Hi everybody, it is your AP Biology teacher, Mr. Poser, and today we are doing our Unit 5 AP Biology recap, and Unit 5 is on heredity. So we're going to be going through all six of these topics briefly, briefly, trying not to ramble too much and make this too long of a video. So here we go.
Topic 5.1 is on meiosis. Topic 5.2 is on meiosis and genetic variation. 5.3 is on Mendelian genetics.
5.4 is on non-Mendelian genetics. 5.5 is on environmental When one this unit is on heredity and what is heredity well This is the transmission of traits from one generation to the next this is how living things pass down their genetic information And why do they have to pass down genetic information well because I don't know if you know this already, but nothing lives forever So you pass down your genetic information to the next generation, and if you're a living thing. That's just what you do That's what separates living things from like rocks and that kind of stuff is that we're always trying to make new copies of ourselves.
We're trying to pass down our genetic information. That's just what we do. And this unit is about how that happens. So just to in order for us to get into meiosis, we also have to talk about mitosis, which is the type of cell division that we've already discussed in this class. And that's how somatic or body cells reproduce.
And they create exact copies. And that works great. That's all fine and dandy for growth and repair. of tissues that works great as far as multicellular organisms go or even if you're like a bacterial cell well bacteria don't do mitosis they do binary fission but um asexual reproduction works well for single-celled organisms um and that's when a single individual is the sole parent and passes on exact copies of the genes and like i said it works for unicellular organisms but not multicellular and why is that well it's because genetic variation is super important um it's really really important for multicellular organisms or complex organisms like ourselves for us to be different from one another genetically.
And how that comes about is through sexual reproduction, not asexual reproduction, in which two parents mix together their genes and give rise to offspring with unique gene combinations, never before seen combinations of genetic traits. And that's super important in this class, that theme that genetic variation is ultimately very, very important. and crucial for the permeation of life, that's super important, and we're gonna come back to that.
But what is a gene? After all, a gene is a hereditary unit, or it's a segment of DNA that produces different proteins and traits, and we're gonna learn all about how those work in unit six on gene expression. As I was saying, variation is important, and sexual reproduction allows for it, while asexual reproduction does not.
If you're just a cell, and you're copying all your DNA, and you're making an exact copy of yourself, Nobody's going to be different from anyone else, except under some other circumstances that we'll talk about also in Unit 6. But everybody's the same if you're doing asexual reproduction, and that's not always a good thing. So sexual reproduction results in a shuffling of the genetic deck throughout every generation. And how does that happen? Well, it happens through gametes, or through sperm and egg cells, which are the cells that are responsible for transmitting genes to offspring.
And fertilization is a fusion of genes between two parents. resulting in a unique, never-before-seen combination. So a sperm cell has a unique combination of genes, an egg cell has a unique combination of genes, and when they fuse to form a zygote, that zygote has a set of chromosomes, never-before-seen, a set of genes, never-before-seen, and therefore it is unique in the universe, really, and that's really important. So in humans, each gamete carries 23 chromosomes, okay? So we can say our haploid number is 23. One set of chromosomes for a human being results in 23 chromosomes.
So sperm cells carry 23 chromosomes, and egg cell carries 23 chromosomes. And when you take 23 plus 23, you get 46, okay, when those two cells feed through fertilization. And meiosis, what this is really about, is through producing these gametes that have this unique combination of genes and one set of chromosomes. As I put here, meiosis results in the reshuffling. of genetic information and creation of new gene combinations.
These two images are what we call karyotypes. You can see one over here. This is called a haploid karyotype, and haploid means that there is only one set of chromosomes.
And what I mean by set is that in a human being, there are 23 of them. Normally, your cells have 23 pairs of chromosomes, but gametes only have, or I should say, yeah, 23 pairs of chromosomes, but gametes do not have pairs of chromosomes. They just have one. Okay, so that way when they fuse with another one, they can make a diploid cell through fertilization. So just to reiterate here, we got to talk about a few differences between mitosis and meiosis.
Meiosis results in four cells. It results in genetically unique cells. It creates sex cells, aka gametes, and those gametes are what we call haploid, and they contain one set of chromosomes.
While mitosis, okay, it results in only two cells, okay? Those two cells are identical to each other. There's no genetic difference. And these are the types of cells called somatic cells, so regular body cells that are gonna be undergoing this type of cell division. They're not gonna do meiosis, right?
They're not creating genetic variation. They're just dividing to do their job. Those are what are called somatic cells and they are diploid.
So there's no reduction in the number of sets of chromosomes as a result of mitosis. So as I've said a couple times already, during fertilization, gametes fuse to form a zygote, which is a diploid cell with unique gene combinations. And this is what a human karyotype actually ends up looking like.
So you can see pairs of chromosomes. So this is chromosome pair number one and they're ordered by size. This is chromosome pair number one.
One of this chromosome here, let's just say this person got that from their mother, and this chromosome here they got it from their father. Same deal over here, okay? Each pair of chromosomes, one came from mom, one came from dad, one came from the egg cell, one came from the sperm cell. And human cells, as I put, have 23 pairs of what are called homologous chromosomes with each set, with one set of sex chromosomes, which are XY or XX. So these two chromosomes, while they are not identical copies of one another, right?
Because one came from mom, one came from dad. Those are what are called homologous, okay? And they're going to pair together during meiosis. As I said, I'm getting ahead of myself a lot here.
Homologous chromosomes are not exact copies of each other. They are the same chromosomes with different versions of the same genes. You get one chromosome from mom and one chromosome from dad.
They are not copies of one another. And that's going to become important when we talk about the process of cell division itself, meiosis. How does it produce genetic variation? That's the main question that topic 5.2 answers. It's crucial for survival and reproduction of populations.
Variation is defined as the differences between organisms based on genetic traits. So for the purpose of evolution and natural selection, variation is very, very important. Now, where does it come from? It comes from this.
We're about to talk about it. Okay, so meiosis results in four cells, right? We just spoke about that in 5.1.
That means that cells have to divide not once, but twice. They go into two and two to four. So thereby it is divided into two phases.
Divided into two phases, meiosis one and meiosis two. Meiosis one is where a diploid cell with copied chromosomes, okay, or duplicated chromosomes becomes two haploid cells with duplicated chromosomes. Or in other words, the homologous pair is split. Okay, so one cell copies all of its DNA just like it would in mitosis. Okay.
And then it's homologous pairs split from one another, okay? So that means chromosome number one is going to be separated from the other chromosome number one. Chromosome two is going to be separated from the other chromosome two, and so on and so forth. Okay, so what we end up with here in step four are two cells that are haploid.
They have copies of all their chromosomes, right? But they are haploid, okay, because they only have one set, okay? They don't have homologous chromosomes.
They don't have two versions of chromosome one. Okay, so meiosis one splits up what are called tetrads, all right, and four chromosomes line up across from each other during metaphase one, okay? And here's an overview of what the phases look like, right?
Here's prophase one, chromosomes are condensing. Tetrads line up along the metaphase plate during metaphase one. Anaphase one is where homologous pairs separate, and telophase two is where two haploid cells with duplicated chromosomes split from each other, okay? So then meiosis two is our second cell division where two haploid cells with duplicated chromosomes become haploid cells with uncopied chromosomes.
So this is where what we call the sister chromatids or the copied chromosomes line up and separate from each other. Okay. And this is, this is kind of more like mitosis a little bit. I don't want us to like say like, Oh yeah, it was just like mitosis because it's not.
Okay. But, but it's more like it, I would say. So here it is.
Prophase two is where chromosomes are recondensing. Metaphase two is where the sister chromatids line up. Okay.
And this looks more, you know, our X shapes, okay. Are lining up in the middle. The anaphase 2 is where the sister chromosomes are separating out, and telophase 2 is where the four daughter nuclei form. And once again, these are haploid cells that are gametes. They only have one set of chromosomes, and they're not even copied, so that when they can fuse with another gamete, they get two sets of chromosomes, and that's called a zygote.
A couple things that are going to make sure that these gametes are genetically unique. One of them is what's called independent assortment, and Mendel talked about this too. We're going to talk about him in a sec. But an independent assortment is defined as each pair of homologous chromosomes separates independently of all the other ones.
So that means the inheritance, this is a law, right? The inheritance of one set of chromosomes does not affect the inheritance of any other chromosomes. And then this is where you can start throwing in some math and probability.
And that's what 5.3 and kind of 5.4 are all about. But the idea that independent assortment results in two equally possible arrangement outcomes, the ways, because no chromosomes are inherited together, meaning that each chromosome is inherited separately or independently, means that you can arrange the chromosomes. during metaphase two.
You could arrange the homologous pairs whatever you want, meaning that this gamete gets this copy of chromosome while another gamete gets this copy of chromosome, but it's equally probable that those could switch, okay? So check it out. Look at this picture here. I think this is a really, really good explanation, right? I have these purple and blue chromosomes, right?
And here's crossing over. We're going to talk about that in a second, right? But it's equally probable for the chromosomes to line up with both the blue ones on the left side and the purple ones on the right side, as this one over here. So they can arrange themselves in a very large number of ways, the more chromosomes that you have. And therefore, the gametes and the chromosomes that the gametes inherit are going to be different from one another.
And the number of combinations, as I said, increases with more chromosomes. If you recall, human beings have 23 pairs of chromosomes, which means that... You can line up the chromosomes during metaphase two in two to the 23rd different ways, which ends up being about 9 million different ways to align the chromosomes.
All right. And that means that there's 9 million different ways that the gametes can inherit chromosomes, which is really increasing the genetic variation. Okay. The other thing that's going to throw a whole lot of genetic variation into it is something called crossing over.
All right. And you should do an activity in your AP biology class about crossing over. and how this works. And this happens during prophase I, where the DNA of non-sister chromatids, aka two different homologous chromosomes, break and rejoin.
This mixes up the genes on chromosomes and it results in recombinant chromosomes. All right, so the same images before with the purple and blue chromosomes, what's happening during crossing over is that the chromosomes literally kind of touch each other and they swap genes while they're in contact with another. So here's a tetrad of homologous chromosomes.
And if they kind of cross over through a process called synapsis, okay, they kind of, they, I don't know, they touch each other. They can swap genes with each other, and that's called crossing over. So now you have chromosomes with completely unique gene combinations.
And this is going to increase genetic variation drastically because that's going to result, mix up the genes even more, okay? So you can mix up the chromosomes, but you can also mix up the genes that the chromosomes carry. And that's going to just...
you know, make genetic variation go crazy. The third thing that is going to increase genetic variation is what's called random fertilization. And that's just the law that no sperm cell has any better probability of fusing with the egg than any other. Okay, so that means that all of the different gametes have an equal probability of being, you know, fertilizing the egg, which means that, you know, it's all up to chance, really. And that ensures maximum possible genetic combinations.
All right. 5.2 genetic variation super important now let's talk about 5.3 let's get into the genetics let's get into the probability let's get into the to the crosses and stuff genetics is the study of heredity and inherited variation it analyzes passage of traits from parent to offspring so for a very very long time human beings have known like oh if you have a kid you know I have blue eyes you know if I have a kid my kid is probably gonna have blue eyes my kid actually has brown eyes but You get the idea, right? We've known that we passed down our traits to our offspring for a long time, but what we didn't know is how that happens, or all the different math and probability laws that are associated with how and why those genes get passed down.
So all living things follow the rules of genetics. All living things have DNA, they have RNA that they make the DNA from, and they have ribosomes that are used to make proteins. Okay, so all living things follow those rules. That's called the central dogma of molecular biology.
That is also unit six topic. But the point is, is that genes are molecular instructions for traits. And where do you get those instructions from? You get them from your biological parents and predictable patterns.
And the first person to start predicting these patterns, we got a plants versus zombies plants over here. I just noticed that for the first time. This image is public domain though. So like I used it.
I don't know. It's kind of cool. Anyway, that's Gregor Mendel. He was an Abbey monk, actually. He failed, I think he failed teaching school or whatever program that they did, an education program through a university or something, but he failed the test to become a teacher, so he became a monk instead, which I think is funny.
And then he becomes a leading figure in the world of science. you know, or biology and figuring out these, uh, how traits get passed down through these pea plants. And he was the first person to study genetics, the father of genetics.
Um, and he did that by cross-pollinating pea plants and determine how traits are passed from one generation to the next. And yeah, they actually look like that where they shoot peas at zombies and stuff. Okay. Um, anyway, so there's a couple of terms that we need to get into before we talk about the crosses. A character is a heritable feature that varies among individuals.
A trait is a variant of a character, right? So, uh, for example, Flower color is a character. Purple flower color is a trait.
White flower color is a trait. Okay, so those are variations or variants of a character. And how Mendel did his experiments, we're going to kind of walk through the most famous one that really illustrates a lot of the main ideas, is that he used true breeding plants, which produce offspring with the same traits. Okay, true breeding means that like it's always been, you know, it's always every generation of those plants has had the same traits. Generation in, generation out.
Okay, so purple flower plants have always bred with purple flower plants, that kind of thing. And he crossed true breeding plants with different traits to study the inheritance of those traits. So here's his first one. He crossed a purple flower, and I drew these flowers myself. You should tell me they're good because I spent a lot of time on them.
Here's a purple true breeding pea plant and a white flower true breeding pea plant. And when he crossed them, what did he got? What did he get? He got all purple flowers, all purple flowers, not any white ones.
He's like, okay, well, that's cool. All right, now let me try crossing two flowers from the F1 generation. And what happened is that, well, look it, there's some white-flowered plants. So it kind of looked like it skipped a generation, and he studied that. Why is it that the white flower trait came back?
And that has to do with what we call dominant and recessive traits and dominant and recessive alleles. The purple flower trait he ended up calling dominant, okay, because it was inherited and when a plant carries a dominant allele, it's going to express the dominant trait, and then he called the white flowers recessive, meaning that they're kind of like hide behind or they recede from the dominant trait, and that's what recessive means, okay? So through his studies, he came up with four concepts.
Number one is that alternative versions of genes, or what are called alleles. account for variations. Okay. So, um, you have, everybody has a gene for any particular trait.
Some traits have a whole lot of genes, but we're going to talk about that in a sec. Okay. Um, but everybody has a gene for a certain trait.
Now, what depends on how you exhibit those traits or your phenotype, as that's called, depends on the version of the gene that you've got. And that's what's called an allele is a version of a gene. Uh, number two organisms inherit two of each gene, one from each parent. Okay.
That's, you know, get one from mom, get one from dad. And the version that you get determines your traits. Number three, dominant alleles determine phenotype, even in the presence of a recessive allele, what I was talking about before.
When there's a dominant allele present, it's going to result in the dominant phenotype. That's why we call it dominant, because it kind of overpowers the other one a little bit. And number four, alleles segregate during gamete formation.
This is independent assortment. The alleles are separated out, and no allele is inherited. The inheritance of one allele does not affect the inheritance of other alleles.
That's called independent assortment. Well, that's not true, but we're gonna get there. So here's the RP generation once again. If we assign some terms to these and we kind of work this out through using Punnett squares, then it becomes clear why the white trait came back.
after a generation. Okay, so if these are two true breeding, these are what we call homozygous dominant and homozygous recessive, and these are what we call genotypes. And genotypes are depictions of the alleles that an organism inherits, right?
So this purple flower pea plant inherited a dominant purple allele and another dominant purple allele, so we call it homozygous dominant. And here's a recessive white flower allele, and here's a recessive white flower allele. It's got two of the same, so we call it homozygous recessive.
Remember, homo means same, hetero means different. Homozygous means two of the same allele for a gene. So we cross two homozygous plants, and what we result in, in the F1 generation, is that we got heterozygous plants, okay? They have two different alleles, all right? And they're expressing the dominant trait.
That's why, you know, purple is dominant. because they have one allele and that's all it takes to express the dominant trait. But these are heterozygous, meaning they have two different alleles. All right.
And if we, you know, cross our two heterozygotes, there is actually a one in four or 25% probability that we're going to end up with white flowers, a homozygous recessive individual. Okay. And a Punnett square is how we show how this works.
Laws and probability can be used to analyze which genes and traits are inherited by offspring. And these are used to make predictions on... genotypes and phenotypes.
So if you hopefully know how to do a Punnett square, okay. Um, something I tell my students all the time is like, Oh yeah, I remember from seventh grade where to put the letters in the boxes, but, um, they don't really remember what it means. Like, Oh yeah, I don't know what this means for, you know, what's the probability that they don't even recognize that. So it's important to know.
Okay. Uh, but here's, here's my parent parental, um, generation, right? My true breeding homozygous dominant purple flower. Here's my true breeding homozygous dominant white flower. If you cross them, check it out, you put that.
You put the alleles in the boxes, right? And then each combination of them gives you a genotype, and then thereby you can analyze the results of the cross and the probability of offspring with particular phenotypes, right? So 100% of the offspring from this cross are going to result in that purple phenotype.
But this one might be a little different. So if you don't know how to do this, try it out for yourself. Pause the video. But I'm going to have a dominant A, dominant A, dominant A, recessive A.
Dominant A recessive A and recessive A recessive A. Therefore, ta-da, there it is. We have a three-to-one ratio, phenotypic ratio, as we call it.
What I just demonstrated here, this is called a monohybrid cross, a cross of two heterozygous. And as I just said, it produces a three-to-one phenotypic ratio where there are three dominant individuals or individuals expressing the dominant trait and one individual presenting the recessive trait or expressing the recessive trait. Okay, so 75% dominant, 25% recessive.
Now, it gets a little more complicated when we cross two traits at the same time. What we just did was a monohybrid. This is what we call a dihybrid cross. A dihybrid cross illustrates what we call the law of independent assortment, that alleles segregate independently of other alleles during gamete formation. All right, so in order for us to discuss this, we're going to talk about another example of Mendel's crosses, right?
And I'm going to give you a spoiler alert here. Hey, you know how we got the, when we cross two heterozygotes for one trait, okay, we got a three to one ratio, three dominant for one recessive. Now, here's another ratio that we're going to result in when we have two traits to cross, okay, this is the magic number, nine to three to three to one, is what happens when you cross two heterozygotes.
And here I have the genotypes for two heterozygotes. You can see there's a dominant recessive, dominant recessive, dominant recessive, dominant recessive for each one. And what are YY and RR? Well, they're... describing the phenotypes of peas, okay, because these are pea plants, right?
So yellow peas are dominant to green peas and smooth Wait a minute. Yes, smooth peas are dominant to wrinkled peas. Okay, I thought I thought I had that wrong for a second Okay, but you can see down here I'm not gonna go through each one But you can see the four different variations of peas that you can get you can have yellow wrinkly green wrinkly yellow smooth or red smooth depending on the pairs of alleles that each pea plant inherits from its parents, right?
So something to note when you're doing a dihybrid cross, okay, maybe I'm getting a little ahead of myself here, but since there are two sets of alleles that are being inherited here, there's several combinations of those alleles that the gametes can get through meiosis, right? They could have, gamete could have a dominant Y and a dominant R. They could have a recessive Y and a dominant R. They could have a dominant Y and a recessive R or a recessive Y and a recessive R. Those are all equally probable.
Okay. So how to kind of set up a dihybrid cross is to use the FOIL method. Okay. All of these are equally probable.
Hence, we put them over here where we put our parents, our parental genotypes. Okay. We put them along the outsides of the... Punnett Square like so, okay?
So each of these are equally probable. So when we cross these, all right, we're gonna do the same thing as we did before, bring the big Ys down and the big Rs across and all that stuff, okay? If you don't know how to do this, okay, I go in more detail in my 5.3 videos, but you should end up with something that looks like this.
All right, you don't have to put the pictures there like I did when you're doing one of these, but check it out. There it is, nine to three to one, or excuse me, nine to three to three to one ratio. But, here's the thing about these dihybrid crosses, is that they aren't always accurate predictors of phenotypic ratios. Now, this is what we could expect, but that's not always what we get.
Because non-Mendelian traits are a thing. Not every single trait in every single gene follows this set of rules and has this pattern of inheritance. So, this is where Mendel was wrong.
Hey, non-Mendelian genetics refers to inheritance patterns that... Oh. don't always conform to what we call the Punnett squares.
And here's a whole bunch of examples, and we're going to try and run through each one of these quickly. So incomplete dominance is the first example of when, you know, Mendelian traits are wrong. Neither allele is completely dominant, or heterozygous phenotype is a mix of the parental.
So if I have a red flower here, and I cross with a white flower, I get a pink flower. And this is what most people think of when they talk about genetics, right? You take some, you know, the offspring are always going to be some kind of mix of the parents, but that's not necessarily true.
This is only true for incomplete dominance. And several traits that even humans have exhibit incomplete dominance. But this red, white, pink flower, I think these are called four o'clock flowers, that exhibits this property very well.
Incomplete dominance is also coupled with co-dominance, where two alleles affect the phenotype in separate distinguishable ways. Instead of having one dominance and one recessive allele for a trait, you have two dominance alleles. So check it out.
If I'm crossing these two fish, there's a blue fish and a brown fish, and you cross them, both of these genes are dominant, so therefore the offspring are both blue and white at the same time. And they are both expressed in the heterozygote. Instead of a mix of them, like you have incomplete dominance, both are dominant, and that's what we call co-dominance.
Both of those traits are expressed. Pliotropy is another example when Mendel is wrong, when one gene produces multiple phenotypes. Well, he actually found out that one gene results in the same or multiple phenotypes in pea plants. I don't remember what they were. I think it might have been flower color and, shoot, I don't remember what the other one was.
But flower color is also inherited with something else, another trait for pea plants. But anyway, polygenic inheritance is another really good example. This is the main one.
And, you know. My students ask all the time like okay so what about like things like skin color and height and eye color and that kind of stuff hair color Well those are here's the thing right those are not determined by one trait those are determined by or excuse me one gene by you know in some cases dozens of genes right because you know skin color eye color hair color those are all gradients okay they're not just you know you know you don't just have one color of brown hair one color of blonde hair right that's or like black hair or whatever There's all sorts of different types of hair colors. So those are inherited by multiple genes, and that's what we call polygenic inheritance. You can't put that on a Punnett square. You just can't, right?
Unless you were gonna make a Punnett square that's 86 genes long, which is ridiculous, right? Another example of when Punnett squares go wrong is epistasis, when the phenotype of one gene alters the phenotype of another gene. So check it out.
I have a dihybrid cross between two brown mice here. And we might be expecting the 9 to 3 to 3 to 1 ratio. Check it out, the agouti, or the kind of brown mice here, that's in our 9. But we only have 3 black mice and 4 albino mice.
So as you can see, check it out, the inheritance of this homozygous recessive C's here is kind of overexpressing the... even the dominant A's here, okay, which is going to result in some different pattern, okay, instead of 93 to 1, or 93 to 3 to 1, we have 9 to 3 to 4, because the C is kind of expressing or like, you know, shoving the other gene out of the way, that's called epistasis. Another example of where Punnett squares don't do the job is over mitochondrial inheritance, mitochondria are transmitted from the egg only, which means that mitochondrial genes are only inherited from the mother.
So if the mother has a mitochondrial disease, all of her children are going to get it. But if a father has the mitochondrial disease, none of his children are going to get it. There you go.
And I didn't have a picture here, but sex-linked genes, genes located on sex chromosomes show different patterns. Biological males inherit only one X chromosome. Biological females inherit two.
Therefore, an X-linked recessive disease, or an X-linked recessive trait, for example, is only going to be inherited by females if they have two copies of the recessive trait, but by males if there's only one copy. And there's another exception to the rule. And I guess I didn't put a picture here, but the last example of how Mendelian traits are wrong are through linked genes, and genes are located on the same chromosome.
This flies in the face of independent assortment, that each one of those genes are, or the law of segregation, I should say, that each one of those genes are inherited separately, and the inheritance of one gene does not affect the inheritance of another. That's not true. Multiple genes are located on the same chromosome.
It says right here, linked genes are more likely to be inherited together since they are on the same chromosome and that breaks the law of Mendel's independent assortment here. Okay, and so we're gonna talk about another set of famous experiments by Thomas Hunt Morgan. He performed dihybrid crosses with fruit flies to determine which fruit flies were linked and how close they are together on a chromosome. So we're gonna walk through another set of experiments and yes, I drew these flies myself, so tell me they're good.
I'm not an artist at all. but sometimes I can make a good fruit fly, okay? So here's a few generations, right?
So what Morgan and his team crossed was what we call a wild-type fly. This is like the normal, these are the kind of traits that you would find on a fruit fly in the wild, hence why it's called a wild-type. It has gray body and normal wings, and wild-type traits usually tend to be dominant, okay? So what he did is he crossed a wild-type fly with a double mutant fly, one with a...
black body and vestigial wings. Vestigial wings means that they're like basically useless. They can't fly around and stuff. It's kind of sad, but whatever.
Um, if they're fruit flies and, uh, these mutant traits usually tend to be recessive. Okay. So I bet you can see what's coming here. Um, if you cross a dominant white or, uh, I should say gray body and normal, uh, wings fly with a double mutant. Okay.
And this is how you write the phenotypes. Wild types are always denoted by pluses. Okay, and pluses tend to be, the wild types tend to be dominant.
Okay, so these are the dominant alleles, and these are what we call the recessive alleles. VG represents the gene for vestigial wings. B represents the genes for body color. And if you cross them, check it out, you get a heterozygote. And this is the genotype that follows for each one.
It gets a little trickier when you're not doing the... capital and lowercase letters, but it's the same principles. Okay.
Once you get the hang of it, it's not so bad. Hey, and check it out. All of the offspring from this trait or from this cross were heterozygous and they all express the wild type phenotype.
Now here's the thing. Here's what's interesting, right? If you cross a heterozygote individual with wild type traits and you cross a double mutant fly, another double mutant fly.
Okay. If you work out this cross here, If you work out this Punnett square, which I suggest you do, pause the video and try it for yourself. You should get a very typical ratio that you would expect. Ready? So if you're crossing it, go ahead, pause it, but I'm going to carry on.
You should end up with this, which, you know, it's going to take a second to analyze, but I'll do that for you. You should end up with an even 1 to 1 to 1 to 1 phenotypic ratio, where 25% of the flies have the... Both the wild type traits 25% of the flies have the gray body but vestigial wings 25% of flies should have the black body and regular normal wings And then 25% should be the double mutants with the black body and the vestigial wings That's what we should expect if you work out this cross Between the heterozygote and double mutant. That's what you should get but that is not what was observed Okay, we should have 25% 575 flies each, okay, based on the results, but we did not get those percentages, which means something was up, okay, so the recombination frequency, or the percentage of the offspring with phenotypes that do not match the parental phenotypes, or remember, the parental phenotypes were the wild type and the double mutant, okay, so these guys over here with the gray body and vestigial wings, that doesn't match the parents, the black body and normal wings, that doesn't match the parents either, okay, that's what we call the recombinance.
If that's not 50%, then that means that those genes did not assort independently. We were expecting, if I go back, we were expecting 50% recombination, new combinations of these traits. But we only got, or they only got, I should say, 17%, which means something is up. Those genes did not assort independently. There is something going on that makes it more likely for these genes to be inherited together.
Yeah, these genes to be inherited together. So this is what it means by these genes are linked. The genes for body color and wing size are linked.
They are located on the same chromosome and more likely to be inherited together. So if you do a double mutant heterozygote double mutant cross and you don't get a one to one to one to one ratio, you have linked genes. Okay?
And the recombination frequency equates to how far apart those genes are located on a chromosome. Recombination occurs during crossing over in prophase one of meiosis. Hence, genes that are closer together, remember crossing over?
It goes like this, right? Genes that are closer together are less likely to, yeah, okay, they are less likely they are to cross over, and therefore they are more likely, if they're closer together, they're more likely to be inherited together. So therefore, these two genes for body color and wing shape, or wing size, are more likely to be inherited together. And what you can do with this is you can make what's called a genetic map, or an ordered list of genetic loci and a chromosome.
Right, so this is a chromosome if you just draw a line like this that's a chromosome Representing one that a fruit fly would inherit and you could put these two dashes here VG and B And you can designate that they are what we call 17 map units or centimorgans apart because 17% of those Flies had their recombination And we had different combination of genes from their parents therefore Those genes are closer together, and they're more likely from that cross to match the parents because those genes are so close together. Recombination frequencies denote how far apart two genes are on the same chromosome. So this is how you would draw a chromosome map.
All right. And this is a more developed image of a chromosome map for a fruit fly. These experiments were done dozens and dozens of times in order to figure out where each of these genes are located on chromosomes in flies.
And that's kind of exciting. All right. So doing a whole bunch of crosses allowed us to do this.
And this has been done for all sorts of different species, right? We know... where the genes are in human chromosomes as well.
So more across, this can be done to make a map that shows locations of various genes on chromosomes. All right, now, a couple more things when it comes to genetic anomalies not following the rules of Mendel, right? 5.5 is all about the environment and what's called phenotype plasticity. The environment also determines phenotype. It's not just genetics.
Identical twins can have slightly different phenotypes, right? It just depends on their environment, how they live, where they live. And that's called phenotype plasticity.
individuals with the same genotype exhibit different phenotypes in different environments. And orchids are a good example of this. I have a list of examples on the next page. So, for example, two orchids might have very, very similar genes.
They might have the same traits that allow for flower color. But if you pot them in different pH soils, they end up having different flower colors, which is kind of amazing. That's phenotype plasticity. For example, this alligator over here, certain reptiles, depending on...
how cool or how warm their eggs are incubated at. While they're, you know, after the eggs have been laid, they have to be incubated. Mom has to like sit on them to like keep them warm, right? Depending on how warm or how cool they are actually determines the sex of the reptiles, which is kind of amazing, right?
Sex is not genetically determined. It's determined by an environmental factor like incubation temperature. That is phenotype plasticity.
Same thing with these Arctic foxes over here, mammals. Like... like the Arctic fox are able to have different fur colors depending on skin, UV exposure.
Okay, same kind of thing with humans. We're mammals, right? Our skin color change depending on UV exposure as well. Other factors are diet, activity, etc. That is also going to affect traits, not just genetics.
Okay, last topic of Unit 5 is on 5.6. And this is all about kind of reiterating here where genetic variation comes from and how chromosomes on the inheritance of chromosomes effects, you know, traits. Okay, so as I put over here, separation and independent assortment of chromosomes, crossing over and random fertilization result in genetic variation.
Those three things, you got to remember those. How chromosomes are inherited and what genes they contain generate variation. And that's very important. Okay, so last part of 5.6 is about what happens, kind of like genetic. diseases, genetic, and how they're inherited, and how you can inherit different traits.
And we're going to talk about one particular having to do with chromosomal inheritance in a second. Hey, but as I put here, human genetic disorders can result from inherited mutated alleles or specific chromosomal changes. So like, for example, a dominant or recessive allele might determine a faulty trait, might result in a mutation in a chromosome, or excuse me, in a gene, and then...
results in a faulty or perhaps altered protein. And these kind of diseases right here, sickle cell anemia, Tay-Sachs, hunting disease, cystic fibrosis, achondroplasia, those are all resulting from a mutated allele on one kind of an autosome, which is a chromosome that's not a sex chromosome, right? So cystic fibrosis is a disease that alters the shape of a chlorite, chlorite.
Chloride ion channel in mucosal lining cells in the airways that produce extra mucus and it makes hard somebody Makes it very hard for somebody to breathe sickle cell anemia results in a change in the HBB gene And alters the shape of hemoglobin Hey Which is the protein that carries oxygen in your blood and it also alters the shape of the red blood cells themselves and that can cause a whole bunch of problems other genetic disorders Hang on my page isn't loading. Okay are resulted from a mutated allele on a sex chromosome rather than an autosome. So, for example, color blindness, hemophilia, and Duchenne muscular dystrophy, those are all inherited on, like, an X chromosome.
So you can, and those follow a different genetic inheritance pattern than the autosomes, right? So think autosomes are like the regular Punnett squares, the sex-linked chromosomes, or excuse me, the sex-linked crosses are with the X and the Y on the outsides. But colorblindness is another example of a genetic disease resulting from a mutated allele.
But another group of genetic diseases like Down syndrome and Turner syndrome are caused by what's called an aneuploidy, having an abnormal number of chromosomes. And most kids know about this. But I just want to dispel something. I have a lot of kids asking like, oh, so inheritance of any extra chromosome results in Down syndrome? No.
That is specifically what's called chromosome 21, or trisomy 21, inheriting three chromosomes of that particular chromosome 21. And aneuploidies, an abnormal number of chromosomes, are caused by non-disjunctions during meiosis, where the chromosomes are not evenly separating either during meiosis 1 or meiosis... No, actually during meiosis 1, and the homologous chromosomes are not evenly separating. So one gamete might get extra chromosomes while the other gamete does not get enough chromosomes, and that can result in diseases like Down syndrome and Turner syndrome. All right. All right.
That is it for this video. Please let me know if you have any questions. I hope I covered everything in depth enough. But if I didn't cover something in depth enough for you, check out my other videos on the topic videos in Unipi.
All right. Have a good day.