Hi. It's Mr. Andersen. And in this podcast I'm going to go over non-Mendelian
genetics or sometimes referred to this as everything that Mendel didn't know. And so
I'm going to kind of build on the work of Mendel. And then eventually get into the work
of somebody named Thomas Hunt Morgan. And so the first few things are going to be just
terms that you should understand. First one is going to be incomplete dominance. Incomplete
dominance sounds a lot like blended inheritance, but basically what happens is, let's say this
one is big W big W. So this is white snapdragons. This one is red. If you cross the two, so
our hybrid when we get one gene from each is going to be pink. And so red plus white
equals pink. Now if we were to really go back to blended inheritance you would cross pink
and your would keep getting pink. But on incomplete dominance if we were to cross pink with pink
and we do the punnett square for that, like that. What we're going to get is a red snapdragon.
We're going to get a pink snap dragon, a pink snap dragon and a white snap dragon. And so
we can get that white and that red back. And so incomplete dominance is when, if you get
one gene from each of these two, then the combination is going to be somewhere in-between
the two. Now something similar to that is called codominance. And this one, if you've
got heterozygous for red and white you're going to have splotches of white and splotches
of red like in the rhododendron and the roan cow. If we have a red and a white cow then
the offspring is going to be red and white. But it's not like pink. That would be cool
to have a pink cow. But it's going to be hairs that are red and hairs that are white. And
even in these red areas you pull one hair out and it's going to be red. One hair out
and it's going to be white. And so in codominance we're basically going to have splotches of
the two different colors. But the genetics are exactly the same as incomplete dominance.
Another term is called epistasis. And so if we were to look at this alligator, what color
is its skin or what color is this guy's hair? Well, we don't know. Because there's a number
of genes that probably determine the color, but there's going to be a separate gene that
determines whether that actual color is added to the hair or not. And so if there's a problem
in that gene, then it's going to result in albinism. Basically epistasis what you should
remember is that there are certain genes that can effect a number of other genes. Almost
like an on off switch. Without that on switch the hair color doesn't get added. And so you
have an albino. Sometimes it's hard to do genetics problems dealing with epistasis.
Sometimes we'll have multiple alleles for a trait. And so an example of that is going
to be blood type. So you could have the A protein. You could have the B protein. You
could have neither protein. So we get the four different blood groups. I'll make a separate
video. Because this is sometimes confusing and explain those. But know that we've got
instead of just two choices, we've got in this case three. Next one as we get into Mendelian
genetics we start to realize as scientists were doing work is that some of the things
that Mendel had discovered didn't seem to be holding true. It was almost as if he lied
to us. And so we call these non-Mendelian genetics. Whoa. That's scary. So the guy I
want you to remember is Thomas Hunt Morgan. And he worked with fruit flies. And he figured
out some pretty amazing things. And this, he kind of discovered the work of Mendel.
But also they had discovered these things called chromosomes. And we were starting to
kind of work out how that comes together. And it was convenient because each of the
traits that Mendel had studied, so flower position, color, pod shape. All of them were
found on separate chromosomes. And so he never had a problem with what we call linkage between
genes. And probably if he ever did do traits where the two traits were on the same chromosome
he probably didn't include that data because he got weird numbers that just didn't fit.
We know that some genes flow together, like freckles and red hair. And that's because
those two genes are going to be found on the same chromosome. This is the experiment that
showed Thomas Hunt Morgan how this works. And kind of stick with me. It's a little bit
confusing, but I think you can do it. And so basically the way we name our genes in
fruit flies is going to be a little different. We basically find the mutation. In this case
you can see that this drosophlila is black. So it's got this bl mutation. And then it's
got these weird vestigial wings. And so we call that the vg mutation. The normal run
of the mill fruit fly is going to be, we just put a plus next to it. So this would be the
wild type. We call that a fruit fly. And so if I were to really write this out using terms
like you're maybe more familiar with, a better way to write it might be like this. V little
v B little b. Then we cross that with little v little v little b little b. But get used
to this. Because it shouldn't be that confusing. And so basically what he did in this cross
is he took one fruit fly that was, oops, let me go back to that. One fruit fly that was
heterozygous for the two traits. And one with homozygous recessive. And so if you do the
punnett square, this one is going to give a vg, vestigial gene. And it's also going
to give a black mutation. And so really this one can only give one type of gamete. But
the other one over here, so if we look at the other parent, so this mom right here,
it could give vg+, so it could give this vg+ and it could give bl. But it could also give
vg+ bl+. It could also give a vg bl+. Or it could give a vg bl. So it can give those four
different combinations. And so this one right here is going to make one that doesn't look
like the parent. But this one would look like the parent. And this one would look like the
parent as well. And so basically according to Mendel you would get two of them that look
just like the parent. And then two of them that are going to be combinations, like this
one right here is black but it has got good wings. And this one is not going to be black.
It's wild type. But it's got these vestigial wings. And so we call these things recombinants
or recombination of the two parent''s phenotypes. And so Thomas Hunt Morgan is crossing these
fruit flies. And Mendel says that he should get 50 percent parental. You can see it. 50
percent parental. These two. And then 50 percent recombinant. And so he knew his genetics and
he knew he should get 50 percent of each but he didn't. Time after time after time he just
kept getting 17 percent of the recombinants. Over and over and over again. And so he couldn't
figure that out. Why is it 83 percent of these and then 17 percent of these over and over
and over again. They were starting to think maybe they discovered some new number like
pi. 17 and it's significance. But sometimes in other crosses it would be like 9 percents.
Some would be like 21 percent. And so basically one of his students, Thomas Hunt Morgan's
student Alfred Sturtevant went home one night. Blew off his homework. And kind of figured
this out. And what he figured out, let me clear this out, is that there are going to
be chromosomes. So the chromosomes look like this. And some genes are going to be found
on the same chromosome. So we might have the bl mutation right. And we might have the vg
mutation right here. And since they're on the same chromosome they're going to follow
each other through generation after generation after generation. And since they're tied together
we're going to have more of the parental types than we are of the others. And you might think
well how do we even get recombinants if they're tied together? Remember during meiosis we
have crossing over where this will actually split. And so there will be crossing over
between chromosomes. And so the cool thing is if those two genes are really close together
on the chromosome, it's rare that they're going to be split in half during crossing
over. And so 17 percent told him that they were, if they're on different chromosomes
we would get 50 percent. But anything less than 50 percent is going to tell us how close
they are. And so let's say the frequency of recombination is 3 percent. That means that
those genes are going to be, there might be another gene right next to this one. And since
they are so close on here, the odds of them being split in half is going to be really,
really rare. And so what he discovered is this idea of gene linkage. That there are
some genes that are found on the same chromosome. And they travel together. Another thing that
we're starting to discover is that most traits are caused by multiple genes. The standard
that biology teachers will say is that you've got a hitchhikers thumb. And it either is
a hitch hikers thumb or a straight thumb. But it's probably not that simple. Because
when I talk to kids is class you'll find that some are really straight and some are in between.
And that's because most traits, almost all traits, are cause by multiple genes interacting.
And so if you flip two die what are the odds that it's going to come up snake eyes or double
ones? Well there's only one way to get that. A one here and a one here. And so the odds
are 1 in 36. But there are going to be some numbers that come up all the time. So if we
look at that, 7 is going to come up all the time. Almost one-sixth of the time. And so
if you ever see a bell-shaped curve in phenotypes, physically what they look like, that means
that there are multiple genes taking place. In this case it would only be two genes and
we can get this nice bell shaped curve. So let's go to something that we're all interested
in. And that's going to be how tall you're going to be. Basically if we go to the simplest
level, height genes, let's just make it simple and say that there are 6 different heights
that you can have. And that's contributed by different genes that you get. And let's
say that you've got Jimmy here and Suzy. And Jimmy and Suzy meet each other, but then they
get back together later in life and they decide to have a family. And they decide to have
a bunch of kids. Let's say they're of average height. We'll call them height 3. And that
means they've got three different genes but they're heterozygous for each of those. So
they've got a tall gene and a short gene. So they're heterozygous for each of those.
And so since they have three tall genes we'll say that they're going to be of average height.
But now let's work out the punnett square with just their genetics to figure out how
tall their kids might be. In other words Jimmy might give a big A a big B and a big C. And
she might give a big A big B big C. And so they'd have a six child. So it is going to
be a giant kid. Or they might give all their short alleles. And they're going to have a
really short kid. And so if we start punching out the numbers what we find is that the odds
of them having a really small kid, and we'll call them height 0 is going to be a 1 in this
would be 64 chance. But as we work our way up to 2s and 3s and 4s and 5s and 6s. What
we'll get is that characteristic bell shaped curve. And so it's going to a bell shaped
curve like this. Most of their kids are going to be of average height. Because they're of
average height. It doesn't mean that can't have a really tall kid or a really short kid,
it just means that they're probably going to have kids that are in the middle. Now how
many genes actually effect height in humans? Dozens and dozens of genes. And so you can
imagine that we're going to get a huge bell shape curve. And that's why we have the bell
shape curve of life. Everything from the length of our thumb to the length of our foot to
intelligence. All these things are caused by multiple genes. And so it's not as simple
as a simple punnett square. And then the final thing that Thomas Hunt Morgan added to the
work of Mendel was the idea of sex linkage. And so he was doing crosses where he would
cross flies that are going to have this white eyes with those that are the wild type. And
he'd find that in the f1 generation they're all going to be the same. But in the f2 generation
only the males would have the trait. And so what he discovered was sex linkage. That there
are some traits that are genes that are actually found on the sex chromosome. In humans we
see this in color blindness. So if you look here there should be, and the color is always
hard to hit, but there should be three numbers that you can see in each of these. And if
you can see any of these, you might be color blind. 37, 49 and 56. And I'm color blind
so I struggle with all of those. So how does that work? Well basically we have some traits
that are carried on the X chromosome. And so let me show you how this works out in my
family. Basically this would be my mom. She is X X since she's a girl. But she has a mutation
on one of her X chromosomes. There's a faulty gene. And so if I were to punch the punnett
square, my dad is not color blind. So if I do this, this is going to be XcX. This is
going to be XcY. This is going to be X X. And then this would be X Y. And so you should
be able to understand what each of these are. This would be a normal female. This would
be a normal male. This right here is going to be a color blind male. So we could say
this is me. So I got one X chromosome that's got a mutation. And my dad gave me the Y chromosome.
And so I'm color blind. If we look at this one, this one is going to be a carrier of
color blindness. And so this could be my sister. Because my sister is not color blind. But
that's because she has one good X chromosome. How do I know that she's a carrier? Well I
have two nephews that are color blind. And so she passed this faulty mutation on to them.
Their dad who's not color blind gave them the Y and so then they ended up being color
blind. And so it's a bummer to be a boy sometimes. Because we only have one gene on our X chromosome.
And so if it's faulty then we're going to become color blind. Now in human population
1 out of ever 10 genes that cause this color deficiency are going to be faulty. And so
boys, since we only have one X chromosome in our population, 1 out of every 10 males
are going to be color blind. So you may be able to figure out in your head how often
is that going to happen in girls? Well since they have two X chromosomes, it's going to
be a 1 in 10 probability on the first X. And it's going to be a 1 in 10 probability on
the second X. And so it's going to be a 1 in 100 probability that girls are going to
be color blind. It's rare that I find girls in my class who are actually color blind.
And that's because they have you know, that extra X chromosome. That back up copy. Which
we do as well in all the other chromosomes inside our body, since we're diploid. Except
the sex chromosome. Another trait that is common here would be hemophilia. Hemophilia
is one that is carried on the X chromosome more common in boys than girls. But I love
evolution. And whenever I see a number like this, 1 in 10, that seems like a high probability.
Perhaps there's an evolutionary advantage to being color blind. And I've read that if
you're color blind when you're hunting or when you're in the military you can actually
pick up camouflage better than you can if you have regular vision. And so maybe there
was an evolutionary advantage at some point for people who were hunting. Especially hunting
in or around night, they could maybe see better and be more successful. And that's why I love
biology. You never know all of the answers but you sure know a lot. And so that's non-Mendelian
genetics. And I hope that's helpful.