now they are haploid (n). So we just finished meiosis I, and now we have secondary spermatocytes. Quiz from Episode 1: Where does crossing over occur? Answer: prophase I of meiosis I. Follow up question: What is pulled to opposite poles during anaphase I? Homologous pairs. If you couldn’t answer those two questions within a second or two, go review meiosis. The secondary spermatocytes then undergo meiosis II and become spermatids. Remember, these are haploid. The little spermatids undergo some further maturing and are called spermatozoa. I remember that spermatids come before spermatozoa in the naming convention because you know how in Spanish they add diminutives to words? Like ‘-ito’ and ‘-ita’. Spermatids—at some point, I added spermati-to to it. So they are diminutive, they are small. Seriously, say it out loud. If anyone gives you weird looks, just tell them you’re learning Spanish, and they will think you are super cool. Spermati-to—so the diminutive would come before the more mature spermatozoa. Question: How many chromosomes does a spermatid have? Answer: 23. Good job! Remember that with meiosis, we can end with four cells that have the haploid number of chromosomes. In spermatogenesis, four sperm (or spermatozoon) results for each spermatogonium. Let’s run through spermatogenesis names one more time, really quick: spermatogonia are the stem cells that live in the seminiferous tubules in the testes. Once the genetic info has been replicated in the S phase of interphase, it develops into a primary spermatocyte. It goes through meiosis I and is now a secondary spermatocyte. The secondary spermatocyte undergoes meiosis II and develops into spermatids, and then it matures into spermatozoa. Spermatogonia sounds like Patagonia, which, yes, is a clothing brand that one of my brothers is super into, but it is also a region at the bottom of South America. And for some reason, my brain accepts this as a way to remember that the starting cells of spermatogenesis is a region at the bottom of the map. Primary spermatocyte—’cause it is first, in the order, it’s primary. Secondary spermatocyte—’cause it’s second Spermatids—or, you know, spermati-to, which are the baby sperm before they mature. Spermatozoa—which is the plural form of sperm. And, actually, the singular of spermatozoa is spermatozoon. All of this is happening in the testes in the highly coiled seminiferous tubules, where there are also Sertoli cells, that are helping to facilitate the formation of spermatozoa. There is a flow chart of all of this on the website, and I’ll post it on Insta, too. I think the flow chart helps to line up the general steps of meiosis with the specifics of sperm and egg production. Now that we have sperm let’s talk about the path the sperm take through the male reproductive system. When I originally learned this pathway, I was taught the mnemonic SEVE(n) UP. I’m betting this is the same mnemonic a lot of you learned. It’s an oldie, but a goodie. So let’s review SEVE(n) UP. Did you guys ever play Heads Up Seven Up in school? SEVE(n) UP S—Seminiferous tubules—where sperm are nourished by Sertoli cells. E—epididymis—sperm can further develop, gain mitochondria and develop flagella, and are stored. V—Vas deferens—which is also sometimes called the ductus deferens, which is the muscle around the vas deferens that carries sperm from the epididymis to the ejaculatory duct. E—Ejaculatory duct—the ejaculatory ducts fuse to form the urethra. Up to this point, there have been two of everything, one on each side. N—the N stands for nothing, like literally nothing. Just ignore the N. U—Urethra P—Penis A little anatomy for you: The sperm drains out of the epididymis and then into the ductus deferens. The end of the epididymis forms the vas deferens, a.k.a. the ductus deferens. The vas deferens is the tube that goes from the posterior of the testes, penetrates the inguinal canal, then enters the pelvic cavity and brings the sperm to the posterior side of the bladder. The seminal vesicles are at the base of the bladder and are considered an accessory gland. The seminal vesicle and the ductus deferens form the ejaculatory ducts. During ejaculation, the ejaculatory duct ejects sperm into the male urethra. So up to this point, males have had two of everything, one on each side. But now the ejaculatory ducts form up to the urethra. The prostate gland surrounds the prostatic urethra. So the ejaculatory ducts join the urethra just below the bladder, and the prostate surrounds it. This part of the urethra is known as the prostatic urethra. Makes sense. The prostate is also considered an accessory gland, and the fluid it secretes goes into the prostatic urethra. Bulbourethral glands are directly under the prostate, and its secretions empty into the urethra. The urethra passes through the penis carrying semen. Remember: Semen is sperm plus fluid secretions from the glands. In males, the urinary and reproductive tracts share a common pathway. This is not the case for females. I mentioned three accessory glands in passing—these glands provide sperm with things that they need on their journey to fertilize an egg. Seminal vesicles—contribute fluid to the sperm, about 60% of semen volume. The fluid here is alkaline to help protect the sperm from the acidic environment of the urethra and the female reproductive tract. The seminal vesicle fluid is also very rich in fructose for the sperm to use for energy on their journey. The prostate gland—makes prostatic fluid. So…more fluid. The last of the accessory gland is the bulbourethral gland, also known as a Cowper’s gland. This gland adds lubricant that helps lubricate the urethra. Now that we know how and where the sperm are produced let’s talk about the sperm themselves. I think everyone knows what sperm look like. They have a big head that carries the genetic information, and then they have a hat on top of their head called the acrosome, which helps in ovum penetration. It’s not a top hat; it’s more of a beanie. On the opposite side of the head is the tail, a.k.a. the flagellum. The part of the tail closest to the head is called the connecting piece, where the mitochondria are located, and then the long tail to help them swim. Because the sperm have a long way to swim, they are going to need a lot of energy, which means they are going to have a lot of mitochondria. Something that I find kinda cool is that the sperm don’t donate mitochondria to the egg and thus the embryo. This is because the mitochondria are located at the spot where the tail meets the head. The genetic information is in the head, so very few, if any, mitochondria are from Dad. This means a couple of things: If someone has an inherited mitochondrial disease, it’s probably coming from Mom. Also, there is, theoretically, a mitochondrial Eve. Google that in your spare time. It’s pretty cool. https://www.sciencedaily.com/releases/2010/08/100817122405.htm Quick Review: The reproductive system is controlled by the brain—the hypothalamus. The hypothalamus releases the gonadotropin-releasing hormone, GnRH. GnRH goes to its neighbor, the anterior pituitary, and the anterior pituitary releases two hormones: luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These two hormones go to the testes. LH acts on the interstitial cells of Leydig to secrete sperm, and FSH acts on Sertoli cells that aid in the development of sperm. Sperm take the SEVE(n) UP path during ejaculation. Sperm contain a head, a mid-piece, and a flagellum. The head is where the genetic material is stored. It is covered by the acrosome, which helps the sperm penetrates the ovum. The mid-piece is where all the ATP is generated, so it has a lot of mitochondria. The flagella is how the little guy swims/promotes mobility. Oh my gosh, we made it!!! So because I want to keep these relatively short—20 to 30 minutes—I think I’m going to split this episode into two. We will talk about the female reproductive system in the next episode. If you are listening to this, I want to thank you genuinely. I am making these podcasts for other students, like myself, and if you are listening, I really appreciate it. It makes it all worth it to know that other people are investing their time in listening to this podcast. Please subscribe, leave comments, recommend this podcast to your friends. Let me know if you have any suggestions, or just general comments, or corrections. Check out the next episode for the female reproductive system. Study hard friends and do me a small favor and listen to a little Salt-N-Pepa https://www.youtube.com/watch?v=qzfo4txaQJA
27 minutes | Dec 31, 2019
Cell Cycle, Mitosis, and Meiosis… and Giant Chocolate Cake.
Hello, and welcome to the Cell-fie Life. Thank you so much for listening! My name is Nikaela and today we are going to be reviewing the cell cycle, meiosis, and mitosis. If you have questions or comments or corrections, please let me know—the best way to reach me is on Instagram with the handle “thiscellfielife”. That’s this C-E-L-L-fie Life. Also, if you follow me on Instagram, I post MCAT prep questions on my story every morning, I hold giveaways, and I will let you know when new episodes drop. Please rate, review, and subscribe. And tell your friends about this podcast. The entire reason I decided to do it is because I wanted to be able to listen and study while working, driving, and doing house chores. I didn’t find a podcast that was providing what I wanted, so I decided to create one. Share with your study buddies! Okay, let’s do this—mitosis and meiosis. There are two main types of cell division that we humans take part in: mitosis and meiosis. Mitosis is the process of making new body cells, so it is how two identical daughter cells are created from a single cell. Meiosis is the type of cell division that creates gametes, eggs, and sperm. Meiosis results in up to four non-identical daughter cells. When I first learned about mitosis and meiosis, I could not keep their names straight. Which one happens in somatic cells and which one creates germ cells? And, because in science we like to name things very similar to one another to make things extra fun—just wait till we get to centromeres, centrosomes, centrioles, and kinetochores, and we will get to those—I had to think of a clever (or dumb) way to remember which one was mitosis and which one was meiosis. And, let’s be honest, I went with the dumbest and most ridiculous way to remember: Have you guys ever seen the movie Singing in the Rain? There is a song that has the line, “Moses supposes his toeses are roses, but Moses supposes erroneously…” And for some reason, I combined “Moses” and “toeses” when I was singing, and it came out “Mos-toesis, and from there it is a really was a short leap to: “Mitosis happens in the toeses”. If mitosis is happening in your “toeses”, well, your toes do not need to create sex cells—your toes are somatic cells. In somatic cells, mitosis is what occurs to create genetically identical diploid daughter cells. So if mitosis is creating somatic cells, then meiosis is happening in germ cells . If my “Singing in the Rain” song wasn’t enough to help you keep mitosis and meiosis straight meiOOOsis happens in your ovaries—or, you know, testes, if you are male. If you guys want to check out the song I’m talking about, “Singing in the Rain”, I’ll post the YouTube clip on the website cellfielife.com. There is also some excellent tap dancing, you know if that’s your thing. To see the whole thing, here’s the YouTube link: https://www.youtube.com/watch?v=zFAlZttXfvE So now that you will never switch up the location of mitosis and meiosis, let’s get into the nitty-gritty: A lot of people approach the cell cycle with a pie chart, which is great—I love pie. And I’m willing to bet that a lot of you have seen this breakdown. I’ll post it on my Insta and on the website, but I’m going to approach the cell cycle, not with a pie chart, but with a cake meme. Remember that cake meme? It’s been on the Internet for years. It’s a cartoon in which a slice of cake is cut from a whole cake, and the person—instead of taking that single slice for themselves—removes the rest of the cake and leaves the single slice sitting on the plate. That almost-whole-cake-slice is what we call “interphase”. Interphase is where a cell spends approximately 90% of its life. The single slice left on the serving dish? That would be mitosis. Mitosis is the process where the one nucleus splits into two nuclei. But first, interphase! Or, how I like to think of it, the correct size of a slice when it comes to chocolate cake. Interphase is where the cell is really just living as a cell: growing, making proteins, and all the other functions that a cell might have. Interphase can be further divided into G1, S, and G2, phases, as well as G0. G “now” is the G with the little subscript zero after it. The G0 phase is sometimes thought of as outside the cell cycle, or as an extended G1 phase. G0 is a phase where the cell is either not dividing or is preparing to divide. It’s simply living its life, carrying out its daily functions. Can you think of any cells that would enter this type of inactive phase and hang out there for their life? I’ll give you a hint: think super-specialized cells. My favorite example is neurons. Okay, G1: G1 is when you have a new cell and it’s gonna start growing. It’s getting bigger. It’s creating more organelles. It’s called the G1 phase because it is the first phase of growing in the cells. The S phase: This is the phase where the cell replicates its DNA so that it has two identical copies. This happens in the synthesis phase. DNA replication happens before mitosis. And this is an important point to remember! DNA replication happens before mitosis—a cell that enters in the G2 phase has twice as much DNA as it did the G1 phase. Remember—DNA replication happens in the S phase; “S” as in “synthesis” phase. In the S phase, one copy of DNA will become two copies. Once a chromosome replicates, it is still considered one chromosome. For example, let’s say we have a cell that has three chromosomes. This cell with three chromosomes enters S phase and all its DNA is replicated. How many chromosomes does this cell have now? The cell still has three chromosomes, despite the fact that it has double the amount of DNA. The DNA strands are still attached, so they are still considered one chromosome. Recall in your mind the traditional X chromosome. Right now, it’s a stringy, loose spaghetti-like X, free-floating in the S phase; it won’t actually get the super tight X shape until mitosis. The middle, where the X’s cross, is called the “centromere”. So, there are two copies of the DNA that are attached in a specialized region called the “centromere”. Because they are still attached, they are still considered one chromosome. Each individual copy can be called a “chromatid”. These are the sister chromatids (I mean, really, they are twins, but they are called sister chromatids). During mitosis, the two sister chromatids will get split apart, and then they will become two separate chromosomes. Centromere: This is the middle point connecting the two sister chromatids. But we’re going to think of it like centroMere. “M”, as in “middle”—this is legit how I remember this. Centromeres are the middle of the two sister chromatids, making them one chromosome. M, centroMere, for middle.` With all of this DNA replication happening, there is also some other additional duplicating happening—the centrosomes duplicate. Side note: I think of centrosomes as centro-SUMS—like they are just “sum” (some) organelle hanging out in the cytoplasm. I put the emphasis on pronouncing it incorrectly so that I can remember what it is and what it does. The centrosomes (centro-SUMS): They are the little organelles close to the nucleus of the cell which will help in the physical splitting of the genetic material. When the chromosomes get pulled apart in mitosis, it is the spindle fibers that are made from microtubules that will pull the chromosomes to opposite sides (we will be going over this is more detail, I just wanted to get the word “centrosome” in early so that it’s in our vocab and I can keep repeating it). After the synthesis phase, there is one more growth phase. This second growth phase is called G2. Also, the cell checks itself before it wrecks itself. The cell has checkpoints where it makes sure that it is healthy enough to continue forward. One really important checkpoint is the one between G1 and S. This checkpoint makes sure that the DNA is looking good, not damaged, and can be replicated. If the DNA is damaged, the cell cycle is arrested until the DNA can be repaired. The protein that is in charge of this checkpoint is called p53. Another checkpoint is the one right before the G2/M phase. This checkpoint makes sure that there are enough organelles, and that it is large enough to replicate. So, at the end of the G2 phase, the cell is now ready for the M phase, mitosis. Yay!!! There are four phases of mitosis: Prophase Metaphase Anaphase Telophase I will talk about each phase individually, but I find it helpful to know what phase is where in the process. For me personally, I don’t have a super clever way of remembering this. I just think PMAT—which sounds kinda like a test, similar to the MCAT, and MCAT is always on the brain, so PMAT kinda just sticks. But I did google some mnemonic devices and my favorite was: Pass Me A Taco. If you have a really great way to remember hit me up on my Instagram and I’ll share them—@thiscellfielife. Okay, so, PMAT… Prophase: the DNA goes from its chromatin form—which is the loosey-goosey, floating-around-in-the-nucleus state—to its condensed form. Remember that we have two sister chromatids connected by a centromere, and now it is in its X shape, which can be seen by a light microscope. So, in prophase, the chromosomes condense and the nuclear membrane starts to dissolve. The centrosomes that were those little organelles that were hanging out in the cytoplasm (close to the nucleus) start migrating to opposite sides of the cell. Metaphase (“M” as in “middle” again): the chromosomes start lining up in the middle of the cell. The centrosomes, the organelles, are now on opposite sides of the cell. Centrioles exist inside the centrosomes; each centrosome has two centrioles. I know that naming is cruel and unusual. Is there a tongue twister f
2 minutes | Dec 30, 2019
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