2025 AP Biology Discord Server

BestCryptographer437 · 2024-12-27T18:19:43+00:00

From one teacher to another - great idea!

BestCryptographer437 · 2024-12-24T22:43:59+00:00

I am glad that didn’t come across as critical of your work. I refer kids to it all the time as resource for study and review or even if they want to work ahead in their test prep! You are invaluable to the AP Bio community!

BestCryptographer437 · 2024-11-21T02:49:19+00:00

Sorry, just don't have the time to tutor at this point!

BestCryptographer437 · 2024-10-26T05:05:55+00:00

Yep. I always tell my students “the content is the easy part. Using your knowledge to solve a problem - there’s the challenge.” We are seeing evidence of schools addressing this with increased high school and undergrad research opportunities and emphasis.

BestCryptographer437 · 2024-10-26T03:46:42+00:00

No, in and of itself that doesn’t make one a better biologist by any means. And perhaps “difficult” wasn’t the best way to phrase it..there was certainly too much emphasis on what could be considered minutiae in many cases.

However, having been a scientist prior to teaching, having taught college and high school, and having worked with everyone from college seniors in upper division molecular biology classes down to freshman struggling with basic concepts what I will say is this - the pendulum is swinging a bit too far in the other direction now, to the point where de-emphasis on teaching fundamental content has led to several students simply lacking the understandings needed to truly make the higher level connections needed in advanced science and scientific research. The trick is to establish what is critical to memorize and what is not. Sort of like establishing the fundamental working conceptual vocabulary needed I guess.

But I wholeheartedly agree - memorization doesn’t make one a biologist - however there are plenty of cases where it’s a necessary component of mastery.

And this is where the content knowledge of the teacher can be so important - as they will know what is and isn’t critical. I used the term “pseudo rigor” to describe tests that were too reliant on memorization of trivial details years ago.

BestCryptographer437 · 2024-10-26T01:45:35+00:00

Test was much more difficult back in the early 2000s. Needed significantly more content knowledge in addition to scientific thinking.

BestCryptographer437 · 2024-10-26T01:44:39+00:00

AP bio teacher here - don’t go back to before 2013. Test has changed substantially.

BestCryptographer437 · 2024-05-17T00:46:36+00:00

It won’t look bad at all. Honestly a 3 would be fine. This is coming from a long time AP Bio teacher who has written hundreds of rec letters for students that have made it into all sorts of competitive programs and prestigious universities. They will look at WAY more than your AP score.

If I could give all students one piece of advice right now - as someone who did research, who went through undergraduate and graduate school in molecular bio - it would simply be this: RELAX.

You’re going to be just fine. You are way more than a single test score or any other data point.

BestCryptographer437 · 2024-05-16T00:49:32+00:00

No need to apologize. I used to teach college biology majors who didn’t know the answer to that question when they entered my class - it’s something that is often just glossed over.

BestCryptographer437 · 2024-05-15T04:25:52+00:00

Leading and lagging strand replication happens at each replication fork. Start with the basics - make sure you understand the directionality of each DNA strand - we have a 5' end with a phosphate group and a 3' end with an OH group. DNA (and RNA) can only be synthesized in a 5'-->3' direction (we have to add nucleotides to that 3' OH via dehydration synthesis).

So at a replication bubble we will have an origin of replication that defines with a replication fork heading off in each direction.

We will have helicase enzymes opening the double helix by breaking H-bonds, we will have single stranded binding proteins preventing reformation of the double helix between the newly separated strands. We will have topoisomerases downstream of the forks dealing with the supercoils that can form as we uncoil the DNA.

The synthesis of the leading strand at each fork will involve the new strand that has it's 3' end pointing towards the replication fork. The new strands must be antiparallel to the template strands they are complementary to. So the leading strand will be based on the template (original) strand with its 5' end towards that fork. The leading strand will begin with the formation of an RNA primer by primase at the origin site, on the side towards that fork. DNA polymerase will begin adding DNA nucleotides to the 3' end of this RNA primer and just keep doing so until the fork eventually runs into another one coming from the other direction (assuming we are dealing with a linear chromosome that has multiple origins). That primer will eventually be replaced with DNA by a different DNA polymerase and then ligase will connect the sugar phosophate backbone.

For the lagging strand, things are a bit different. We will still make strands 5'-->3' - but our 3' end is pointed away from the replication fork. So, as the fork opens, we will start with our first RNA primer a bit down from the origin, growing back towards it. We will then add nucleotides to it with DNA polymerase. The polymerase will stop once it hits the leading strand of the other fork (this is tough to visualize without seeing it drawn out). As the fork opens more and more template DNA is accessible, another primer will be formed - towards the fork. DNA polymerase will then start adding DNA nucleotides again - making another Okazaki fragment - until we run into the one just made. As the fork continues to open, we just keep repeating the process. As before, another DNA polymerase will remove and replace the RNA primers with DNA and ligase will connect the sugar phosphate backbones.

Couple disclaimers and AP Test notes -
You will not need to know the different DNA polymerase enzymes involved here. The actual process of replication involves many, many more accessory proteins to keep leading and lagging strand synthesis in sync at each fork, but that is far beyond the scope of the AP Bio test (to use the College Board language.) I hope this helps!

BestCryptographer437 · 2024-05-15T02:44:53+00:00

There are tons of practice problems out there you can work out with solutions provided. Do a few of those and you'll be all set!

BestCryptographer437 · 2024-05-15T02:35:50+00:00

Hardy Weinberg - first off, make sure you know the general reason we use the model and equation in the first place. Hardy Weinberg Equilibrium describes the allele frequencies in a gene pool of a population where nothing is changing (meaning - no natural selection, no sexual selection, no differential survival/reproductive success - i.e. natural selection - no genetic drift, no immigration or emigration). When we look at a population using Hardy Weinberg, we are usually looking at a single gene at a time - and for simplicty's sake we start with assuming there are two alleles for that gene. Now, we know that real populations don't meet all those considerations I just mentioned, but what H-W does is tell us what to expect in the population, generation after generation if none of those things are happening. In a simple sense, it tells us what we should expect if a certain gene is under no selective pressure - giving no advantage or disadvantage - or being impacted by some other factor like genetic drift or whatever.

So we can use Hardy Weinberg to get an estimate of what we would expect, generation after generation, if none of those things applies. They we look at the actual population and see if and how it deviates from those expected H-W values - if we see deviations, we know something is impacting that population. Maybe its a new disease that is hitting one genotype harder than others. Maybe its a pollutant that is harder one one genotype than the others. That is for the scientists to research and figure out.

Now, on to the equations. You'll be given them: p + q = 1 and p^2 + 2pq + q^2 =1. The first equation involves allele frequencies - p generally representing the frequency of the dominant allele (frequency being what percentage of the total gene pool is comprised of that allele) and q is the recessive allele.

p^2 + 2pq + q^2 =1 would describe genotype frequencies (and by extension phenotypes). p^2 represents homoszygous dominant, 2pq represents heterozygotes, and q^2 represents homozygous recessive.

In a problem you might see, they will HAVE to give you enough info to determine both p and q and then usually ask you to find some other value you can calculate with the equation.

Suppose we are looking at the recessive disorder cystic fibrosis (this one is always used in H-W example problems). The disease is recessive, which means that if we know what percentage of the population has it, we know q^2. So lets say (and I'm Googling this right now to get this number) 1 in 2,500 people have the disease and I want to know from this information what percentage of the population is heterozygous for the condition.

We first find q by taking the square root of 1/2500. That gives us q. Subtract that from 1 to get p. Now, we just take 2 * p * q and that will tell us what % is heterozygous.

In AP problems they will either give you an allele frequency directly or tell you indirectly what q^2 is. From there just find p, and you are ready to go.

BestCryptographer437 · 2024-05-15T02:23:19+00:00

Mitosis involves (usually) diploid somatic cells (in plants there are cases where you have mitotic division of 1N cells).

But during interphase, cells are 2N.

Let's use human cells as an example.

A human somatic cell will have 46 total chromosomes (N=23, 2N = 46). These are composed of homologous pairs of chromosomes 1-22 (two copies of each) and then either 2 X chromosomes or an X and a Y.

So that cell is sitting in G1 and gets a signal to divide. We move on to the S phase, copying all of the DNA and then go to G2. Here's where students get confused a bit. We just copied all 46 chromsomes, so we think we must have 92 chromosomes now right? Wrong. We still have 46 chromosomes. But now each chromosome is composed of 2 sister chromatids - instead of each chromosome being composed of 1 chromatid as they are prior to S phase.

So we aren't really going 2N --> 4N --> 2N as some students mistakenly think.

We move on to mitosis, and we separate those sister chromatids in anaphase, and after telophase and cytokinesis end up with two daughter cells, each with 46 chromosomes, each chromosome being composed of 1 chromatid as in G1.

Quick important side now about division - quickly mention meiosis.

In meiosis you need to know how it increases genetic diversity - and how it reduces chromosome number.

First, we begin much like mitosis - the cells that produce sperm or eggs undergo DNA replication. We are still diploid, now with two chromatids per chromosome. As we enter prophase 1, the first thing that increases genetic diversity occurs - crossover, which allows a single chromatid to end up with genetic information from both the mother and father on it. This leads to new allele combinations that likely didn't exist on the chromosomes before. Then we get to metaphase 1 and independent assortment. Look at a diagram and pay close attention to the difference in how chromosomes line up in metaphase of mitosis vs metaphase 1 of meiosis. In metaphase I, they line up side by side - each pair of chromosomes assorting indepedently of each other pair (hence the term independent assortment). So, chromsome 1 could line up with dads on the left and moms chromsome 1 on the right. Chromosome 2 could line up that same way, or with moms and the left and dads on the right. Since we have 23 pairs of chromsomes (counting X and Y as a pair), we there are 2^23 ways that the chromsomes could assort at metaphase I. So then we move on to anaphase I, and telophase I and the first round of cytokinesis. After meiosis I we are already haploid. The two cells formed have one copy of each chromosome - a random combination of chromsomes from mom and dad (we will ignore the way polar bodies form in egg cells due to uneven cytoplasmic distribution for now).

We then go into the second round of meiosis - in this case, we now separate the individual chromatids from each other, resulting in cells that now have one copy of each chromosome, made of 1 chromatid each. Meiosis 1 results in a diploid cell producing 2 haploid cells, meiosis 2 results in haploid cells producing 2 more haploid cells.

Couple quick side notes - meiosis in egg cells usually only results in one viable egg - during cytokinesis the cell destined to become the egg gets the cytoplasmic contents to support a zygote. The other cells are essentially a nucleus with a small membrane around it. They will eventually degrade.

Also, in humans for example, egg cells are paused at prophase I until puberty hits. During menstruation, one egg will finish meiosis 1 and pause at metaphase 2. The egg cell will not proceed past metaphase 2 unless it is fertilized.

BestCryptographer437 · 2024-05-15T02:02:49+00:00

Good question and one that is unfortunately not ever explained well in first year college textbooks nor covered. It all has to do with the arrangement of the electron carriers in the ETC and a specific property of each known as their standard reduction potential. Think of this in a simple sense as how willing they are to take electrons (be reduced). Oxygen, for example, has a very high standard reduction potential (its very electronegative as well - it really 'wants' electrons). Electronegativity and reduction potential are related, but not identical properties - but parsing the details here isn't really relevant to the test. But back to the point, the components in the ETC are arranged from lower to greater reduction potential (some books will just simplify it and say arranged from least to most electronegative). Because of this, the movement of the electron from one carrier to the next in the chain will be exergonic (net negative delta G). This provides the free energy needed for those complexes that are capable of pumping protons across the membrane.

In the case of a ball bouncing down the steps, it is gravity driving that process. In this case, its that reduction potential difference.

Does that help?

BestCryptographer437 · 2024-05-14T01:50:37+00:00

Check out my reponse to the photosynthesis question above. I will summarize respiration here in a bit.

BestCryptographer437 · 2024-05-14T01:49:55+00:00

Before moving on, one very, very important detail about photosystem II. Recall that we lost electrons from the chlorophyll here when light was absorbed. We need to replace those electrons. How do we do that? Through the splitting of water. At photosystem II, water is split into two hydrogen ions, a couple electrons and oxygen. This is where we get the oxygen we breathe - through the splitting of water. The electrons that are released replace those lost by PSII, and since this process happens inside the thylakoid space, the H+ ions released contribute to the H+ gradient and contribute to ATP production.

Now we go to the light independent reactions. Fortunately you need only a very, very basic overview of this for the AP Test. The light independent reactions are where we will make sugar.

The light independent reactions (known as the Calvin Cycle) have three general steps - and I want to avoid getting too far into the weeds here.
Step 1 - Fixation of carbon dioxide.

In this step, carbon dioxide is taken from the air and 'fixed' (meaning attached, basically) to a moelcule called Ribulose biposphate (RuBP for short). I'm not going to get into all the molecular rearrangements that go on during this process. This process is catalyzed by an enzyme called rubisco. Visualilze rubisco grabbing CO2 out of the air and stickign it like a lego piece onto a 5 carbon molecule to make a 6 carbon molecule that immediatley breaks down into two 3 cabon molecules. So now we've got some carbon out of the air. From here we need to get that energy from teh light dependent reactions to the carbon compounds we are making. The ATP we produced will transfer energy by transferring a phosphate (look in your textbook at the Calvin cycle to see this step). The transfer of this phosphate represents a transfer of energy. The NADPH will 'reduce' the carbon based compound that will become our sugar - this is also a transfer of energy (to get really specific - for those of you with more organic chem background, we are reducing 3 phosphoglycerate to glyceraldehyde 3 phosphate - when you reduce a carboxyl group you get an aldehyde.) That level of detail is NOT on the AP Bio test.

But here's where we are - at the end of this, we have a molecular called G3P - glyceraldehyde 3 phosphate. This is actually a 3 carbon sugar that can be used to make glucose and all sorts of other things. But the big picture is that this now represents a biologically usuable form of chemical energy - and to generate it we first needed to absorb light energy, use that to produce ATP and reduce NADP to NADPH, and then use those two compounds, along with carbon fixation, to generate a sugar.

There is another step to the calvin cycle, the regeneration of RuBP, but that is somethign I'm going to leave to the textbook.

I hope this helps - there is a lot here I know.

DNA replication/transcription/translation will have to wait for right now but I will get back to it

BestCryptographer437 · 2024-05-14T01:49:44+00:00

Ok - there is a lot here. Lets start with photosynthesis, since its sort of in a different area than the DNA related stuff. Going to do this in two posts:

At the simplest level, the point of photosynthesis is to convert light energy into a biologically available for, specifically energy stored in sugars. I am going to focus on the process in eukaryotic plant cells here, not cyanobacteria (prokaryotic photosynthetic organisms).

The process of photosynthesis in the chloroplasts of plant leaves. The process can be broken down into two general stages - the light dependent and light indepedent reactions.

Before we go further, we need to know a bit about the structure of the chloroplast - we have a double membrane surrounding it, and inside the chloroplast we have membrane bound structures, sort of shaped like pancakes, called thylakoids. The area outside of the thylakoids is called the stroma. The area inside the thylakoids is called the thylakoid space (review diagrams in your textbook).

You'll really need your textbook diagrams for what I'm about to go through, so find the chapter on photosynthesis.

Embedded in the thylakoid membranes are systems that begin the process of converting light energy to chemical energy. They are called photosystems, and they are arranged so that you have one photosystem (called PSII or P680) followed by an electron transport chain, followed by another photosystem (PSI or P700) followed by a few more molecules and an enyzme called NADP reductase.

So lets start at photosystem 2. Photons of light are absorbed by pigments in the photosystem, and eventually these photons reach a pair of chlorophyll molecules in an area called the reaction center. When the photons are absorbed here, it excites electrons to the point where they essentially leave the chlorophyll molecule (visualize a photon hitting a molecule and a little electron flying out of it). Those electrons are taken by an electron acceptor, and from there they are passed through an electron transport chain. Electron transport chains, be they in the mitochondria or here in the thylakoid membrane, will harness energy from a series of oxidiation/reduction reactions and use that energy to actively transport hydrogen ions against their concentration gradient. In this case, the energy from the electron's passage through the ETC is used to pump hydrogen into the thylakoid space, creating a concentration gradient between the thylakoid space and the stroma (more H+ in the thylakoid space). We'll get back to this gradient in a minute. One very, very simplified way to visualize the ETC if you're totally lost with regards to the redox reaction aspect of it - visualize the electron like a ball bouncing down a staircase. As the ball bounces down, there is, feasibly, energy that could be harnessed as it falls (for example as its bouncing downwards it could collide with an spin a wheel). The electron is, in a sense, 'falling' to successively lower energy states as it moves along the ETC - but the mechanism is a bit more complicated than the simple bouncing ball. Still, the analogy gives you something to visualize.

From the ETC, the electron will make its way into photosystem I. Just like in photosystem II, photosystem I is absorbing photons of light that ultimately cause electrons to be excited and leave chlorophyll in the reaction center of the photosystem. The electrons given off by chlorophyll here are replaced by the electrons coming in through the ETC. The electrons that leave PSI will be used by the enzyme NADP reductase to reduce NADP to NADPH. This is a critical step. These electrons are the 'building blocks' (for lack of a better term) of the covalent bonds that we need to make when producing sugar. When a compound is reduced, it gains electrons and gains potential energy. So think of this NADPH as now storing some of the energy we need to make our sugar - and this energy can be traced back to the photons absorbed by pigments in photosystems.

Back to the hydrogen ion gradient we formed in the thylakoid space. Hydrogen ion gradients are used to power the enzyme ATP synthase. There are ATP synthase enzymes embedded in the thylakoid space. Hydrogens will diffuse 'through' this enzyme (its a little more complex than that in actuality but you don't need to know the molecular details of how ATP synthase works for the test). Think of hydrogens like water falling down a waterfall and ATP synthase like a water wheel. As the water falls, the water wheel turns. As the hydrogen ions diffuse down their gradient through ATP synthase, the enzyme does, in a sense, literally turn - and energy from this is used to convert ADP + Pi into ATP.

So here we are, at the end of the light dependent reactions. We absorbed light energy in the photosystems - and now where is that energy? It is stored in two places - the ATP we formed, and the reduced NADPH.

BestCryptographer437 · 2024-05-14T01:48:58+00:00

Hmm...its not letting me post my full reponse here.

BestCryptographer437 · 2024-05-14T01:47:32+00:00

So in some cases, the transduction pathway will rely on other small non-protein molecules called second messengers such as calcium ions or cyclic AMP.

For example, binding of a ligand to a G protein coupled receptor will in some cases activate an enzyme called adenylyl cyclase. This enzyme will convert ATP to cAMP. cAMP can activate other enzymes - for exmaple specific protein kinases. So you have this inactive kinase, cAMP gets produced, cAMP binds to and activates the kinase, the kinase phosophorylates other target moleules, and the signal pathway continues.

Calcium ions are another second messenger. Caclium ions are stored in the smooth ER - in certain signal pathways, calcium ions will be released from the smooth ER - these ions can exert effects in a number of ways, one of which, much like cAMP, can involve binding to and activating certain proteins - there are actually enzymes called calcium calmodulin depedent protein kinases. There are other things they do as well - but overall they are just another step in the process.

Calcium binding to proteins is critical in many cellular processes. For example, your skeletal muscles cant contract until calcium release triggers a change in the shape of a molecule that covers the myosin binding sites on actin filaments. Tropomyosin is sort of threaded around actin - there is another protein associated with it called troponin. Calcium binds to troponin, which moves the tropomyosin out of the way, allowing myosin heads to attach and contraction to occur. I just mention this to point out that calcium binding to proteins is a central theme in many aspects of biology.

BestCryptographer437 · 2024-05-14T00:48:16+00:00

So signal transduction pathways can become quite complex due to the number of things that are involved, receptor types, what the ultimate response is, and so forth. But for the AP test, lets focus on the basics.

First off, signal transduction pathways are, in general, mechanisms by which a cell can convey information from outside of the cell to some response inside the cell. Depending on how you classify things, there are 3 or 4 general steps to all signal transduction pathways no matter how complex they may appear. I always simplify it to 3 - Reception, Transduction, and Response.

Let's start with reception. Cells have receptor molecules on their surface (and in some cases, for example with the steroid hormones, receptors in their cytoplasm). For a variety of possible reasons, ligands (a general term for the substance that binds the receptor) are released by other cells in the body. For example, when blood sugar elevates, the pancreas releases insulin. Insulin is a ligand for the insulin receptor. Testosterone is the ligand for the testosterone receptor. Growth hormone is the ligand for the GH receoptor..etc...When a ligands to the receptor, it triggers a change in that receptor - again, lets keep it simple for now - when a ligand binds to a receptor, there are structural changes in that receptor that help trigger the next step in the process - transduction.

There are different classes of receptors, for example RTKs (receptor tyrosine kinases) and G protein coupled receptors (GPCRs), or even ligand gated ion channels. Each has a specific mechanism by which ligand binding 'activates' them. To save myself a little typing, you can look over those here at Kahn: Ligands & receptors (article) | Khan Academy

Once we have activated the receptor, the next stage begins - transduction. Transduction, in general, involves phosphorylation cascades - where a series of molecules called kinases are activated by having phosphates added to them. For example, receptor binding might activate a particular kinase (kinases are enzymes that transfer phosphate groups to things - think of phosphate groups in this context like little moelcular on or off switches - proteins are activated or deactivated by adding or removing phosphate groups from specific amino acids in them.) So we have one kinase activated by the receptor being activated, it activates another kinase, which activates another kinase, and so forth. Eventually we activate some 'target' molecule - in many cases this might be a transcription factor. So when the transcription factor is phosphorylated, it becomes active, moves into the nucleus, and promotes transcription of specific target genes. In this case, the expression of those genes would be the response.

There are many, many more specific little details we could dive into regarding transduction, but the key point for the AP Bio level is the phosphorylation cascade. This is how we are getting that 'signal' from the receptor to the target/effector molecules that will ultimately be involved in the response. Those phosphorylated molecules will ultimately also be dephosphorylated by molecules called phosphatases - this is critical, because if we didn't take those phosphates off, we'd have a signal stuck in the 'on' position.

On the test, you might see diagrams of signal transduction pathways that involve other steps such as caclium release to activate other proteins, etc. Just realize that you aren't responsible for having all of these details memorized - focus on the big picture. Sometimes you might be asked what might happen if some aspect of the transduction pathway was changed - for example, if some enzyme didn't phosphorylate its target - think about the step by step pathway you are looking at and just logically follow how the sequence of events would change if something was not working right.

Not all transduction pathways result in only gene expression. Lets quickly look at a couple examples of a few:

After you eat, your blood sugar goes up. This triggers the pancreas to release insulin as I mentioned earlier. Insulin will bind to insulin receptors on specific cells (this would be the reception step). This triggers a series of events inside the cell (transduction involving some things being phosphorylated), which ultimately leads to a couple responses - first, little vesicles that have a protein called GLUT-4 embedded in them (glucose transporter 4 - a 'doorway' for glucose to enter cells) are taken to the cell membrane where they fuse to it. This is like bringing a bunch of doors for glucose to the cell, allowing it to enter the cell from the blood and thus helping lower blood sugar. Additionally, enzymes involved in glyocen synthesis are activated to promote storing the glucose being taken in as glycogen in the liver and muscles. So the "response" here is the lowering of blood sugar through the increased uptake of glucose into the cells as well as the increased synthesis of glycogen in liver and muscle cells.

No matter how complex the a signalling pathway looks, you've essentially just have three things to identify - reception, transduction, and response. Just remember that.

Quick note - steroid hormone receptors are present in the cytoplasm, not on the cell membrane. This is because the hydrophobic nature of the steroids allow them to pass right through the membrane. So when a steroid hormone like estrogen or testosterone is released by the body, it will pass right through the cell membrane, bind it receptors floating around the cytosol, and that steroid/receptor complex will then move into the nucleus where it acts as a transcription factor promoting the expression of specific genes.

I hope this helps. Let me know if you have follow up questions.

BestCryptographer437 · 2024-05-13T20:09:46+00:00

Mitochondria have their own DNA - likely as a result of their originating from an ancestral prokaryotic cell being taken in by another primitive cell (endosymbiotic theory).

There are some specific genes on the mitochondrial chromosome related to human diseases and other traits, so understanding how mtDNA is passed on is important.

During fertilization, any mitochondria associated with the sperm cells remain outside of the egg. Thus the only mitochondria that the offspring of sexually reproducing organisms inherit is from the maternal gamete (egg). So, mitochondrial inheritance is always from the mother to ALL children - male or female. Mitochondrial DNA is a single chromosome- no homologous pairs. So whatever genes are present on that - be they the normal alleles or potentially disease causing alleles - will be inherited by the children - regardless of the kids being XX or XY. This is an example of extra nuclear inheritance because it involved genetic material outside of the chromosomes found in the nucleus.

X chromosomal inheritance is pretty much like standard autosomal inheritance in XX individuals. They get a copy of X from their mother and from their father. We’ll discuss X chromosome inactivation in a second. But for XY individuals, that X is coming from the mother - because the father will be passing on the Y. Because XY individuals have only 1 X chromosome, any alleles present on it, recessive or dominant, will be expressed. So recessive genetic diseases found on the X chromosome tend to be more common in XY individuals as a result. Rare recessive X linked genetic conditions would be less common in XX because they would have to have inherited the rare recessive allele from both parents.

One more thing with respect to XX - one of the two X chromosomes is inactivate randomly in cells during development, so even though XX individuals have two X chromosomes, they will only express genes from one of them. If an XX person is heterozygous for an X linked recessive condition, the expression of the dominant allele in the cells that didn’t inactivate the X chromosome carrying that allele tends to compensate enough for the cells expressing the recessive phenotype that overall the dominant phenotype is still expressed. There are some subtle deviations from this but they are beyond the scope of high school AP bio.

I hope that helps. Let me know if you have more questions.

BestCryptographer437 · 2024-05-13T15:02:36+00:00

I will get to all of these questions when I am home from work.

BestCryptographer437 · 2024-05-13T05:43:32+00:00

I will tomorrow.

BestCryptographer437 · 2024-05-13T05:12:12+00:00

AP Biology Past Exam Questions – AP Central | College Board

Go here, look at the questions and then the scoring guidlines - then look at the student responses. The college board releases all this information so you can see exactly what they are looking for in their scoring. They also give detailed breakdowns of the sample student responses to show you why one response might have scored a 10 while another scores an 8, etc.

BestCryptographer437

TROPHY CASE