Population Genetics: When Darwin Met Mendel – Crash Course Biology #18

Population Genetics: When Darwin Met Mendel – Crash Course Biology #18


Hey look! It’s our friend Gregor Mendel,
the supermonk who discovered the basic principles of genetics. Hopefully you remember all of this. Both parents contribute one
version of each of their genes called an allele,
to their offspring. And some of those alleles are
dominant, or always expressed, while others are recessive and
only expressed when they’re not paired with a dominant one. Oh, and here’s our old friend
Chucky D, he lets me call him that. All this information that Mendel
figured out would have been really quite interesting to him,
because Darwin spent his whole life defending his ideas of
Natural Selection as the primary force for Evolution. But, Darwin had no idea how traits
were passed on to their offspring, even though these two guys were
living and working at the same time. Both Mendel and Darwin died not
knowing how their ideas fit together. So today we’re going to introduce
them, and their ideas, to one another, through the
science of population genetics, which demonstrates how genetics
and evolution influence each other. And I have good news! It involves a lot of math! Population genetics, on the
surface, is not a complicated idea. It’s the study of how populations
of a species change genetically over time, leading to
a species evolving. So let’s start out by defining
what a population is. It’s simply a group of individuals
of a species that can interbreed. And because we have a whole bunch
of fancy genetic testing gadgets, and because, unlike Darwin, we
know a whole lot about heredity, we can now study the genetic
change in populations over just a couple generations. This is really exciting and really
fun because it’s basically like scientific instant gratification. I can observe evolution happening
within my lifetime, so cross that off the old bucket list. Now part of population genetics,
or Pop-Gen, I know, we’ve got fancy abbreviations for everything
now, involves the study of factors that cause changes in what’s
called allele frequency. Which is just how often certain
alleles turn up within a population, and those changes
are at the heart of how and why evolution happens. So, there are several factors that
change allele frequency within a population. And just like Fast and Furious
Movies, there are five of them. And unlike Fast and Furious
movies, they’re actually very very important and are
the basic reason why all complex life on earth exists. This main selective pressure is
simply natural selection itself, Darwin’s sweet little baby which
he spent a lot of his career defending from haters. Obviously, we know this,
Natural Selection makes the alleles that make animals
the strongest, most virile, and least-likely-to-die more
frequent in the population. Now, most selective pressures are
environmental ones, like food supply or predators or parasites.
But at the population level one of the most important evolutionary
forces is sexual selection, and population genetics gives it
special attention, particularly when it comes to what’s called
nonrandom mating. Which is a lifestyle that I
encourage in all of my students. Do not mate randomly. Sexual selection is the idea
that certain individuals will be more attractive mates than others,
because of specific traits. This means they’ll be chosen
to have more sex and therefore have more offspring. The Pop-Gen spin on things is that
sexual selection means mating isn’t random. There are specific
traits that are preferred, even though they may not make the
animals technically more fit for survival. So sexual selection
changes the genetic makeup of a population, because the
alleles of the most successful maters are going to show up more
often in the gene pool. Maters gonna mate! Another important factor here,
and another thing that Darwin wished he understood,
is mutation. Sometimes when eggs and sperm are
formed through meiosis, a mistake happens in the
copying process of DNA. “Bad” errors in the DNA could
result in the death or deformation of the offspring, but not all
mutations are harmful. Sometimes these “mistakes” can
create new alleles that benefit the individual by making it
better at finding food, avoiding predators or
finding a mate. These “good” errors, and the
alleles they made, are then passed to the next generation,
and into the population. Fourth, we have genetic drift,
which is when an allele’s frequency changes due
to random chance. A chance that’s greater if
the population is small, and thus happens much more quickly
if a population gets knocked way back by a tornado or something. Genetic Drift does not cause
individuals to be more fit, just different. Finally when it comes to allele
game-changers, you gotta respect the gene flow. Which is when new individuals
with different genes find their way into a population and spread
their alleles all over the place. Immigration and emigration are
good examples of this, and as with genetic drift its
effects are most easily seen in small populations. Again, our factors: Natural Selection: Alleles
for fitter organisms become more frequent. Sexual Selection: Alleles for
more sexually attractive organisms become more frequent. Mutation: New alleles pop up
due to mistakes in DNA. Genetic Drift: Changes in allele
frequency due to random chance. Gene Flow: Changes in allele
frequency due to mixing with new, genetically different populations. Now that you know all that,
in order to explain specifically how these processes influence
populations, we’re going to have to completely
forget about them. This is what’s called the
Hardy-Weinberg Principle. Godfrey Hardy and
Wilhelm Weinberg were two scientists in 1908 who
independently, at the same time, came up with the exact same
equation that describes how, under the right circumstances,
Mendelian genetics works at the scale of a whole population. But those “right circumstances”
assume that none of the factors I just mentioned are at play. Hardy and Weinberg’s simple
equation shows us the frequency with which you could expect
to find different alleles within a hypothetical population
that’s not evolving. This weird hypothetical
state is called the Hardy-Weinberg Equilibrium, in which the frequency of alleles
in a population remains constant from generation to generation. And to make sure that happens,
NO FUNNY STUFF is allowed to go on. To wit, the Hardy-Weinberg
Equilibrium requires: 1. NO natural selection, which means that no alleles are
more beneficial than any other, so the better alleles will not
be selected within a population. 2. NO sexual selection, which means mating within the population must be
completely random no individual can have a better
chance of getting it on than other. 3. NO mutations, because mutations modify
the gene pool. 4. Hardy-Weinberg demands a
gigantic population size because the smaller the population,
the more likely you are to get genetic drift. 5. Finally, NO gene flow, that means nobody can bring over
their hot cousin from the next island over, because that
would significantly mess with the allele frequencies, if you know what I mean. So, clearly, no fun
and lots of rules. Hardy and Weinberg, they figured
this out at the exact same time, so it can’t be that complicated,
because it wasn’t some kind of stroke of Einsteinian inspiration,
they just figured out a thing that was pretty simple. So the question
is, can we do the same thing right now? Can we figure it out on our own? What we’re looking for is the
relationship between the phenotype and the actual frequency of the
genes in the population. So how do we proceed from here? Alas…earwax. The consistency of earwax
is a Mendelian trait. Wet earwax is a big W because
it’s dominant and dry ear wax is recessive so it’s a little w.
Now let’s call the frequency of the dominant, wet allele
of the population p and the frequency of the
recessive, dry allele q. Which if you’ve ever noticed,
q is kind of a backwards p. Since there are only two alleles
for this gene in the entire population, p + q=1. So if the frequency of p is 75%,
the only other thing it could be is q,
so that’s going to be 25%. Which is 1. So imagine we go to this
hypothetical, no-fun, Hardy-Weinberg island and
there are 100 people. We poke every single one of them
in the ear and 9 of them have dry ear wax. So that’s 9/100 or 9% or 0.09.
You know math? But this is not q. It’s not the frequency of the
little w, it’s the frequency of the homozygous ww. So this is the expressed phenotype.
It’s not the genotype. We don’t know that yet.
We know the frequency of ww. But you know there’s got to be a
lot of other w alleles hanging around in heterozygous pairs. So how do we figure out where
those are, how many of those there are? Well, I have no idea.
I now, am stuck. I do not know.
I am lost. When I’m stuck in situations like
this, what I do, is I go back to what I DO know. And what I know is that the
frequency of Big W plus the frequency of little w=1. But that’s in the entire
population, and in each individual, we want to know their genotype,
so two different alleles. So what’s happening is this is
happening twice in every individual, so what we
need to do, is square it. And when we square that equation,
if you remember algebra at all, you get: p^2 + 2pq + q^2=1 And that, my friends, is what
Hardy and Weinberg did, and IT is the
Hardy-Weinberg equation! So p squared is the odds
of it being a WW. This 2pq here is the heterozygotes,
and the q squared is the homozygous recessive. Well good news! We know ww. We know the homozygous recessive
is 0.09, so we already have that information. We know what q squared is,
it’s 0.09, and in order to get what q is we just take
the square root of that. That was a horrible square root symbol. Which is 0.30 or 30%. A 30%
frequency of the q allele in the population. Then we just use the simplest
equation in the world to figure out what p is. This minus 1. And that’s 0.70. Now, using our Hardy-Weinberg
equation we can go beyond the frequency of the alleles and
actually talk about the frequency of the genotypes. So the frequency of the WW
homozygous dominant is p squared. We have p. So we just square this
and that equals 0.49. Or 49% of the population
is homozygous dominant. Now the math gets even easier
because we know p and q. So to figure out how many
heterozygotes there are, we just do 2 times p
which is 0.70 times 0.30,
which is q, which is 0.42. Which is math that
I did beforehand. No, I didn’t just know that. So 9% of the population is
homozygous recessive, 49% is homozygous dominant, and 42% heterozygous,
displaying wet earwax, but with that little w
in there as well. What’s awesome about all of this
is we can see Mendel’s ideas work in a big population, and when
things aren’t lining up with this equation, then we know that
there are one of those 5 factors at work. Probably more than one. For example, a bunch hot surfers
moved to the island, and they all happened to have dry earwax. And they start spreading their hot
surfer genes all over the place. Nonrandom mating: it always goes
out the window whenever the hot surfers get involved. I don’t know about you,
but this stuff’s pretty beautiful to me. So don’t give me too hard of a
time in the comments, where you can ask questions! Or on Facebook or Twitter. Thank you for watching this
episode of Crash Course Biology. We will see you next time.

100 comments on “Population Genetics: When Darwin Met Mendel – Crash Course Biology #18

  1. Stephen Raj Post author

    "Just like Fast and Furious movies, there are 5 of them" lol if only you knew

    Reply
  2. Department of Analytics Post author

    Basically Hardy-Weinberg Equilibrium = Communism.
    Function: Measure Economic Freedom.

    Reply
  3. Serban Kline Post author

    Animals were created as they are by the lord, children do not listen to this fiend

    Reply
  4. Elfa Norisda Post author

    wow, thank you so much Hank, for explaining in a fancy-understandable explanation that enlighten me on my research topic. Really being helped by this video to begin with. Go and good luck for your next can't-wait video! XD

    Reply
  5. rs5352 Post author

    One scientific caveat – the Fast & Furious movies are also really important, and are also the reason why we have complex life today.

    Reply
  6. Tony Vasi Post author

    Hey! I realize this videos pretty old at this point but if someone happens to be reading through comments still, I have a question!

    I’m having trouble figuring out why you square the equation (p + q) instead of multiply it by 2 or something. I’m sure the answers simple and I just haven’t realized it yet. Thanks!

    Reply
  7. Mohamed Dadamouny Post author

    What are the difference between Intra-individuals (Qi) and inter-individuals intra-population genetic variance and what could it tell us?

    Reply
  8. Hopeyfish Post author

    This was explained so much more clearly in 12 minutes then in the 2 hour lecture I just struggled to keep notes through.

    Reply
  9. RiBread Post author

    My AP Bio teacher doesn’t teach. Thank you so much for this series! It’s my only thing to help me pass😂😭

    Reply
  10. Emily Marques Post author

    I'm confused, with those calculations, the final product amounts to more than 1. 0.49+0.42+0.3 =1.2, which therefore doesn't satisfy the equation?? Does it? Please help clarify!

    Reply
  11. James Carmody Post author

    You explain Hardy-Weinberg better than Khan Academy. These 11 minutes made more sense to me than Sal's entire microlecture.

    Reply
  12. Kasey Brown Post author

    The serious problem with this video is that it's making the Hardy-Weinburg thing sound like it's something totally unrealistic that you should definitely ignore. As though it's a debunked theory. I'm about to take my bio test and as it turns out, no, the Hardy-Weinburg thing is actually a very real equation that's taken very seriously.

    Reply
  13. Christian Houghton Post author

    Good Work, all of you have made something that we need 4 months in the University! jajaj…really, it´s was really helping. Just one thing I´ll say to correct in the future: there is no direction of the evolution…at least we don´t have probe of that, not enough. Keep working please, we need you=)

    Reply
  14. Jimmy Gravitt Post author

    Anbd of course here comes Harvey Weinstein makes an appearance spreading his alleles about… What's that? Hardy Weinberg? Right then.

    Reply
  15. Jiggelmeister Post author

    how did he do the drawing? was their a glass surface in between him and the camera? special effects?

    Reply
  16. petr shv Post author

    Mendel and Darwin died without knowing that their ideas fit together, while plank and Einstein died knowing that their ideas didn't fit together.

    Reply
  17. Pop Culture Collective Post author

    HA now there are like 8 F&F movies with a spinoff series coming too. Man 2012 was such a simpler time. looks longingly into the distance

    Reply
  18. Big Chungus Post author

    So you're saying the Fast and Furious movies aren't the leading cause for the start of life in the universe? Vile heathen. kappa

    Reply
  19. Matt S Post author

    Is it that weird that im watching all of this stuff without being in school? I am preparing for college though.

    Reply
  20. Sara H. Post author

    Did anybody else realize that the Darwin finger puppet changed the second time he brought it out? It was originally Darwin, then switched to Albert Einstein…..(0:30 is Darwin, 5:05 is Einstein)

    Reply
  21. Randy Harris Post author

    How often would you say that there is a beneficial mutation? Frequency of 1 every 1000 was what was suggested to me; I only wondered what you thought. Good video BTW.

    Reply
  22. Kaden Howell Post author

    05:48 NO SEXUAL SELECTION! Aw man, but what about my girlfriend from Hawaii? No, jk i dont have a girlfriend. ☹️

    Reply
  23. Mel Soderlund Post author

    The info in these videos is fantastic and super useful, but the inflection in Hank’s voice sounds condescending.

    Reply

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