Patrick Roisen

M.Ed., Stanford University
Winner of multiple teaching awards

Patrick has been teaching AP Biology for 14 years and is the winner of multiple teaching awards.

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Non-Mendel Genetics

Patrick Roisen
Patrick Roisen

M.Ed., Stanford University
Winner of multiple teaching awards

Patrick has been teaching AP Biology for 14 years and is the winner of multiple teaching awards.


When students are studying genetics, most kids get the whole difference between dominant and recessive traits and they understand Mendel's two laws. Then they hit the AP Biology exam and they'll see a question that might start off like this; a plant seller breeds an orange flower and a white flower and produces 31 orange and 28 whites. Then they take two of those white flowers, cross those and you get 14 orange and say 30 whites. Explain these inheritance patterns.

The student starts off saying okay that first generation, that’s a 1:1 ratio. I know what’s going on here I’ve got a homozygous recessive being crossed with a heterozygote, I’m good to go. Let’s take a look at that next generation, where I’ve got two of my heterozygotes being crossed. I know I’m going to get a 3:1 ratio. I look at the numbers and it’s a 2:1 ratio. What’s up with that?

It turns out, things are a lot more complicated than Gregor Mendel knew. It’s kind of ironic that this man got lucky. Instead what happened is, when he studied those pea-plants, he happened to pick traits that all follow the same basic rules or pattern of inheritance and those are simplest ones of them all. It turns out as we’ve gone on and studied more about how inheritance happens, there’s lots of complications.

What I’m going to do today is, I’m going to go through all those complications, and I’m going to start off with some of the variations on Mendel’s Complete Dominance. We’re going to be looking at Co-dominance and Complete Dominance and things like that. Then, I’ll go into some of the ways genes can interact with each other like Epistasis. Then I’ll go into how you can have linked genes which violates Mendel’s second rule. Then I’ll look at sex-linked traits which completely blow through Mendel’s rules.

I need to warn you that I’m going to be flinging around a lot of term today like gene and allele, heterozygous and homozygous like an angry chimp t the sewage plant. So you need to be really sure that you’re aware of these terms and know what they mean. If you don’t, I really recommend that you go to your textbook and read that portion of it, or even better, watch my videos on Mendel two laws.

Assuming that you do know all these sort of things, let’s go into some of the exceptions of complete dominance. Now Mendel talked about dominant and recessive traits. Now, to understand what that means it really is helpful to go down to the molecular level and figure out why is a trait dominant? Or why is it recessive? Generally, what it turns out, is that a dominant version of a gene simply is dominant, because it makes something. It’s a section of DNA that codes for a protein that actually gets made and then actually does something.

The recessive version of that gene instead is just same section of DNA, but because the sequence of ATCs and genes will be different, it winds up not turning on, so no protein is made. Or the protein that is made is faulty in some way or doesn’t do the job it’s supposed to. That way if you get one copy of the gene that’s dominant, you make that enzyme, that enzyme can do whatever function it needs to. If you get two copies, yeah, you still can do it. If you get a non-functional copy so long as you have that backup of functional copy you’re fine. You do show that our recessive trait for example. However, if you get two non-functional versions of that gene for example I can roll my tongue. Those of you who can’t, you actually don’t have any instructions in your DNA that tells your body when you’re deep within your mummy’s womb at a certain period of fetal development to start building some muscle fibers going this direction on your tongue. I did have at least one copy of that, so I turned that on, I can roll my tongue. That’s it.

Now that seems pretty simple once you understand it, but what happens if there’s more than just two versions of a gene? What if you have three? Well, let’s go ahead and take a look at how this could work.

Let’s imagine there is protein that your cells could possibly use for cellular identification. It’s a protein that should shove up on the membrane and it allows your immune system to recognize who belongs and who doesn’t.

Let’s say there’s a version of that gene that I’ll call A. So if you get one copy of the A allele, if this is one of your cells, you can make proteins called A. I’ll just write them as the letter A. Proteins do not look like letters; I just want to make sure you get that. If you get one copy of A and another copy of A, then you’ll be happy making As all over your cells.

Let’s say there’s a version of the gene that doesn’t make anything. I’ll call that zero. If you get A and zero, you get the instructions to make A and nothing. You’ll still make A.

Let’s imagine you had a test to detect whether or not you had As on your cells. Well, you do your test and with somebody’s A, A you would find those A. Somebody who is A, zero, they would still make a cell that ha s As on it like this. They may not have as many, but they’ll have some. A lot of times your DNA can be regulated to increase its output to compensate for the fact that it’s missing the normal amount of the copies of gene. But this person has these As on their cell, this person has As on their cell, so we’ll say they’re the same basic kind of cell. All right, so far so good.

What if they had two versions of O? Then they would make nothing and then they would make some more nothing. So this person would have our type zero cells. So everybody is fine so far? Let’s make this back up a little bit. Let’s get rid of some of these things here. Let me see if I can just make this go away like that. Perfect. So now let’s look at a version of this gene that makes a different protein. It’s similar to A, but different enough that we’ll call it protein B. So allele B, if you get one copy of it, you make B proteins on your cells.

If you do two copies, you make B proteins on your cells. So somebody who has B and B, they make B proteins. Somebody who has B and 0, they make B proteins and nothing which is still; if we do our test, we can detect they’re type B. So, so far things are pretty simple. A is dominant to zero, B is dominant to zero, so zero was recessive. Now the question comes up, what the heck is going on if we have somebody who has the A version of this gene and the B version of the gene?

Well, what does A tell you to do? It tells you make A proteins. So that cell will make A proteins. This section of the DNA says make some B proteins, and the cell will happily do what the DNA is telling it, and it will make some B proteins. So when you do your test, you’ll detect they’ve got As and they’ve got Bs. So what do we call this? We call this type AB. So one type is type A, another type is type B. A third type is type AB and then there is that zero.

Now I’ve been using letters, so how about I just change the numbers zero to the letter O? That looks similar. Wait a second, that’s blood types. A, type B blood, type AB blood and type O. That’s how blood typing works. Now what do we call the relationship between A and B? Because they’re both dominant to what I used to call zero and now we’ll call O, because that’s the correct way to call it. They’re both dominant to O. How are they related to each other? They are both expressed equally. So we call that co-dominant. So the A allele for blood typing and the B allele for blood typing are co-dominant to each other, completely dominant to O. So now you know how blood typing works and that’s a great example of co dominance.

Now some of you maybe wondering what about the A positive or O negative stuff? That positive or negative is referring to a separate gene called the Rh factor. The positive just means that you got at least you’ve got one copy of how to make it, the negative means you have two copies of the non-functional. You can’t make the Rh factor protein.

What’s another example of co-dominance? Well, roan cows would be. So let’s take a look at what a roan cow is. So if we take a look at this, this is a kind of cow called a roan cow. Now a roan cow from a distance looks pinkish. But if you get closer and closer, you’ll see it is actually covered with red hairs right next to some white hairs, not pink hairs. So how do you get a roan cow?

Well, it turns out, a roan cow is produced when you mate a white cow, with I hope, let’s pretend this is a bull. So here we see a red cow and to make a red cow, it has two copies of the red version of the hair color gene, big R, big R. This white bull here it has two copies of the white version or allele of the hair color gene. So when they mate, we produce a offspring that has the big R and the big W alleles. They’re co-dominant to each other and that tells this daughter cow here, actually that’s a son. It tells this son here to make some red hairs, and it’ll make some white hairs. So you’ll see red hairs, white hairs, red hairs, white hairs all over its body. From far away it may look pinkish, but up close you’ll see both equally expressed. That’s a trick to spotting co-dominance. You see both equally expressed.

Now let’s take a look at the thing that’s very often confused with co-dominance, and that’s incomplete dominance. The common example, standard example of incomplete dominance, is snapdragons. Snapdragons are a kind of flower. Now there’s red versions of the snapdragon, and there’s white versions of the snapdragon like with the cows. This is why people always get confused.

If you cross a red snapdragon with a white snapdragon, the red ones are big R, big R kind of like our cows. The white ones are big W, big W kind of like the white cows. If you cross them, you get pink. Now it’s pink from a distance and it’s pink up close. When you get really close down to the cellular level, you’re just going to see a pinkish cell. You’re not going to see a red cell next to a white cell. That would be co-dominance. Instead, we see this blending which is what the characteristic trait of incomplete dominance.

You can see what pops up when we cross a pink big R big W snapdragon, with another pink, big R, big W snapdragon. You’ll see one of your offspring is red, one of your offspring is white, and then your two heterozygotes are pink. This is the quite essential ratio that will allow you to spot right away a incomplete dominant trait; if you see a 1:2:1 ratio. That kind of thing will say, or scream out to you hopefully, by the time you’re done doing all these reviews with me, that that’s either incomplete dominance, or sometimes it could co-dominance. When you get to these two hybrids and they’re different from their parents, start looking. Is it blending? Incomplete dominance. Are equal expression? That’s co-dominance.

Now let’s go back to that first thing that I started off, where I was talking about orange and white flowers. So, when we made it a orange flower with a white flower, we wound up getting 31 oranges produced from that P1 generation, and 20 white flowers produced. So you think when you look at this 31 to 28, that’s almost equal numbers. So that’s a 1:1 ratio, or I prefer to call it a 2:2 ratio? Why do I prefer that 2:2? Notice how many boxes, how many offspring we have here? That’s a total of four. I always try to get numbers that are equal to the number of boxes I have to fill in.

So if it’s a 2:2 ratio, then let’s say orange, orange, white, white. Well, I could have a white here, and an orange here. Let’s see will that work? Let’s see white, orange, orange, orange, orange. If orange is recessive, this would work. If white is dominant that would work. This would give me a white parent and this would give me an orange parent which is what I had. This would give me half and half. So life is pretty good so far.

Now you’ll discover that you can arbitrarily make orange dominant to white. You get the same results. So we’re not quite sure, but it looks like it’s our standard dominant recessive thing. But remember, we took two of these creatures here. Two of the white ones and we mated them. Let’s see what happened when we did that. When we did that, we wound up with 14 orange and 30 white. You look at that ratio, these are not equal. In fact, this is pretty darn close to a 1:2 ratio. Well if my parents are orange and white, orange and white, let me start putting that in. I have three boxes. This is a 1:2 ratio. That’s only three. What’s going on over here? When I start doing this step here, there’s four offspring and I only got two. What if I added in some information that a bunch of the seeds roughly 14 of the seeds never sprouted? Wait a second, so 14 of the seeds never sprouted? They died?

If you get this combo, you die. This is an example of a lethal allele, where W is dominant to orange. So if you get two copies of the recessive orange, you’re orange. If you get one copy of the dominant W and one of the recessive orange, you’re alive. But if you get two copies of the dominant white, you die. Now there’s lots of reasons that could happen, overproduction of some proteins can cause major problems. Now you’d think well if it’s lethal, why hasn’t natural selection eliminated it? A lot of times natural selection will eliminate lethal alleles pretty quickly. But sometimes, it turns out that there may be advantages to being a heterozygote. For example if you’re a flower, and you’re being bred by flower people, they may like white flowers. So they’ll go with this.

Let’s talk about an example with humans. There is a trait called sickle cell anemia. If we take a look at what sickle cell anemia does, it’s a version of the normal hemoglobin gene. Now the normal hemoglobin makes normal red blood cells like these. The sickle cell trait makes red blood cells like this. What will happen is that, these sickle cell hemoglobin red blood cells don’t carry themselves through the blood system very well. They tend to precipitate out and you’ll have major problems with joint pain, or typically die pretty early.

Now why is anybody suffering this when they die? Natural selection should eliminate them real quick. Well, it turns out, that if you have one copy of the normal and one copy of the sickle cell, the one advantage of this has, is if you are in an area with malaria, because the malarial parasite infest red blood cells. The thing is if it gets inside one of these, it’s trapped, because the sickle cell red blood cell, as soon as the malarial parasite gets in, it goes and dies. Trapping that malaria parasite inside instead of giving it a free ride on normal red blood cells.

So people who are heterozygous for sickle cell anemia. Their body is able to make enough red blood cells that are normal for them to be able to function in their normal everyday life. But they also are making half the red blood cells as special traps just for those malaria parasites. That gives them enough advantage in areas of the world, where there’s lots of malaria such as regions of Africa and regions of Asia. You’ll find large portions of the population, are actually carriers for sickle cell anemia. So that’s how we’ve done variations on Mendel’s normal dominance.

So far we’ve been talking about how one gene interacts between the two alleles. Now let’s take a look however, at how multiple genes can interact with each other, or interact with their environment. So let’s take a look first at something called epistasis. Epistasis is one gene can interact with and affect the behavior of another gene. The standard example of this is black and brown mice. Now with black and brown mice, when you mate a black mice with a brown mice, you see all of the children are black.

Then when you mate those children who are heterozygous for the black trait, so big B is black, little b is brown. Here is two heterozygous black mice. You normally expect, and you actually do normally see 3:1 ratio, our standard result of a heterozygous cross. But sometimes, instead of getting a 3:1 ratio, you’ll get a 9:3:4 ratio. That’s 9 black, 3 brown and 4 white. But where do white come from? Wait a second, we add up those numbers that’s 16 offspring. 9 plus 3 plus 4. How could that be? I smell a di-hyrid cross.

Let’s take a look at this cross. Here is our heterozygous for the brown versus black gene. Take a look at this C gene. If we take a look here, we can see I’ve colored in a bunch of them that are black.

A bunch of them are brown. What are these guys down here who are white? Notice how they have two copies of the recessive C gene. What’s that C gene? It turns out that the C gene is coding for an enzyme that allows the mice to actually make the black or the brown pigment. So if you get two recessive, remember, that means non-functional versions of the enzyme that allows you to build your black or brown pigment, then you don’t make any pigment whatsoever. That makes it white, i.e. albino mice.The simple way to think of epistasis is one gene, in this case the C or coat color gene, acts as an on-off switch for others. It can be a lot more complicated than that, but that’s the easiest way to remember.

So what are some of the other ways that you can have genes interacting with each other? The next one is polygenic inheritance. Now polygenic inheritance is actually one of the more common forms. You’ll see this in things like height. You know that there’s not just tall people and short people, instead you see there’s gradation between people like Yao Ming who're up here and little we people we here. That is an example of a polygenic inheritance.

What’s going on there? Well, there’s lots of genes that can influence your height. You can have genes that allow your bones to grow faster, while you can also have genes that allow you absorb calcium really fast. If you’ve got the low calcium absorption gene combined with the fast growing gene, instead of growing really fast, your fast growing gene will try to make you tall, but you don’t have the building materials coming in the calcium that you need to build your bones. They’re not coming in fast enough, so you’ll wind up being normal height like me.

On the other hand if you’ve got the really fast absorption of calcium combined with the slow building, you’re going to be getting lots of building materials and you’ll still be normalish height. There’s all sorts of gradations in between.

Another really good example of polygenic inheritance is intelligence. I’ve seen some estimates where some people think that there’s well over a thousand genes involved in making what we call intelligence. That’s why you see not smart people or dumb people, you see a bell curve, and either end, there’s people are just freaky smart on everything. Then there’s a lot of people somewhere in between.

Now intelligence is not only a good example of polygenic inheritance, it’s also a good example of environmental inheritance. Say for example, you’re the son of Albert Einstein. And you get all these genes for being smart and really good at Math. Well, you’d be skippy if you never take a Math class, you’re never going to be develop those genes. So yes, you’ll be able to be really good as you’re walking down to the grocery store, you’ll be able to just add up the number of oranges that you’ve put in the pile in your head. But you’re never going to know how to do Calculus if you never take that class.

Another common example of environmental effects is Siamese cats. With Siamese cats interestingly enough, their pigmentation gene is turned off by heat. So in their coldest parts of their bodies like their paws and their ears and the tip of the nose, they can actually make their dark pigment. But in the warmer parts of their body like their torso and upper legs where they tend to be warmer, that gene is turned off by the high temperature. So they are very pale color. So there you go. That’s environmental effects.

Now while things like co-dominance and polygenic inheritance were never dreamed of by Mendel, you can sill use his first law to figure those things out. That well is like most people treat the speed limit. So what about Mendel’s second law? Any violations there? It turns out there is, because stop to think about it. There’s something in the region maybe 25,000 different in the human genome, yet we only have 23 pairs of genes. If you do the Math that’s somewhere around a thousand genes per chromosome. So we call these genes that travel together on the same chromosome during meiosis, we call those linked genes. Because if you recall, Mendel’s second law is all about how one gene separation and again it doesn’t influence the other genes separation in the gametes.

Let’s take a look at how this can work. Remember that thing I talked about before in another episode, or you’ve read about in your textbook called Testcross? Let’s take a look at that. So with the Testcross, that’s when you’re crossing somebody who’s showing dominant phenotypes, with someone who is homozygous recessive for both traits. Now with a homozygous recessive for both trait person, they can only make one kind of gamete; little r and little e. That’s what we see here. That’s the gametes of this parent.

If we had non-linked genes that means that we have genes that are not on the same chromosome, somebody who’s big R, little r, big E, little e, their Rs will separate, their Es will separate. But the big R has an equal chance of winding up with the little e, as it has with the big E. That’s because of the way that the homologous chromosomes pair up during prophase one and then separate. How one pair of analogous chromosome separates, has no influence oh how the other one does.

You remember that during meiosis, during prophase one, those homologous chromosomes are tumbling all over the place. So there’s no way that one’s tumble will influence another pair’s tumble. But what if they are on the same trait, on the same gene?

Here we see a pair of homologous chromosomes. This one’s from daddy. Daddy happens to give you a big R and a little e on his copy of this chromosome. Mummy gave you a little R version of the R gene, and a big E version of the e gene. So let’s take a look at what would happen with this set up. Remember these homologous chromosomes pair up, and then they separate. This one goes off to form one sperm or egg. This one goes off to form the other sperm or egg.

So instead of having four possible outcomes, you instead have only two possible gametes being produced by you, since the r and the e gene are on the exact same chromosome. They are linked genes. So instead of seeing 25%, 25%, 25% possible offspring, instead we have 1/2 this way, one-half that way. A 50-50 or a 1:1 ratio.

So you think about that, hopefully you know enough about meiosis to say, but wait a second, there’s not just the jumbling of the chromosomes during prophase one, what other event happens? Luckily for us, because remember the whole purpose of sexual reproduction is to create variation, and this greatly reduces variation. Remember that when those chromosomes pair up, they not only jumble, but they also break. Then, we take portions of your mummy’s chromosome, and we attach it to one of your daddy’s chromosomes like this.

That event is called crossing over. And this crossing over reintroduces some variation. Now, how often will that happen? Not a whole lot. It depends on how far apart the two genes are from each other. If they’re close together like they are on this paper chromosome, it doesn’t happen all that often, because the crossing over points are essentially random. But if I put the r here and e there, then the chance of crossing over happened between them and separating this little r, from the big E over here, becomes higher and higher.

What you’ll see is that instead of 50% and 50% like this; let me add in my percent sign. Remember on the essays always put your units whether it’s percent or anything else. You forget to do that, and you lose your points. If instead I see say 5% RRee, you have 45% of these guys, 45% of these guys and then 5% of my rrEE.

If I see this weird ratio of five to 45 to 45 to 5, that 5% represents the number of times that I wound up creating this molecule. Every time I create one of these, of course you know I’m creating one of these. So this crossing over event, tells me roughly how far apart they are. If they’re much further apart, then this number starts to increase approaching 25, as this one also approaches 25%. If one was way at this tip and that one was way at the other tip, then I would see almost all the time there’ll be enough crossing over. So Gene mapping is allowed by linked genes. We look for the number of times that you have crossing over events. Roughly, to cover this very quickly, to figure out how far apart they are, all they do is they add this number plus that number. And then you just call them map units. So how far apart are these genes? 5 plus 5, 10. 10 map units.

Now the guy who figured this out, his name is Morgan, T.H Morgan. So sometimes they’ll call them Morgans. Or actually they measure them in milliMorgans or Centimorgans. So this is either just 10 generic map units or 10 Centimorgans. I highly recommend that you go online, check out your bonus materials. I’ve put a link to the virtual version of the official AP lab where you actually have to do some gene mapping. Go through it. It will turn out to be pretty easy to do.

While linked genes bend or break Mendel’s second law and Co-dominance and things like that mess with Mendel’s first law, what about something that can break and bend both? That’s sex-linked inheritance. So let’s take a look at that.

What is sex-linked inheritance? Well, the word link should clear you in that it’s talking about something about genes all on the same chromosome. That’s what it’s talking about.

Remember that, there’s those 22 pairs of chromosomes that you get from your mum and dad equally, what’s that 23rd pair of chromosomes? Those are called the sex chromosomes. Girls have two copies of the X chromosome. Guys have one copy of the x chromosome and one copy of the Y chromosome. You’ve got to remember those are the sex chromosomes. and then the other 22 those are called Autosomal chromosomes, or the Autosomes. So one thing to look for if you see the phrase. Autosomal recessive trait that just means it’s not sex-linked.

When you’re taking a look at a sex linked trait, remember because guys only get one X chromosome, they break Mendel’s first law which says you get two copies of every factor. Because girls have two copies of it, they do follow Mendel’s first law. Guys they don’t follow Mendel’s first law, because they only have one X chromosome. What about that Y chromosome, does it have anything significant? Well, for guys yes it does. It has a gene on it called TDF or SRY depending on which textbooks you use. That’s the gene that’s about six weeks or so plus or minus a bit. During fetal development it says make the testicles now. Assuming that it does, you’ve made testicles then. Those of you who don’t have that gene, you don’t have testicles.

Are there any other significant genes on the Y chromosome? Not that I’m really aware of. So we basically ignore it. It’s the X chromosome; however, that’s huge and has a bunch of really important genes on it. Say for example the genes for color blindness and the genes for hemophilia, what’s sometimes called bleeder’s disease, because they have problems with blood clotting.

So how would you write a sex-linked trait? Well, let’s take a look at a standard problem. Remember, girls are XX, guys are XY. To indicate that a gene is located on the X chromosome, you just put it as a superscript floating up high here. So, this is a standard kind of sex-linked problem where, here is a girl. We know she’s a girl, because she’s XX, here is a guy. We know it’s a guy because, he’s XY.

This girl is a carrier for a particular trait. Let’s pick color blindness. So she does have normal vision, because she’s got one version of the dominant normal color vision, but she is carrying the recessive color blind trait. The guy is also color blind.

So if we take a look at this, we’ll see that he’s got the big B. So I’ll change that to a big B here. So this normal vision guy and his carrier wife, they have children. He produces X big B sperm and Y sperm. That winds up creating this daughter here and this daughter here. Notice both daughters are completely normal. They have at least one copy of the normal vision trait. So phenotypically, they look the same. This daughter is a carrier getting a little b from mummy. This son over here, he’s got normal vision. This son here however, is completely color blind. That’s the trick to spotting a sex-linked trait.

If you see 100% of the girls and I’ll just put that up here. 100% of the daughters are one way, while 50% let me redo my fives, I’m getting sloppy today. 50% of my sons are normal. 50% are different. You see this difference here, that’s sex linked. Now the AP Biology people are going to try to a hide this. They’re going to give you a problem where they going to talk about multiple generations. So let’s take a look at how they’re going to try to hide it.

If you look at this here we have a trait. Now let’s say instead of color blindness, let’s go with eye color. Let's say a brown-eyed woman and a blue-eyed man they decide to have children. Do you think? Okay that sounds fine. When they mate, this brown-eyed woman, and this blue-eyed man, they have a 100% of their daughters brown-eyed. 100% of their sons are brown-eyed.

You think okay, dominant versus recessive. It’s probably autosomal. Here comes the switcher, they take two of the offspring. Don’t do this with your family please. They take two of the offspring. This son mates with this daughter. And on the AP they’re not going to use men and women, they'll use gerbils or hamsters, because that way nobody has any issues. But let’s go with people, because it’s more salacious that way.

So we take this son and this daughter and we cross them. What do we see happen? They produce 50% of the sons are brown-eyed. 50% of sons are blue-eyed while a 100% of daughters are brown-eyed. Again, you see the 50-50 on the men while a 100% on the women? That means it's sex linked. So when you see these multi-generational crosses, first, if they’ve given you two generations, you know something tricky is going on with generation number two.

Earlier I talked about the lethal alleles, now I’m talking about the sex-linked. So if you see a multi-generational crossing, you know something tricky is going on. If you see a 50-50 split, it’s sex-linked. Something else, then it’s one of those other things that I talked about like the lethal alleles or Epistasis.

To reinforce this, I strongly recommend that you go back through your textbook, read that section on sex-linked. Or even better, go online in your bonus materials and again do the virtual lab, because since it’s one of the 12 official labs, the AP Biology people will be asking questions about it either in the essay, or in the multiple choice question.

So now you know how non-Mendelian genetics works. So your standard tools, the Punnett Square, and things like that, you can still use. You just have to think a little bit more through these problems. If you do that, just think of it like a brain teaser. So, you know that there’s those weirdness’s on dominance; Co-dominance or incomplete Dominance.

Just remember blending versus seeing both at the same time. You also know that if you see ratios that don’t match the standard 3:1, instead if you see 2:1, that’s probably a lethal allele. If instead of 9:3:3:1, you see 9:3:4, that’s probably Epistasis. You also know about those linked genes. Remember to figure out how far apart the genes are on the DNA molecule, add together the recumbent ones.

The last thing I’ll remind you about, are those sex-linked traits. Remember, with women they’ve got two copies of the X chromosome. So they can be a carrier for a trait, but still appear normal for things like color blindness or hemophilia. We guys, we’ve got our single X chromosome, we don’t have that luxury. I recommend that you go online, do the virtual lab like I suggested in your bonus materials. Or do at least the genetic problems that I’ve provided for you. You do that to help cement this knowledge, and you’ll do just fine on the AP essay.

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