DIP Episode 56 - Cell Biology Review For The USMLE Step 1 (Part 1)

Hello, welcome. My name is Divine. I am a Fiji Y1 Transitional Year resident of Gwynn in Turidiology. This is the 56th episode of the Divine Intervention Podcasts. And here I'm going to be talking about Cell Biology. And I mean I've got a bunch of questions about this from people like why exactly do you do these podcasts? Well, I mean as you can tell from my name, as you can tell from the name of the website, you can tell them probably Christian. And the thing is I sort of see my main purpose on this earth as I've, I mean I sort of see like one of my purposes on this earth, sort of spreading knowledge in an accessible fashion. So I sort of look at it as a calling, almost like a ministry. So that's, I'll say that's probably like my primary motivation. I'll probably say some more things about that in the future. But back to Cell Biology, right? So Cell Biology is a very high-yield part of Step 1, right? And the thing is it is often ignored by many people. The only problem is it contains enough questions to pull you down score wise, if you don't understand the concepts, right? So I'm going to be doing this in a couple of parts. And my main goal is to discuss Cell Biology, explain like the core of Cell Biology, but also try to integrate to like Pharmacology and other subject areas that are tested on Step 1. So this will be me doing a lot of explaining. It's almost like a freestyle format, if you may.

Although I have like some big topic headers that I'll use to sort of keep things organized. And then I have a very nice Step 1 worthy question at the end. So let's begin, right? So obviously if you're dealing with Cell Biology, you want to worry first about the Central Dogma of Cell Biology that involves DNA and RNA and protein and all that stuff, right? And the thing is basically you want to know a few, you want to understand a few basic processes that relates to the Central Dogma, right? So the first thing you want to understand is how you go from DNA to DNA. If you're making DNA from DNA, right? That process is known as replication. You have DNA is basically making copies of itself. If you're going from DNA to RNA, right, you're going in the realm of transcription, right? Because again, think about it. DNA is like the original, sort of like the original blueprint, right? So you don't want to use the original, right? So you want to make a copy of it, which is RNA in the process of transcription, and then you'll continue down the protein synthesis pathway. And then if you're going from RNA to protein, right, that's known as translation. They're sort of putting that DNA language in a format which is protein that can be used by the cell to achieve certain functions. And I mean, if you're going in reverse, right? We say that going from DNA to RNA is transcription. If you're going in reverse from RNA to DNA, that's reverse transcription, okay?

And don't forget that that's done by reverse transcriptase, for example, classically, that's tested on step one in the context of HIV, right? And the thing is DNA, right? Usually is double stranded. You can actually convert DNA from being a double stranded form to being a single stranded form. I mean, you can do it in one of two ways, right? You can do it through a catalytic mechanism, which is what obtains in cells under the action of helicase, okay? But another thing you could actually do is you could actually just apply heat to DNA, and that double stranded DNA will become single stranded DNA, right? That process is known as a denaturing DNA. In fact, if you sort of want to integrate that with PCR, right? In PCR, you basically apply heat to DNA, that the nature's DNA converts it from being double stranded to being single stranded. And then you mix in primers, right? Those primers, as the DNA cools down, if heating made DNA, the nature, right, broke those two strands apart. Cooling down DNA can bring two strands together, right? So if you mix in primer, those primers could potentially re-enmail with single stranded DNA, and that's basically what is done in multiple cycles, in PCR, right? And the thing is, if you want to compare DNA synthesis to, which is, again, replication to RNA synthesis, which is transcription, you probably want to be able to recognize some key similarities and differences, right? So in DNA, your, in replication, you're trying to make DNA, right?

You're trying to make a polymer of DNA. So it should make sense that the DNA polymerase is the enzyme that will help you make that happen. But in transcription, right? You're trying to make RNA, you're trying to make an RNA polymer. So it should make sense that RNA polymerase should help you with that process. And the thing is, if you kind of look at the cell cycle, right, you want to remember where these two process, like during what phases of the cell cycle, this you want to remember the phases of the cell cycle that have these processes, right? So replication in general, right, happens in the S phase of the cell cycle, the S of the synthesis phase of the cell cycle, while transcription happens in essentially every phase of the cell cycle with the notable exception of mitosis, okay, with the notable exception of mitosis. And with the notable exception of mitosis, right? So basically every phase of the cell cycle minus mitosis basically represents interface, okay, interface. So transcription, right, production of RNA from DNA happens during interface. Replication happens specifically during the S phase of the cell cycle. And I'll just take a quick detour and discuss the phases of the cell cycle, right, because these are tested quite commonly in the context of step one, right?

So remember, we have like the G zero phase, we're basically cells that are not dividing like quiescent cells, right, like your neurons, your permanent or stable cells, if you may, they sort of sting the G zero phase. If your cells want to begin to divide, they go to the G one phase, okay, and then from the G one phase, you go to the S phase, from the S phase, you go to the G two phase, right? I remember again in the S phase, that's where you have DNA replication, and then from the G two phase, you proceed to mitosis. The high u thing you want to remember is that if you're going from the G one to the S phase, right, we know that, oh, if you go through G one to S, you're essentially in a sense, like almost committing yourself to proceeding with the G two phase. To proceeding through the cell cycle to ultimately divide, right? So they are very many, there are a ton of factors that control that process of going from the G one to the S phase, and I'll probably talk about that in later podcasts, right? So like growth factors and all that stuff, they control those processes. And then if you want to sort of think about from ecology, it's actually very high u to know the drugs that act on the different phases of the cell cycle. For example, if you're like, okay, what drugs work in essentially like every phase of the cell cycle, you're probably thinking about, you are collecting agents, right, like cyclophosphamide, right?

Remember, that's the thing that can cause hemorrhagic status that you prevent with mesna. Another thing that sort of works everywhere in the cell cycle, like your platinum analogs, okay, like this platinum, cable, platinum. I remember those drugs are auto toxic and never toxic, and you can prevent the never toxicity of the platinum agents like cisplatin with, with, with, with, amyphostin, okay? And don't forget that cisplatin is actually a serotonin receptor agonist, right? That's why it can cause profound motion vomiting. In fact, that is how on dancetron, right, which is a serotonin receptor antagonist was actually discovered as a potential treatment. For chemotherapy induced, the MSS. And then if you sort of jump to the G2 phase of the cell cycle, the G2 phase of the cell cycle is actually inhibited by bleomizing. It's actually just pretty high auto-onders, like just know that factoid. And please don't forget, right, bleomizing, I mean, I've talked about this in podcast in the past that bleomizing can cause pulmonary fibrosis. And don't forget that that's also a property that's shared by methyl tracksate, okay? And also a property that's shared by amylder, remember, it's a class three anti-rhythmic. And if I'm not mistaken, that's also shared by nitrofyrantoin. Nitrofyrantoin is an antibiotic used to treat this status, especially in females. It can also cause pulmonary fibrosis.

And then if you're looking at the S phase or the synthesis phase of the cell cycle, right, we have drugs like five-flour urethyl, okay? Remember, five-flour urethyl is an inhibitor of timelolate synthase. I talked about this in the biochem, in the biochem review, right? So it inhibits timelolate synthase. And I mean, use it for many things like you can treat cancers, you can treat atinic erotosis, all that fun stuff with five FU. Another high u-drug that works in the S phase, right, is methyl tracksate. Remember, that's the drug I said that causes pulmonary fibrosis, but in addition to doing that, it also inhibits dihydrofolyl reductase, okay? And by inhibiting dihydrofolic reductase, you do not convert the oxyredine monofosthase to the oxyredine monofosthase. Okay, remember, methyl tracksate is the drug of choice. It's a demard for the treatment of rheumatoid arthritis. It's also a pretty nice drug for the treatment of, of like molar pregnancy and also like multiple cancers. So sort of keep that in the back of your mind. And then if you're looking at the M phase, right, the mitotic phase of the cell cycle, you don't want to forget your drugs like your taxines, okay? Remember, your taxines prevent micro-tubial depolymerization, okay? We prevent micro-tubial depolymerization. So the cell is almost arrested in metapheys if you may, okay? And then don't forget your vincu-alcolics like the increase in them blasted. Those drugs basically prevent micro-tubial polymerization, okay?

Very high u to know that. Don't forget that those drugs can cause a peripheral neuropathy, right? Because remember, you need micro-tubial to appropriately transfer newer transmitters from the cell body of the neuron all the way to the synapse, very high u to know that. Okay, so back to our differences between replication and transcription. We said again, replication, you use DNA polymerase for that transcription, use RNA polymerase for that, right? And then we said before we took that long detour through the cell cycle to say that replication happens in the S phase, the synthesis phase of the cell cycle, while transcription happens in essentially all phases of the cell cycle with the exception of the M phase, okay? And basically if you take all phases of the cell cycle minus the M phase, that is what is known as interface, okay? And the thing is you want to remember that replication basically happens in the same way, in every kind of cell, every kind of tissue, right? Because if you want your cells to divide, you need to copy the entire genome, right? Versus transcription that actually occurs in relatively unique ways in different cell types, right? So if you're a renal cell, if you're a kidney cell, you probably express different proteins, at least for the most part, in comparison to like a hepatocyte, the liver cell. So you want to keep that at the back of your mind. And again, in replication, right?

Again, you're making the, you're basically copying the entire genome versus transcription, where you're copying some but not all of the genome, okay? And then the last thing you want to remember is where these processes occur, right? So if you're looking at a eukaryotic cell, okay? Replication actually occurs in the nucleus, right? You make DNA in the nucleus, but transcription actually occurs in the cytosol, in the cytoplasm. Versus a prokaryot, where replication actually occurs in the cytoplasm, right? And also, replic transcription occurs in the, in the cytoplasm as well for prokaryot. Remember, prokaryotes in general do not have, do not have a nuclei. They can very easily make this an electron micrograph question, where they say like, oh, what's the site of synthesis of blah, blah, blah? And they can just point to, they can just put, put like ABCD and E, and then you sort of have to pick out exactly where those processes occur. And another one that they love to test in that context is the nucleus, right? For the synthesis of ribosumal RNA. Now, let's then discuss, let's say some more words about DNA, right? So we know that DNA, if you remember from the bio-camera review, I said that you sort of build it up in steps, right? So you start with a mitrogenous base and then you go to a nucleoside and then you go to a nucleotide, okay? So the thing is that mitrogenous bases, right? They can be one of two, they can be one of two things, right?

You can have your purines or you can have your pyrimidines, right? So you can have your purines or your pyrimidines. Your purines, if you remember from the bio-camera review, have two rings, okay? So your purines have two rings, okay? And your purines include adenine and guane, okay? Adenine and guane. And the thing is your pyrimidines, right? They have one ring, right? And they're three pyrimidines. We have like cytosine, we have uracil, we have thymine, okay? We have cytosine uracil and thymine. And the thing is, I mean, you don't need to memorize the structures of these amolecals. We kind of want to be able to recognize them, right? And they kind of, there are some nice mnemonics and tricks that can help you recognize these agents, right? So like, it's like, if you look at adenine and guane, the difference between adenine and guane is that adenine. And just look at the top of the molecule, look at the top of the molecule. Adenine has an amino group. Remember the A in adenine for the A in amino, okay? And guane does not have that amino group. In fact, guane has more of like the ketone, like a carbono group at the top of the molecule. In fact, if you know that adenine has an amino group and guane does not have an amino group, it should make sense that a deamination reaction will convert adenine to guane, right? And I mean, if you sort of keep going with that, right? What's the enzyme that would deaminate adenine to guane?

I would hope that you think of that, think of the enzyme as being adenosine deaminase, okay? Adenosine deaminase. And that is actually high yield in the context of immunology because if you have a deficiency of adenosine deaminase, that's actually one of the most common causes of autosomor recessive severe combined immunodeficiency, okay? That's like a combined B and T cell defect where you're susceptible to recurrent like bacterial and viral and fungal infections. Now, if we jump down to our pyrimidines, right? Our pyrimidines have one rank, okay? And pyrimidines, like I said, we have cytosine uracel and thymine. And again, you don't need to memorize structures where you probably want to be able to say like, oh, this is this, this is that, okay? And the thing is, if you actually look at cytosine and uracil, the primary difference is an amino group, okay? Cytosine has an amino group, uracil does not, okay? So again, that should make sense that if you want to go from cytosine to uracil, you probably want to use an enzyme known as cytosine deaminase to make that happen. And why is that important? That's actually important if you're thinking about an AIDS patient with meningitis, right? If a patient has AIDS and they have meningitis, right? I really hope that you're thinking of them potentially having meningitis from cryptococcus new formants. Remember, that's India-ing positive. We tend to treat cryptom meningitis with amphoteria, right?

So amphoteria is in B and five flu cytosine. How does five flu cytosine work? I've talked about this in a previous podcast. The thing is, five flu cytosine is converted by cytosine deaminase, okay? To five flu or uracil. And then that five FU goes ahead to inhibit thyme deletes and thase and cryptococcus new formants, okay? So again, uracil has no amino group of cytosine does, okay? And then if you sort of follow like a logical progression from uracil to thymine, okay? Remember the THY-thymine for the THY-methyl? Thymine has a methyl group, okay? Thymine has a methyl group, right? So think about it. If you're an enzyme that is making thymine, what should that enzyme name? Potentially B, right? It should be thymidylate synthase, right? Thymidylate synthase. And if you know that the difference between uracil and thymine is a methyl group, it means that you need some kind of one carbon donor for that reaction to work. That one carbon donor, if you remember from the bio-camera reviews, can be either SAM, right? So like, S-a-denocel methyonine, but it could also be folic acid, okay? And it so happens that folic acid is the donor for this reaction, right? So if you want to, for example, go from DUNP to DTMP, use thymidylate synthase and remember that that enzyme is inhibited by five-flour yourself. Now, again, those are your nitrogen basis, right? If you take a nitrogen base and add it to a sugar, okay?

You form a nucleoside, and then to that nucleoside, if you add a phosphate group, you form a nucleotide, okay? You form a nucleotide, you form a nucleotide, very high, you'll know that. And if you're looking at two structures of, if you're looking at two different structures, you're like, wait, oh, the fine, which one is DNA, which one is RNA? Look at the three prime group, I mean, sorry, the two prime group on the sugar. If the two prime group, if the two prime carbon has a hydroxy group, then that means you're dealing with RNA. But if the two prime has no hydroxy group, that means you're dealing with DNA, okay? That's why it's known as deoxy, deoxyribonucleac acid, okay? And the thing is that sugar, that sort of makes up the structure of a nucleotide, right? The sugar on the one prime carbon, that's actually where you add the nitrogenous base, okay? Which could be a purine, which has two rings of a pyramid, which has one ring. Another thing you could add to that sugar is that the two prime carbon, if you add a hydroxy group, that tells you you're dealing with RNA, not DNA. At the three prime carbon, there is always a hydroxy group, that three prime hydroxy group is actually used in the formation of the phosphodistroborns. Right, I remember that three prime hydroxy group also forms the three prime end, if you're sort of reading DNA, in the five prime to three prime direction. And then on the five prime carbon, that is where you have the phosphate, right?

That helps with forming the phosphodistroborns, okay? Again, very high yield to understand those. So I guess now that we sort of like leave that foundation, we sort of talk about a few properties of DNA, okay? The first property you kind of want to understand is basic property, DNA is double stranded, okay? That's a pretty easy one. And another easy one to remember is that DNA, right? Sort of moves in the five is red, in the five prime to three prime direction, right? And again, remember, the five prime three prime refers to the carbons on the sugar, right? The sugar that makes up the ribose sugar that makes up DNA, okay? And remember that at the five prime carbon, you have the phosphate, the three prime carbon, you have the hydroxy group, okay? And again, you read DNA in the five prime to the three prime direction. And the thing is, DNA is anti-parallel, that's another high yield property, okay? So it's like you don't have like a five prime end, pairing up with another five prime end, right? And you kind of think of it as like, wait, you have these two bulky phosphate groups, they both have negative charges, they're sort of like tossing with each other, so you don't want that to happen, right? So you probably kind of make some sense that you have the five prime end of one strand, pairing up with the three prime hydroxy end of the other strand, right? So of the complementary strand, if you're trying to be a little more specific, okay? So that's why DNA is anti-parallel.

And then please do not forget, in fact, just keep repeating this after me. 82 GC3, 82 GC3, 82 GC3, 82 GC3, 82 GC3. That helps you remember that pure ends pair with primidines, right? And if you're looking at that 82 GC3 no more neck, add an in pairs with thining, okay? And there's two hydrogen bonds between those molecules. And then if you're comparing guanine and cytosine, or guanosine and cytosine, you have three hydrogen bonds forming between those molecules, right? And again, this should help you answer certain questions on step one, right? Because again, think about it. If you have three hydrogen bonds, what obtains between guanine and cytosine, right? You can see that because it's a larger number of bonds, those bonds are more difficult to break, right? So the one way they can do this on step one is they can basically give you a question where they give you like long sequences of DNA. And then the as which one has the higher melting point or the higher melting temperature, you probably want to pick the one that contains more G Cs and Cs, okay? Because by containing more G Cs and Cs, it means you have more hydrogen bonds existing in that region of DNA, right? So that region of DNA will be harder to break because again, there's just more hydrogen bonds around, okay? And DNA, there's like the, there are many kinds of DNA, it is like ZDNA, there's like I think YDNA, there's like BDNA. Just remember that the BDNA is the form that's found predominantly in humans, okay?

So what else do I want to discuss here? Because I want to try to keep this podcast to less than 30 minutes. Well, I guess I can talk about some more stuff with DNA structure, right? So I guess let's sort of answer the question, like how does DNA actually feel in itself? Because I mean DNA, DNA, DNA genome is like a ton, like a crapton on nucleotides, crapton of my Georgianos basis, right? So how does DNA exactly feel in itself, right? So the thing is I said that the basic structure of DNA is that it sort of hangs around as a double helix, okay? But the thing is that double helix, if you want to make it kind of compact, right? You add protein to that double helix, the protein you add in this case, proteins known as histones, okay? Proteins known as proteins known as histones. And the thing is histones are kind of unique in their own right. The thing is histones, think about it, you're making a protein that wants to bind DNA. Well, you know that DNA has a negative charge because of all those phosphate groups that are on it, right? So if you want to compact DNA, you want to make a protein that binds to DNA, you want that protein to potentially have a positive charge, right? For example, there are amino acids like lysine, right? Like arginine, remember, arginine is a product of the urea cycle, like lysine, like arginine, like histidine, right? Those are positively charged amino acids.

It so happens that lysine and arginine are the positively charged amino acids that are found in histones. And the thing is basically that there are a couple of histones that you sort of want to keep at the back of your mind, right? There's like histone H2 A, histone H2 B, histone H3, histone H4. You actually use dimers of each, right? So you kind of form like an octomer. And those octomers sort of wrap around DNA twice, okay? To form a basic unit known as a nucleosome, okay? Another name that's actually used to describe nucleosomes is they're called like 10 nanometer, whatever, okay? Just think of, remember the term 10 nanometers with nucleosomes, okay? But the thing is you can actually stack those nucleosomes on top of each other to meet DNA even more compact, right? So you can see like, oh, nucleosome 10 nanometer, let me stack it up another nucleosome 10 nanometer, let me stack it up another nucleosome 10 nanometer to form like a 13 nanometer fiber, okay? The thing is you can make bonds between those fibers, those bonds actually made by histone known as histone H1. H1 is kind of like the middle man between those 10 nanometer thingies that ultimately makes like the 13 nanometer DNA structure, okay? And the thing is those 13 nanometer things, if you keep compacting them more and more and more and more and more, you ultimately make something known as heterocromatin. Heterocromatin is the most condensed form of chromatin.

It is essentially transcription, it's like transcriptionally inactive, okay? Versus double stranded DNA that's more along the u chromatin end of the spectrum, that is more transcriptionally active, okay? So u chromatin is transcriptionally active, but if you keep going from u chromatin to nucleosome or 10 nanometer, whatever it's called to a 30 nanometer, whatever it's called, and then you go to heterocromatin, you actually decrease in the access that the enzymes that you need for replication have to DNA transcription, and then you don't end up working on that DNA molecule. In fact, if you're sort of thinking about your heterocromatin, they kind of look dark on electron microscopy, and again, that should kind of make sense, right? Because if you're something that's very compact, you don't let a lot of light sort of go through you, right? Because you're dense, right? So you don't let light go through you, and if light does not go through you, sort of show up as dark spots on the microscopy. Versus u chromatin that looks a little lighter on electron microscopy, again, they love to give electron micrographs on step one, so look at electron micrographs of the cell before you take your exam. And if you're thinking of heterocromatin, I mean, if you're looking at females, females have an excromosome that is inactivated, right? That excromosome, right, basically has a lot of heterocromatin, right?

So you sort of show those, shows up as like a dark thing, if you're looking at the female cell, grossly, right? That's what's known as a bar body, as a bar body. Okay, now, one other high-yield thing you want to know is that if you want to make DNA transcriptionally inactive, you want to methylate that DNA, okay? But if you want to make DNA transcriptionally active, you actually want to acetylate that DNA. And again, kind of think about this for a second. If you add an acetyl group to DNA, acetyl groups have negative charges. By plastering your license and arginines and all that stuff with acetyl groups, that sort of disengages the histones from DNA, because those negative charges, right, that you're blessing them with from the acidulations, right? Those negative charges sort of like bang up with the negative charges of the phosphates on DNA. And that can make, you can basically like make DNA more transcriptionally active that way. And then, one other thing you want to remember with all of this is that, what did I want to say? Well, it's kind of done out of my memory. So I guess I'll just jump to the question we have here. So this question is a host of researchers working on elucidating the cause of death in a stillborn unit. One of my examples are obtained and sent for genetic analysis. Results obtained from multiple experiments reveal the following. So we have DNAX contains 40% adenine and 10% cytosine. And then we have DNAY containing 40% adenine and 25% cytosine.

Now, the question is, DNAX and Y are a likely mixture of what? Option A says human and hep B DNA, option B says human and EBV DNA, option C says hep C and EBV DNA. Option D says HIV and human DNA. And then option E says human and parrho B 19 DNA. I'll encourage you to sort of pause here, think about the question, and then resume the recording to get your answer. But the answer here is actually E, okay? Human and parrho B 19 DNA. So let me talk about why this is true. The thing is, think about this for a second. I said that, remember 82 GC3, no money, correct? So I said adenines always pair with thymines. And cytosines always pair with, no, sorry, adenines always pair with thymines, right? So 80 and then one ends always pair with cytosines, right? So GC. So if those pairs always happen, it should make sense that the number of adenines in a cell should equal the number of thymines. I mean, if you're looking at like, I guess let me put it this way. If you're looking at like a double strand of DNA, right? The amount of ad, if you take those two strands, count all the nucleotides, number of adenines should equal the number of thymines. The number of guanines should equal the number of cytosines, okay? So if you look at DNA X in this question, it contains like 40% adenine, right? So if you know that the number of adenines, you know that adenines always bind with thymines. If there's 40% adenines, there should be 40% thymines, right?

And if there's 10% cytosines, there should be 10% uers guanines or whatever, yeah, if there's 10% cytosines, there should be 10% guanines. And if you add up all those numbers, like 40% adenine, 40% thymine, 10% cytosine, 10% guanine, that makes up 100%. So the math works out. But look at DNA Y. It contains 40% adenine and 25% cytosine. Let's do the math for a second. So 40% adenine, 40% thymine, that's 80%. 25% cytosine, 25% guanine, that's 50%. 80% plus 50% is 130%. You cannot have more than 130%, you cannot have more than 100% DNA, right? So the math does not work out. So since the math does not work out, that should tell you that you're not dealing with double stranded DNA for this case. You're actually dealing with single stranded DNA, okay? And is there a single stranded DNA thingy that's among the five answer choices I have here? Well, I hope you're thinking about Parvabine 19. Remember, it's probably the only high yield single stranded DNA virus that you need to know for, for step one. So the answer is actually E, okay? So DNA X obeys the rules that we sort of lead at the beginning of the question. So it makes sense that it should be human DNA, human DNA is double stranded, okay? But DNA Y does not obey that rule. So it probably makes sense that that is single stranded DNA. So the answer here is E. If you're sort of like thinking like, divine, what kind of rule are you talking about here? I would encourage you to maybe go back to undergrad and look at Shargav's rooms.

That's kind of what I illustrated in this question. But one last thing I'll mention here is that doing well on step one is not just knowing your concepts. I mean, it's great to know your concepts, but it's also great if you're kind of like a good test speaker, right? So let's talk about test-taking strategy here real quick, right? The thing is, even if you did not know the concept that was being tested, this question talks about a stillborn unit, right? The thing is, if you just look at that demographic, there are very few things that make a newborn, stillborn. In fact, if you've studied adequately for step one or paid any kind of attention during your preclinical years of med school, there are probably only two things you want to be thinking about under those circumstances. The two things you probably want to think about are one, either like hydrops fatalis from a kid that has a, well, I guess maybe three things, right? So you can think of like hemolytic disease of the newborn from like R-HN compatibility, that's one. Another thing that could cause that is if you have like a weird thalacemia, right? So like hemo globin barks, where you have like gamma-4, so like a profound severe loss of like four genes for your alpha globin chains. And the thing that could also cause it is parvo B19, right? Because it can infect your red cell precursors. In fact, that's why I said, in this question I said, bone marrow samples were obtained.

So if you do that analysis, you can see that, okay, there are only three things here that can kind of give you this kind of presentation, right? So the only answer here that sort of agrees with those three things I've come up with is parvo B19. That's why the answer is E. So notice, you could also have got in this answer if you're just a good test-eaker, okay? So I'm not saying to not study study, but being a good test-eaker certainly helps on the very difficult questions. So I hope you found this to be helpful. I will continue this series. This is obviously something I love discussing. And we'll talk about this in a few, I would say some more things about cell biology in a future podcast. Have a wonderful Saturday and I'm very glad that Manchester United won a game from Tunnel to 32. I was pretty happy with that. So God bless, I'll see you in the next podcast. Thank you.

Reverse transcriptase (e.g., used by HIV).

Replication occurs in the nucleus during the S (Synthesis) phase.

RNA contains a hydroxyl group ($\text{OH}$) at the 2' carbon, whereas DNA has only hydrogen (deoxy).

Acetylation.

Heterochromatin; it is generally transcriptionally inactive.

5-Fluorouracil (inhibits thymidylate synthase) and Methotrexate (inhibits dihydrofolyl reductase).

Purines have two rings (Adenine, Guanine); Pyrimidines have one ring (Cytosine, Uracil, Thymine).

Lysine and Arginine.

Histone H2 A, H2 B, H3, and H4 (forming an octamer) wrapped around $\text{DNA}$.

Transcriptionally inactive.

Adenosine deaminase deficiency.

Compaction increases (from 10 nm $\rightarrow$ 30 nm $\rightarrow$ highly condensed); transcriptional activity decreases.

Purines have two rings (Adenine, Guanine); Pyrimidines have one ring (Cytosine, Uracil, Thymine).

Lysine and Arginine.

Histone H2 A, H2 B, H3, and H4 (forming an octamer) wrapped around $\text{DNA}$.

Transcriptionally inactive.

Adenosine deaminase deficiency.

Compaction increases (from 10 nm $\rightarrow$ 30 nm $\rightarrow$ highly condensed); transcriptional activity decreases.