Mendel’s Laws, excerpt 2 | MIT 7.01SC Fundamentals of Biology

second law– this thing over here about a
three to one ratio about a single trait being controlled
by a pair of alleles, and those alleles being distributed
independently of each other to the offspring, the
stuff you always learned about Mendel– that's often referred to
as Mendel's first law. Mendel, by the way, didn't call
it Mendel's first law. It's considered– you don't write that in your own
papers or something like that, right? So Mendel did actually observed
some other things beyond this independent
segregation of the alleles for a single trait.

Mendel began to cross his peas
together and try to make combinations. He had rounds and wrinkles. He had greens and yellows,
talls and shorts. He started making
combinations. How about a plant that was
wrinkled and yellow? Green was the normal color. Round was the normal shape. But he had yellows. He had wrinkleds. How about making
a combination? So he begin to make plants that
bred true for different pairs of phenotypes. So for example, he had a pure
breeding line here that was both round and green. That was the stuff he could
pick up at the market. But he made a line here that was
both wrinkled and yellow. What is the genotype of this
round, green strain? At the round gene– the gene for roundness-
what is its genotype? Big R, big R. It's a pure
breeding strain. It was homozygous– we're just testing our words
here– homozygous for the big R allele. Green is controlled by
a different gene. It has an allele big G. It's
pure breeding for this. And we call it big G, big G.

Convention, when we use capital
letters, it tends to mean that the associated
phenotype is dominant. OK? It'll make you think that the
allele is dominant, but it's the associated phenotype
that's dominant. Now, wrinkled– what
was wrinkled? Wrinkled was a homozygous
wrinkled– little r, little r. And what was the genotype
at the yellow locus? Little g, a little g is
how we'll denote it. Geneticists use four or five
different kinds of notations. We're going to use this notation
today of big R's and little r's and little g's. But you'll get used to other
kinds of genetic notations. So when we cross these guys
together, this F0 generation here of these two pure breeding
parental strains, we get an F1 generation. The F1 generation– what is it phenotypically? What did it look like? Round and green, yep–
round and green.

What was in genotypically? Big R, little R, big
G, little g. Now we could self
these plants. And our head would hurt with
the nine to three to three to one ratio. So instead, why don't we cross
these plants back to the wrinkled, yellow strain to
make our life easier? Little r, little r, little
g, little g– and when we cross that back,
what is the segregation that's going to happen? Well, what are the possible
gametes that could emerge from this parent? We could get a big R and a big
G. We could get a big R and a little g. We could get a little r and a
big G.

We could get a little r and a little g. Those are the four possibilities
that could be contributed by this parent. What could be contributed
by this parent? Little r and little g–
that's it, right? No other options. So that's what our little
Punnett square looks like here of our options– parent number one, parent
number two. What will this be? This will be big R, big G over
little r, little g, big R, little g over little r little g,
little r, big G over little r little g, little r little
g over little r little g. In other words, this will
be round and green. This'll be round and yellow. This'll be wrinkled and green. And this'll be wrinkled
and yellow. And what will be the
ratio of these? One to one to one to one,
provided that those gametes were all equally frequent,
provided that that parental plant made each of those four
types in equal proportions. That one to one to one ratio
in the gametes will necessarily translate into a one
to one to one ratio in the phenotypes observed in
the next generation.

When we cross back–
not by selfing– but when we cross back to the
parent that has the recessive phenotypes, we'll often
call this a backcross or a test cross. If I haven't done a backcross
or a test cross where I crossed back to the wrinkled,
yellow parent, I would instead have had to make a square here
that had 16 boxes in it, and I would have had to add up to 16
boxes to figure out how many were round and green– nine out of the 16. How many were round
and yellow? Three out of the 16. How many were wrinkled
and green? Three out of the 16. And how many were wrinkled
and yellow? One out of the 16. But for the purposes of using
the white board up here, I did the test cross or
the backcross, because it's simpler. But you can also do the four by
four matrix and figure out what it looks like. That was news. It didn't have to be
that way, right? Maybe it was something else. This is pretty cool.

What it tells you is not just
is it the case that here the alleles segregate
independently. It's a random coin flip
which one you get. It tells you no correlation
between the two traits. They're independent. This is called independent
assortment. Mendel's second law is the law
of independent assortment. All right. So Mendel publishes the paper. 1865, it comes out. Here's a copy of
Mendel's paper. It's translated into English
from the original German. So I got Mendel's paper here. There's no Punnett squares. It's kind of messy notation.

Look at that. Look at all that– big A, little b. He's got A's, B's, C's. He's got three factor crosses
running around in here. Mendel really goes to town. It's a beautiful paper here. But it just goes on and on. It's incredibly hard to read. Look at this. It takes a lot to
read this thing. But in a way, it's simple. It's nothing so sophisticated. Oh yeah, here. Look at this– long, green,
inflated, constricted– all this kind of stuff. It's pretty cool. You should look it up. It's online. You can find Mendel's paper. What happens to Mendel's
paper? Nobody reads it. It sinks like a stone. It's this cool paper and
nobody reads it. Nobody reads it for
a lot of reasons. Scientific communication wasn't
so big in those days. Oh, well. Mendel also ends up getting
promoted to become the abbot of the monastery, and that's
pretty much the end of his scientific career,
in my opinion.

He got too many administrative
duties, doesn't do more science there. Also, he has some
poor choices. The next plant he works
on is hawk weed. Hawk weed turns out to have
really weird genetics that totally leads him astray. Basically, this is
the one important paper Mendel ever publishes. It's an incredibly
important paper. It's so important because it
contains the clue to what Darwin, living at exactly
the same time, wished he understood, which is what the
basis of genetic variation is. Wouldn't it be great if Darwin
had read Mendel's paper? Darwin actually owned a copy
of Mendel's paper. He received a copy of
Mendel's paper. In those days, the way they
printed books, there were folded pages and you had to
slit the page to read it. Darwin never slit the pages of
the copy of Mendel's paper. So we know he's never read
Mendel's paper, but he has one in his library. He had Mendel's paper. He had the answers sitting
there on the shelf, but never read it. The stuff sinks like a stone.

Nobody really pays much
attention to it. And Mendel goes on,
dies that's it. [LAUGHTER] PROFESSOR: Until the end of
the 1800s, right at the beginning of the 20th century,
along comes cytology– looking at cells in
the microscope. Microscopes began to get
good in the late 1800s. And cytologists began to see in
their microscope that when cells divided, these funny
structures began to appear– these long, thread-like
things. And the German chemical industry
being developed at that time had invented
all sorts of dyes. And cytologists began
experimenting putting dyes on these cells. And the dyes let them see really
clearly these funny things that were condensing
out when cells divided. And they had no clue what these
funny things were other than that they took up dyes. And so in the absence of any
clue what were, they called them chromosomes, meaning
colored things. That is what chromosome means. They called them colored thing
Chromos colored bodies, colored things.

That's all they knew. And they observed that these
chromosomes, these colored things, did really interesting
choreography. When cells divided, when they
underwent mitosis, what would happen is that the chromosomes
would line up along the midline. And they would have, at that
point, these funny X-like structures. And I'll draw four of
these chromosomes lining up like this. And what would happen
during mitosis? The cell would divide, and each
of the two cells would get one half of the X. So if you
started with four of these X's, you ended up with
four like this.

There you go. That was the chromosome being
somehow tugged apart. Now, anything that gets tugged
apart when a cell divides– that's kind of interesting. Then those chromosomes
would disappear. You couldn't see them again for
a while until the cell was ready to divide again. And when the cell is ready to
divide again, darned if those single lines hadn't
turned into X's. Somehow the cell had turned the
single lines into these two pieces, these X's,
and they were ready to divide again. And that was mitosis– the process of ordinary
cellular division. But there was another process. Folks observed meiosis. That's what happens when
you make gametes. So when gametes get made, the choreography was a bit different.

Instead of all the chromosomes
lining up on the midline as individuals, they lined
up as pairs. They line up as pairs. When the cell divides, you
end up with now only two X's, not four X's. Then what happens is those
cells divide again. And you end up with those
straight lines– but not four of them,
only two of them. The first step gets called
meiosis number one– meiosis I. The second is
called meiosis II. The second step looks just
like mitosis, doesn't it? Chromosomes are lined up
along the midline. They separate it. It just looks like mitosis,
ordinary cell division. But that first step
is special. That first step says, somehow,
the chromosomes come in pairs, and the cell picks one from
each pair and gives to its gametes– its sperm
or its egg– one from each pair.

And what do you think happens
on fertilization? Well, you had one from each
pair, one from each pair, it comes together and it
restores a pair now. And you know what folks said? They said this sounds just like
what that dead monk was talking about. Pairs, particles of
inheritance– particles that come in pairs and
you give to your gametes one of the two pairs. These colored things must be
the basis of inheritance or genes or something. Wow, because it fits Mendel's
model beautifully. It explains the first law. What about the second law? What about Mendel's
second law? How could it explain the big R
and the big G being inherited independently of each other
with no correlation? What would that have to mean? They're on different
chromosomes. The genes are on different
chromosomes. Because if big R is on one
chromosome and big G is on the other chromosome, then it's a
coin flip whether or not the big R might be here and a little
r might be there or the big G might be there or
maybe it's over there.

It's a random draw which
way it's going to go. So it perfectly explains
Mendel's second law. Unless– what happens if big R and big G
are on the same chromosome? Then they're going
to go together. I'm not going to have
independent assortment. I may have totally dependent
correlated assortment. If big R and big G are on the
same chromosome, they're going to be inherited together. Mendel's second law is
going to be wrong. So why did Mendel find big R
and big G going together? Maybe was lucky and he picked
traits on different chromosomes. But what about his next trait? Lucky again? Lucky again? Mendel studied seven traits. How many chromosome pairs
do peas have? Turns out, seven. But anyway, what happens? What's going on? Mendel's second law can't be
right if the chromosome theory is right when the genes are
on the same chromosome. They would be dependent. They won't be independent one
to one to one to one.

So which is it? Is Mendel right, my hero? Or is this chromosome
theory right? Because they can't be both
perfectly right. So which is it? Oops, we've run out of time. [LAUGHTER] PROFESSOR: Next time.

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