Hi. It's Mr. Andersen and welcome biology video essentials 54. This is on population
variation and how that applies to population dynamics. And so basically it's that same
old idea that variation is important. And in this case we're talking about genetic variation
within a population. This right here is a tasmanian devil. Tasmanian devil live on Tasmania
which is an island state, about 150 miles south of Australia. Basically the Tasmanian
devil is nocturnal. It's usually found out at night. They have a really disproportionately
large head. Really powerful jaws. They go out at night and basically feed on dead and
dying material. They're also very aggressive. They have these loud screams and they'll fight
for territory. And they'll fight other Tasmanian devils for food. But they've been plagued
by a disease over the last decade. And it's called devil facial tumor disease. It started
in 1996. And it's spread across Tasmania. And it will probably lead to the extinction
of the Tasmanian devil. In this facial tumor disease, they get these nasty tumors that
build up on their face. Eventually they make it impossible for them to feed and to breathe.
And then they die as a result of that. But it's awful. But what's weird about the disease
is it's transmission. It's not a conventional virus. It's literally cancerous cells that
are transferred from one Tasmanian devil to another. In other words when these Tasmanian
devils are fighting, tissue is being transferred from the sores of one Tasmanian devil to another.
And since they lack genetic variability, all the Tasmanian devils are essentially the same,
cancer can be transferred from one to another and create cancerous cells there. Now can
you pick up cancer from somebody else? Not at all. And the reason you can't is that genetically
we're so different that our cells, our immune system is essentially going to recognize that
as not part of ourself. And it's going to destroy those cells. But in the Tasmanian
devil, since they decrease that genetic variability they're transferring cancer between each other.
And they'll eventually go extinct. There's a captive breeding program that's trying to
keep them alive. And it looks like there's a few females that are immune from this cancer.
So basically in this podcast I'm going to talk about genetic diversity. And how a lack
of genetic diversity can lead to extinction. An example I'll give you is the black-footed
ferret. But how genetic diversity is very good. And having a different response to a
disease is important. I'll talk about HIV immunity in humans and how some humans are
actually immune from picking up the virus or immune from AIDS. And then how we can look
at the numbers of those individuals through Hardy-Weinberg equilibrium. And we can work
backwards to figure out the allele frequency of this CCR5 Delta 32 mutation. And so basically
variation is good. Let's start with the story of the black-footed ferret. The black-footed
ferret is a nocturnal weasel. They feed on prairie dogs almost exclusively. They'll got
out, hunt at night. But black-footed ferrets, we thought, went extinct. And that's because
we decreased the amount of prairie dogs and their population had dropped off. And so by
the 1900s, the late 1900s we thought that they were gone. Until a dog in Meeteetse Wyoming
showed up on a doorstep with a dead black-footed ferret. And so they discovered another group
of these black-footed ferrets that were alive is outside Meeteetse Wyoming. And so the problem
was that there were few of them left and those eventually died off. In other words their
population was so small, they had so small amount of genetic diversity that a few diseases
eventually wiped them out. So in 1981 I think they were extinct in the wild. But there's
been a captive breeding program to bring back the black-footed ferret. And so they've been
breeding them in captivity. Releasing them I think they're in a number of western states.
And they're making a comeback. I think there are around a thousand of them left. But if
you think about it, they've gone through a huge bottle neck. When the only black-footed
ferrets are the ones we actually had breeding in zoos, and then releasing those, we've reduced
that genetic variability. It's going to make them more susceptible to any kind of a disease
or any kind of a genetic disease. And so again variation is important. AIDS is something
that's interesting. When we were looking at the AIDS outbreak in the 1980s we found that
there were people who should be getting AIDS that weren't getting AIDS. And we've now discovered
it's because they have a mutation. And so if we look in Northern Europeans we find that
in some areas, especially like in Sweden, I'll show you in a second, up to 3% of the
population actually are immune to getting the virus, HIV. So let's look at how it's
transferred. Remember it's a RNA virus. It's a retrovirus. So basically they have proteins
on the surface that allow them to infect T lymphocytes. There's a CD4, so this is going
to be a CD4 receptor that's going to allow the attachment of the HIV and then entry of
the genetic material into the cell. But what's important is there's this protein right here,
excuse me, right here called the CCR5 protein. It's in the membrane of a T4 lymphocyte. And
if you don't have that proper protein here, the CD4 receptor can't link up with that HIV
and so it can't move in. And so if you can't make that protein, then you can't be infected
by HIV. Now where did this come from? We think it came from, if we look at the selective
pressure in Northern Europe, it probably either came from the plague or the black death. Or
small pox outbreaks. In other words with both of these diseases there were people who were
immune to the disease. And it's because they had a mutation in this one protein right here.
So they couldn't pick up the disease. And so what's happening right now, well here's
the number of people who are living currently with AIDS. So in the United States its over
a million. But if you look here in sub-Saharan Africa all of these countries, in each of
the countries we have millions of people in each of these countries that are dying as
a result of AIDS. But within that population, since there is variability, we're going to
find people there that are naturally immune to HIV. And so if we were to come back a thousand
years later, we'll find that those allele frequencies are going to be higher in those
areas where we had greatest prevalence of HIV. And what's interesting now is that these
diseases years ago are offering protection to some of the people today. And so you can
see why it's important in a population to have variability. Because a few of those people
will be immune. Just like a few of the female Tasmanian devils are immune from this facial
tumor disease. And so that will give them a chance at least of surviving. Now how do
we know that this person who had this first mutation started in Sweden? Well if you look
at the allele frequencies we find that they go from zero all the way up to around 0.18
as we get up into Scandinavia. And so how do you figure out these numbers? Well basically
what you're looking at are the people in the population who should be getting the HIV but
aren't getting it. They then identified where that is and now they've been able to identify
the gene. And so we can apply Hardy-Weinberg Equilibrium to that. So if we look at, let's
say the high end. So if we're looking way down, way up here in Scandinavia. So if I
grab a value. So that means that we have 0.18 percent of the population. So what is it telling
us? That is our q value. And so that means that 0.82 of the population is going to be
our p value. And so in our population, 18% of the frequency, or 18% of the alleles actually
have this delta 32 mutation. So you can't get the HIV. And so if we want to figure out
how many people are actually immune to it, well you have to have two copies of the gene.
And so that's 0.18. So that's going to be 0.18 squared. And so that would be like 18
over 100 times 18 over 100. So that would be 324 over 10,000. So if we move this over
two, so that would be 3.24%. So where the allele frequency is the highest, where it's
0.18, 3.24% of the population actually can't get AIDS. Or at least can't pick up this one
strain of HIV. And so what percent of those are going to be carriers? Well to figure out
that I'd take 2 time p times q and that would tell us the number of individuals in this
high area that are actually carriers for the disease. And so again we're tying together
all those things we've learned this year. The idea that natural selection can be a selective
pressure on those people. That we can see it in the genes. And those genes are expressed
in the phenotypes that we have. And we can look at where those are and apply Hardy-Weinberg
equilibrium to figure out the allele frequency. And so that's populations. That's variation
in populations. And remember variation is good. And once we decrease the size of a population
or that variation we're more susceptible to disease. And so I hope that's helpful.