ADAM MARTIN: Well, first of
all, nice job on the exam.
We were quite pleased
with how you guys did.
And so from now
on in the course,
Professor Imperiali
has been telling you
about information flow, but
information flow within itself,
so information flow from
the DNA to the proteins that
are made in the cell, which
determines what that cell does.
And so we're going to
switch directions today.
And we're going to start
talking about how information
flows between cells--
so from a parent cell
to its daughter cells.
And we're also going to talk
about how information flows
from generation to the next.
And this, of course, is
the study of genetics.
And what genetics is
as a discipline is it
is the study of genes
and their inheritance.
And the genes that you
inherit influences what
is known as your phenotype.
And what phenotype
is is simply the set
of traits that define you.
So you can think of it as
a set of observable traits.
And this involves your
genes, as you probably know.
I mean, just this morning, I was
dropping my son off at school,
and he was comparing how tall he
was compared to his classmates.
And as he went in, he was like,
thanks for the genes, dad.
So I expect that
many of you are going
to be familiar with much
of what we'll discuss,
but we're going to lay
a real solid foundation,
because it's really
fundamental for understanding
the rules of inheritance
and how that works.
So genetics is the
study of genes.
So what is a gene?
You can think about
genes in different ways.
And what we've been
talking about up until now,
we've been talking about
molecular biology and what
is known as the central dogma.
And the central dogma states
that the source of the code
is in the DNA.
And there's an information
flow from a piece of DNA,
which is a gene.
And the gene is a
piece of DNA that
then encodes some sort of
RNA, such as a messenger RNA.
And many of these RNAs
can make specific proteins
that do things in your
cells in your body.
So that's one very
molecular picture of a gene.
You can think of a gene as
a string of nucleotides.
And there might be a reading
frame in those nucleotides that
encodes a protein.
So that's a very molecular
picture of a gene.
The field of genetics started
well before we knew about DNA,
and its importance, and
what the DNA encoded
RNA which encoded proteins.
So the concept of a gene
is much older than that.
And so another way you
can think of a gene
is it's essentially the
functional unit of heredity.
So it's the functional
unit of heredity.
I'll bump this up.
So I want to just briefly
pause and kind of give you
an overview of why I think
genetics is so important.
So what you saw up here
is you saw a cell divide.
And I showed you this
in the last lecture--
you saw the chromosomes,
which are here,
how they're segregated
to different daughters.
And this is-- basically, you're
seeing the information flow
from the parent cell into
the daughter herself.
But we saw this, so I'm
just going to skip ahead.
So why is this so important?
I'm going to give you a
fairly grandiose view of why
genetics is so important.
And I'm going to say that
we can make a good argument
that genetics is
responsible for the rise
of modern civilization.
Humans, as a species, began
manipulating genes and genetics
even before we had any
understanding of what
was going on.
So this is more of an
unconscious selection.
And so 10,000 years ago,
humans were hunter gatherers.
They'd go out, and try to
find nuts and seeds, and hunt
animals.
And that's how we got our food.
But around 10,000 years
ago was the first example
of where humans, as
a species, really
altered the phenotype of
a plant, in this case.
So wild wheat and wild barley,
the seeds develop in a pod.
And the biology
of the wild wheat
is such that the pod
shatters, and the seeds then
spread on the ground
where they can then
germinate into new plants.
But 10,000 years
ago, humans decided
that it would be more ideal if
we had a form of wheat which
didn't shatter, which is
known as non-shattering wheat
in which the seeds
remain on the plant.
And that allows it to
be easily harvested
at the end of the season.
So 10,000 years ago is
one of the first examples
where humans really
genetically altered
the phenotype of a plant.
And they selected for
this non-shattering wheat,
which then allowed for
the rise of agriculture.
In addition to wheat, we also--
about 4,000 years
ago was the rise
of domesticated fruit and nuts.
So here are some almonds.
If you would like an almond,
feel free to have some.
You guys want some almonds?
No.
If you have a nut
allergy, don't eat them.
Great.
So wild almonds,
when you chew them,
there's an enzymatic
reaction that
results in cyanide forming.
Rachel just stopped chewing.
Don't worry.
These are almonds that are
harvested at Trader Joe's, so
you're safe.
And so the wild
almonds, obviously,
were not compatible
for consumption.
But 4,000 years
ago, humans again
selected for a form
of the almond, which
involved just a single
gene, which was non-bitter
and known as a sweet almond,
which was also not toxic.
So this doesn't just go for
foods, but also for clothing.
So humans have selected
for cotton with long lint.
And that served as a basis
for clothing and sort
of allowing us to have fabric.
And I just want to end with a
little story about the almond,
which is part of the
archaeological evidence
for when almonds
were domesticated
was when King Tut's
tomb was unearthed.
And they found a pile of
almonds next to the tomb,
because the Egyptian
culture, what they did
is they buried the dead
with food to sustain them
in the afterlife.
So that just gives you
an idea as to how far
back the importance
of genetics goes.
If we think about
nowadays, right now
you are always seeing
genetics in the news.
And you also have
the opportunity
yourself to sort of do your
own genetic experiment.
And so now you guys
are undoubtedly
aware of all these
companies that
want you to send them your DNA.
And they also want
you to send them
money, such that they
can give you information
about your family tree and also
information about your health.
So this is now a big business.
But if you don't
understand genetics,
this is not as useful
as it could be.
So I'm just curious.
How many people here have
used one of these services
and had their DNA genotyped?
Cool.
And do you think
that really changed
your view of who you are?
Or was it kind of, eh?
AUDIENCE: We actually--
I don't know if we even
looked at where we came from.
We looked for genetic disease.
ADAM MARTIN: So you're
looking for genetic disorders.
And you don't have to tell
me anything about that.
Yeah, so I have not done
this, but my dad has done it.
And he will go
find his relatives
and bore them with our ancestry.
So this is one example
of how genetics is really
in play today.
And not everyone
knows how this works.
I've had people at Starbucks
in the morning come up
to me with their 23andMe profile
and ask me to explain stuff,
because they know who I am.
It's a little awkward.
So we can also use
genetics for forensics.
And so this is kind of a--
I had a lab manager in
the lab, and he told me
that people were doing
this in senior homes
in Florida, which I
thought was kind of funny.
What I find hilarious about
this is the mug shot of the dog.
That dog looks so guilty.
But you can use DNA to--
you can use DNA
to genotype poop.
You can genotype
your neighbor's dog.
You can get evidence that
they're the one that's
pooping on your lawn.
So that's a
not-so-serious example.
But there are more
serious examples
of where DNA genotyping
is really having
an effect in our society.
And this is something I
mentioned in the intro lecture.
Just this past
spring, someone was
suspected as being the
Golden State Killer.
This is a cold case.
The killings happened
40 years ago,
but the break came from
investigators getting DNA
from the suspect's
relatives to implicate
this person in this crime.
So they had DNA from the crime.
And they saw that there were
matches to the DNA at the crime
to certain people.
And then they can
reconstruct who
might be the person in the
right place to commit the crime.
So this is--
I think this is
interesting, because it also
leads to all sorts of
privacy issues, right?
Who's going to gain
access to your genotype
if you submitted to
these companies, right?
I mean, this is
probably a case where
I'd argue there's probably a
beneficial result in that you
can actually figure out if
someone's committed a crime.
But there are other
issues in terms
of thinking about
insurance companies
where we might be interested
in having our information not
publicly available to
insurance companies.
And maybe this is something
we can discuss later
on in another lecture.
For today, I want to move
on and go through really
the fundamentals of genetics.
And what I'm going to do is I'm
going to start with the answer.
OK?
I'm going to present
to you guys today
the physical model for
how inheritance happens.
OK?
So today, we're going to
go over the physical model
of inheritance.
And this physical model
involves cell division,
which you saw in
the last lecture
and also in my opening slide.
It involves cell division
and the physical segregation
of the chromosomes
during cell division.
So also chromosome segregation.
OK, so this is how I'm going
to represent chromosomes.
And I just want to step you
through what it all means.
So I have these two
arms that are attached
to this central circle.
The circle is meant to
represent the centromere.
So this is the centromere.
And you'll remember from
the last lecture on Monday,
the centromere is the
piece of the chromosome
that physically is attached
to the microtubules that
are going to pull the
chromosomes to separate poles.
OK?
So that's called the centromere.
And usually, it's denoted,
it's like a constriction
in the chromosome
or a little circle.
OK?
These other parts of the
chromosome are the chromosome.
So that you have the
arms of the chromosome.
Now I'm drawing what's known
as a metacentric chromosome.
It's not important that
you know that term.
But it just means
that the centromere
is in the middle
of the chromosome.
There are other types of
chromosomes with the centromere
might be at the end.
OK?
So there are different
types of chromosomes.
All right, now,
for all of us, we
have cells that have different
numbers of chromosomes.
OK?
Some of our cells are
what is known as haploid.
And what I mean by
haploid is there
is a single set of chromosomes.
Now the cells that we have that
are haploid are our gametes,
so they're our eggs
and our sperm cells.
OK?
So these include gametes.
OK, but most of the
cells in your body
are what is known as diploid.
And diploid means there's two
complete sets of chromosomes.
OK, and you get one
set from one parent,
the other set from
the other parent.
OK?
So one set from each parent.
OK, and I'll draw the
other set like this.
And what I'll do is I'll
just shade in this one
to denote that it's different.
OK?
So these two
chromosomes then are
what is known as homologous.
They're homologous chromosomes.
Homologous.
OK, and what I mean by
them being homologous
is that, basically,
these two chromosomes
have the same set of genes.
OK, so they have the same genes.
They have the same genes.
But they have different
variants of those genes.
OK, so different
variants of these genes.
And these variants are
referred to as alleles.
OK?
So if you have the same gene
but they differ slightly
in their nucleic
acid sequence, then
they're distinct
alleles of those genes.
So often, the way
geneticists refer
to these different
variants or alleles
is we use a capital letter
and a lower case letter.
OK, so this chromosome
over here might have
a gene that's allele capital a.
And then this
homologous chromosome
will have the same gene but
a different allele, which
I'll denote lowercase a.
OK?
So in this case,
big A and little a
are different alleles
of the same gene.
They might produce a
slightly different protein,
which would result possibly
in a different phenotype.
OK?
So everyone understand
that distinction?
Oh, I want to make one
point because this came up
last semester and was
one of those cases
where I forgot the
part about the head.
So we often just have two
alleles when we teach genetics.
But I hope you can see
that because a gene is
a long sequence of DNA, there
is a ton of different alleles
you can have within
a given gene.
So one nucleotide
difference in that gene
would result in a
different allele.
OK?
So we often refer
to two alleles,
but there can be more than
two alleles for a given gene.
OK?
Does everyone see how
that manifests itself?
OK, great.
Any questions up until now?
Yes, Carmen?
AUDIENCE: So when you say
that there's more than one,
more than just the two alleles,
I don't have more than one
on each chromosome.
So they're just more than one--
ADAM MARTIN: In the population.
So Carmen asked,
well, can I have
like five alleles of a gene?
And that's a great question.
And so thank you,
Carmen, for asking that.
What I mean is if we consider
a population as a whole, right?
You have two alleles
of each gene,
unless it's a gene that
somehow duplicated.
And so when we're
considering the population,
there can be more than-- right?
I mean, I see we
have people with--
hair color is not
a monogenic trait.
But we have people with
black hair, with blond hair,
with brown hair, right?
There is more than just
two possible alleles
with possible phenotypes.
OK?
All right, let's
go up with this.
All right, now I want to
start at the beginning.
So most of our
cells are diploid.
And the origin of our
first diploid cell
is from the union
of two gametes.
OK?
So I'm going to draw
two gametes here.
Each is one n.
And I'm just going to draw one
set of chromosomes for this
here.
So we might have a male
gamete and a female gamete.
And what I'm referring
to when I say n here,
n is basically referring to
the number of chromosomes
per haploid genome.
So when you have one
n, it means you're
haploid because you have only
one set of haploid genome.
But early in your life,
we're all the result
of a fusion between a
male and female gamete.
And so that creates
a diploid cell.
OK, so now, this
diploid zygote, so this
is referred to as the
zygote, is diploid
and now has a set of
homologous chromosomes.
OK?
So I'm only drawing one set of
homologous chromosomes here.
So on the board, I'm going
to stick to just one,
so I don't have to
draw them all out.
In the slides, I have three.
OK?
So each of these
represents a chromosome.
These are different chromosomes.
Different chromosomes are
either different color
or have a different
centromere position.
And then these down
here that are colored
are going to be the
homologous chromosomes.
OK?
Do you see how I'm
representing this?
OK, so once you have
the zygote, right,
so you guys are no
longer one cell, right?
You guys each are tens
of trillions of cells.
So this zygote cell had
to reproduce itself,
and your cells had to
divide, so that you
grew into an entire
multicellular organism.
I'll just quickly erase that.
OK, so when most of your cells
divide, and most of your cells
are known as somatic cells.
When cells of your body or
your intestine and your skin,
when they divide, they
genetically replicate
themselves.
And they're undergoing a type of
cell division known as mitosis.
OK?
In mitosis, it's essentially
a cloning of a cell.
Or ideally, it's the
cloning of a cell.
So you have a diploid cell.
It has to undergo
DNA replication .
And when a chromosome
undergoes DNA replication,
it will, during
mitosis look like this.
OK?
And these two different
arms or strands, they're
known as sister chromatids.
OK?
So that's just another
term you should know.
These are sister chromatids.
OK, and the sister chromatids,
if DNA replication happens
without any errors,
should be exactly the same
as each other in terms
of nucleotide sequence.
OK?
So after DNA
replication, this cell
will essentially have four
times the amount of DNA
as a haploid cell.
And it will split
into two cells.
And again, they'll
both be diploid.
OK?
And I'll just
point out, if we're
thinking about our pair
of chromosomes here,
right, this parent
cell has both homologs.
And the daughter
cells, because they
should be genetically identical,
also have both homologs.
OK, so that's an example
with just one chromosome.
I'll take you through an example
with these three chromosomes
here--
all six chromosomes.
So you have--
these are homologs.
These are homologs.
These are homologs.
And during mitosis, all
of these chromosomes
initially are all
over the nucleus.
But during mitosis,
they will align along
the equator of the
cell and what is
known as the metaphase plate.
Metaphase is just a fancy
term for one particular stage
in the mitotic cycle.
And then what will
happen is the spindle
will attach to either one
side or the other side
of these chromosomes.
And it will physically segregate
them into different cells, OK?
And what I hope you see here is
that this has six chromosomes.
This has six chromosomes.
And these two daughter
cells are genetically
identical to the parent cell.
OK, so this is known as
an equational division,
because it's totally equal.
OK?
And again, the daughter
cells are both diploid, OK?
So that's mitosis.
Any questions about mitosis?
OK.
Moving on, we're going to talk
now about another type of cell.
And these are your germ cells.
And these germ cells
undergo an alternative form
of cell division
known as meiosis, OK?
And your germ cells--
germ cells produce
your egg and sperm.
And so meiosis essentially is
producing gametes, such as egg
and sperm cells, OK?
So what's the final
product going to be?
What should be the genomic
content of the final product
of meiosis?
It should be one end, right?
Who said that?
Sorry.
Yeah, exactly right.
What's your name?
AUDIENCE: Jeremy.
ADAM MARTIN: Jeremy.
So Jeremy is exactly right.
Right?
The germ cells-- in order
to reproduce sexually,
they should be haploid
cells, so that they
can combine with another haploid
to give rise to a diploid, OK?
So the ultimate
result that we want
is to have cells
that are one end.
But most of our cells
to start out with
are diploid, so
they're two end, OK?
So what's special about
meiosis is you're not just
going from two end to
two end, but you're
reducing the genetic
content of the cells.
You're going from two end
to a one end content, OK?
So again, meiosis starts
with DNA replication.
But in this case, the first
division, which is meiosis I,
is not equal.
And it actually segregates
the homologs, such
that you get one cell that has
one of the homologs duplicated
and another cell that has
the other homolog duplicated.
OK?
And I'll show this.
I'll show it right now.
So this is the same cell now.
It's undergone DNA replication.
As you can see, each
chromosome has two copies.
But instead of all the
chromosomes lining up
in the same position of the
metaphase plate, what you see
is that homologous chromosomes
pair at the metaphase plate.
And what happens here is that
the homologous chromosomes are
separated--
two different cells.
And now, you have two cells that
are not genetically identical,
OK?
So because there
is not equational
and there's a reduction in
the genetic material that's
present in the
cells, this is known
as a reductional division, OK?
So that's meiosis I. And
that's a reductional division.
And then-- but this
is not yet haploid.
And so-- here, I'll just
stick another one in here.
These cells then undergo
another round of division,
which is known as meiosis II.
And during this meiosis,
these sister chromatids
are separated, such that you're
left with one chromosome.
And my drawing-- at least one
chromosome per gamete, OK?
So each of these, then, is 1n.
OK?
So again, you have
the chromosomes.
But this time, you have them
aligned like in mitosis.
They align.
The sister chromatids
are physically separated.
And now, you see this
cell is genetically
identical to this cell.
And this cell here
is genetically
identical to this cell, OK?
So that's meiosis II.
And that's an
equational division
much more like mitosis, OK?
Because the product of the
division of those two cells--
each of those is equal, OK?
And finally, the
result of meiosis II
is that you're then
left with gametes
that have a haploid
content of their genome.
OK, I want to end lecture
by doing a demonstration.
Let's see.
So this could either
be amazing, or it
will be a complete disaster.
So we're totally going to do it.
So everyone come up.
Right here.
Here.
Evelyn, you can leave
when you have to go.
And we'll have a
chromosome loss event.
OK?
It has to be a multiple of four.
If we have extra people label,
then the people can supervise.
Go.
Oops, sorry.
All right.
What do we got here?
Here you go, Bret, Andrew.
Sorry.
I hope I'm not hitting anybody.
AUDIENCE: [INAUDIBLE]
ADAM MARTIN: What's that?
Yeah, that's the
advantage of these.
All right.
Here you go, Myles.
Let's see.
Here you go.
Sorry.
Someone take this.
All right.
What do we got here?
Just got a little
chromosome here.
AUDIENCE: [INAUDIBLE]
ADAM MARTIN: Oops, sorry.
All right.
Who doesn't have a chromosome?
Everyone in the class
has a chromosome?
All right.
One of you want to come in here?
All right.
We'll see how constrained
we are in terms of space.
I've never been this ambitious
and had this many chromosomes
before, so I'm excited
to see how this works.
So you each have a Swim Noodle.
They're different colors,
so different colors
represent different chromosomes.
And then you also have Swim
Noodles that have tape on them.
And these represent
different alleles
from your other chromosomes.
So these two chromosomes would
be homologs of each other, OK?
Does that make sense?
OK, great.
All right.
Now, the metaphase plate will
be along the center of the room.
So let's first reenact mitosis.
So why don't you guys
find your sister chromatid
and then sort of align in
the middle of the room here?
Sister or brother chromatid.
How are we doing?
Do we have enough space there?
It's a little packed.
You can see how the cell--
can you imagine how packed
it is inside a cell?
OK, everyone found
their sister chromatid.
Normally, the sister
chromatids-- they replicate
and they get held together.
So there's no finding of
sister chromatids, but--
all right.
Great.
So segregate and we'll
see how you guys did.
All right.
And the goal is that you guys
would be genetically identical.
So how-- OK, great.
That looks like one
short red, one short red.
OK, that's good.
They look genetically
identical to me.
All right.
So that was my mitosis.
Now, we're going to do meiosis.
OK, why don't you guys align,
like what would happen during
meiosis I. OK, you
guys can come back.
Think about who you're
going to pair with.
[SIDE CONVERSATION]
All right.
So what were you looking
for when you were pairing?
Who were you looking for?
AUDIENCE: Longest chromosome.
ADAM MARTIN: Your longest
chromosome, right?
OK, great.
All right.
Why don't you guys segregate?
All right, so that
was meiosis I. Meiosis
I looks successful to me.
And now, we have to
undergo meiosis II.
So maybe what we could do
is you guys can rotate.
And the metaphase spindle can
be sort of in this orientation.
AUDIENCE: [INAUDIBLE]
ADAM MARTIN: Yeah,
that will-- we
want a group over there, a
group over there, a group here,
a group here.
And those will be
our four gametes.
[SIDE CONVERSATION]
All right.
You guys set?
All right.
Go.
[SIDE CONVERSATION]
OK, terrific.
Everyone haploid?
Looks like everyone is
haploid, which is good.
Right?
So let's just take a minute and
think about probability here.
So what was the
probability that a gamete
would end up with this orange
allele on the red chromosome?
AUDIENCE: Half.
ADAM MARTIN: Half, right?
Because there are two, right?
So these two gametes
have that allele.
These two should not, right?
OK, great.
And we just had a
chromosome loss,
so that gamete is in trouble.
But maybe we could get a TA
to rescue this chromosome.
Either one of you is fine.
There you go, David.
[SIDE CONVERSATION]
All right.
That was great.
Now, let's-- as
you're doing this,
you get a sense as to how things
could get mixed up, right?
And you think inside
the cell, right?
So I don't--
I've lost track of
how many chromosomes.
We have 1, 2, 3, 4, 5, 6, right?
How many chromosomes do we have?
AUDIENCE: 23.
ADAM MARTIN: We
are-- a haploid set
for us is how many chromosomes?
AUDIENCE: 23.
ADAM MARTIN: 23.
Exactly.
Right?
So it'd be even worse
for a human cell
to get this to go right.
So why don't you guys line up
in the mitosis configuration?
And we'll consider some
things that could go wrong.
All right.
Who here is good friends
with their sister or brother
chromatid?
Is anyone very good friends
with their sister or brother
chromatid?
[LAUGHTER]
AUDIENCE: [INAUDIBLE]
ADAM MARTIN: Yeah.
Someone become good friends
and become inseparable, OK?
Would someone volunteer
to be inseparable?
OK, great.
You guys are now
inseparable, OK?
Now, segregate.
OK, great.
Now, what happened there?
AUDIENCE: [INAUDIBLE]
ADAM MARTIN: What's that?
AUDIENCE: He stole her.
ADAM MARTIN: Yeah,
that's cell stole her.
OK.
So now, we have two-- a
duplication of that chromosome.
What's happened over here
with this daughter cell?
AUDIENCE: It's
missing a chromosome.
ADAM MARTIN: It's missing
a chromosome, right?
AUDIENCE: Right.
ADAM MARTIN: So
these are the types
of mistakes that can be
associated with a cell becoming
cancerous, right?
Because let's say
there was a gene
that suppresses growth
on that chromosome.
And it wasn't on that homolog.
Then you might result in a
genetic sort of mutant or loss
of that gene that would result
in uncontrolled proliferation.
Also, picking up
the extra copies
of genes that
promote growth could
allow that cell to have a
proliferative advantage, OK?
We're going to-- this is sort
of foreshadowing what we're
going to talk about later.
But I just want to
plant the seed now.
OK.
Why don't we go
back and do meiosis?
[SIDE CONVERSATION]
OK.
Now, anyone see any friends
looking across the aisle now?
All right.
Great.
You guys are now inseparable.
Why don't you guys segregate,
except the inseparable ones?
Oh, but your sister chromatids
still have to stay attached.
There you go.
See?
Great.
Right.
So just like last
time, this is known
as a non-disjunction event
where the chromosomes don't
separate when they should, OK?
Great.
Now, why don't you
guys do meiosis II?
[SIDE CONVERSATION]
All right.
You can segregate.
All right.
Now, you see these
two gametes over here
are lacking an entire
orange chromosome.
And these two gametes here have
picked up an additional copy
of an orange chromosome, OK?
So these two gametes
are no longer
haploid for the
orange chromosome.
And if one of these
gametes were to fuse
with a haploid gamete that
has an orange chromosome,
then now you have
a zygote that has
three copies of the orange
chromosome, which is abnormal,
OK?
So if that were
chromosome 21 in humans,
that would result in something
that's called trisomy 21, which
is down syndrome, OK?
So you see how mistakes in
how chromosomes segregate
can result in human disease.
OK.
Why don't we give
yourselves a hand?
Good job.
[APPLAUSE]
OK, you can just throw the
Pool Noodles on the side.
And I just have one
slide to show you
where we're going next.
[INAUDIBLE]
[SIDE CONVERSATION]
AUDIENCE: So I have a question.
ADAM MARTIN: Yeah?
AUDIENCE: When the
homologous chromosomes split,
can you share alleles?
Are there alleles
preserved in this portion?
ADAM MARTIN: You're asking
if there's crossing over?
AUDIENCE: Yeah.
ADAM MARTIN: There
is crossing over.
Yes.
And that will get its
own entire lecture.
Yes, good question.
OK, so just to give you guys
a preview of what's up next.
So in the next
lecture, we're going
to talk about Mendel
and Mendel's peas.
And we'll talk about the
laws of inheritance, OK?
And realize Mendel
was way before DNA
or what our knowledge
of a gene was, OK?
Next, we'll talk about fruit
flies, and Thomas Hunt Morgan,
and seminal work that led to the
chromosome model of inheritance
and also resulted in
the concepts of linkage
and also genetic maps.
OK, we're going to go--
well, just to sort of anchor
yourself, the structure of DNA
was published in 1953.
So these seminal
genetic studies up here
were done before
we knew about DNA.
So geneticists were studying
genes and their behavior
well before we knew DNA
was what was responsible.
And then we'll talk about
sequencing and the sequencing
revolution.
We'll talk about cloning,
and molecular biology,
and how one might go
from a human disease
to a specific gene
that causes it.
And then, finally,
we'll start talking
about entire human genome
and genome sequences.
OK, so that's just a preview
of where we're going,
so have a great weekend.
