DNA and RNA – Part 1


Hi. It’s Mr. Andersen and welcome
to biology essentials video number 27. This is on DNA and RNA. I want to start with a
picture of a peanut plant. Right here we have the same peanut plant in both of these. On
the left side it’s being decimated by the larvae from a corn stalk bore. The one on
the right however you can see the bore sitting right here but it’s not eating the peanut.
And the reason why is this one over here has been engineered. They’ve actually added a
gene from a bacteria called bacillus thuringiensis. And it produces a toxin that the larvae doesn’t
like. So it takes a couple of bites. Quits eating it. So there are two things that I
wanted to show you with this picture. Number one is this idea that no matter what you are,
a virus, a bacteria, eukaryote, like a plant or an animal, you have the same genetic material.
And that’s called DNA. The other thing that’s interesting is that humans can tamper with
this. We can actually transfer DNA from one organism to another. We can transform that
organism. And that whole field is called genetic engineering and it’s exploding right now.
So in this podcast I’m going to try to accomplish five things. First of all we’re going to talk
about the history of DNA. How these three experiments, the Avery-MacLeod-McCarty, the
Hershey-Chase and finally the Watson-Crick-Wilkins and Franklin experiments showed us what DNA
looks like. Where it is and how it works. Next I’ll talk about how DNA is organized
in chromosomes. Both prokaryotic and eukaryotic. We’ll talk about the structure of DNA and
RNA. Mostly how they’re different. And then how DNA makes copies of itself. We’ll then
discuss the Central Dogma. How DNA is transferred through transcription into RNA. Which is then
translated into proteins which then makes you. And then finally we’re going to talk
about this brave frontier of genetic engineering. And how we can do things like transform bacteria
to make important things. Especially for diabetics, like human insulin. And so that’s a lot to
do. So we better get started. Let’s start way back in history with the Frederick Griffith
experiment. This was in 1928. He was a medical doctor. And so what he was looking at was
bacteria. And they would do serological testing. So they’re trying to figure out what bacteria
causes disease and they were using a mouse as a lab experiment. So right here they’re
using streptococcus pneumoniae, they’re taking one type of that. It’s called rough, because
when you grow it in plates it has a rough appearance. They would inject that into the
mouse and the mouse would be happy. They’d then inject a different type of that streptococcus,
a virulent type. This one is smooth. They’d inject it into the mouse and then it would
die. And so he hasn’t learned anything at this point. He then took this evil smooth
strain of streptococcus. He heat killed it. So he heated it up. And he found when he injected
that heated into the mouse, the mouse was good to go. So we haven’t learned anything
yet. What he then found, and this would be that discrepant event, is that when he took
the rough strain, which normally doesn’t hurt the mouse at all, he then mixed it with the
heat killed smooth strain which normally doesn’t hurt the mouse at all. The mouse died. And
so what did he learn from that? Well he learned a lot. And the big thing he learned is that
there was a transforming factor. Something was being transferred from these dead smooth
strain to these live rough strain. It was transforming them into a virulent type of
a bacteria. He didn’t know what it was, but we took the next 30 years to figure out that
is was DNA. And we figured out the structure of that. So the first step came through the
Avery-McCarty-MacLeod experiments. And this is in the 30s and 40s. And what they did is
looked at Fredrick Griffith’s experiment and they tried to figure out what was this transforming
factor? What was being transferred from these heat killed smooth strain over to these rough
strain? And so they broke down the bacteria. They then isolated the major molecules inside
that. And so what they had was RNA. They also had proteins. And then the last thing that
they found was DNA. And we knew what DNA was. We’d known it for you know 50 years before
then. And so what they then used was enzymes that broke down each of these. And then they’d
see if you could transform the bacteria again. So they add a ribonuclease and broke down
the RNA and it still was able to transform. They added a couple enzymes, trypsin and chimotrypsin
that break down proteins. It was still able to transform. And then they added a deoxyribonuclease
which breaks down DNA and then they couldn’t transform. And so what did Avery-McCarty-MacLeod
figure out? DNA was this transforming factor. Now most of their work was largely ignored
and the reason why is most scientists thought DNA was not complex enough to be the stuff
of life. It only has four different letters and we’ll talk about that in just a second.
And so that couldn’t be the stuff of life. And so a lot of their work was actually ignored.
But in retrospect we look back and they show that they were the ones who figured out it
was DNA. Where was the definitive answer? Well most of the argument came form is it
DNA? Or is it proteins that are actually being transferred? And proteins are very complex.
And so most of the people were thinking that it’s proteins that was the genetic material.
Not DNA. And so the Hershey-Chase experiment, sometimes called the blender experiment, used
bacteriophages. And a bacteriophage is simply a virus that infects a bacteria. It looks
kind of like lunar lander. It lands on the bacteria. It injects its hereditary material
in. And then it hijacks that bacteria to make more of the bacteriophage. And so what Hershey
and Chase did, it’s a really elegant experiment, is they used two different atoms. They used
in one experiment sulfur. And in this case the sulfur is labelled red. They used a red
dye to dye the bacteriophages in this experiment. They then infect the bacteria, blend it all
up. They precipitate it out and see what color came out. Now why was it important they use
sulfur? It’s because sulfur is found in proteins but it’s not found in DNA. They then used
a different dye to dye phosphorus. Phosphorus is found in DNA but it’s not found in proteins.
And so what they were able to show is that the only one that was doing the transforming
was this green dye. That means that it was the phosphorus. And that means that it wasn’t
proteins that were transferring the information. That it was DNA. And so the Hershey-Chase
experiment was definitive proof that DNA was the hereditary material. And so this is in
the 50s. And now the race is on to figure out, not only, mostly to figure out what’s
the structure of DNA. How’s it all work. These are interesting people. Apparently Hershey
and Chase, they worked together. Their lab was totally silent and they just worked very
effectively together. Sadly Martha Chase goes crazy later in life. But a really cool experiment.
Now we go to the ones that you’re probably familiar with. The names that you’re familiar
with. And that’s probably Watson and Crick. James Watson and Francis Crick are mostly
given credit for discovering the structure of DNA. But there were three other, probably
even more people that played in this discovery of this structure of DNA. One of those is
Maurice Wilkins. Maurice Wilkins was really good at x-ray crystallography. So that is
taking pictures of crystalized material. It’s kind of like shining light through a chandelier
and then figuring out what the structure of the chandelier is. He was working with Rosalind
Franklin. They didn’t get along that well. And Maurice Wilkins is an interesting guy.
Died just a few years ago. They didn’t work well together but they had the best data out
there. This is a picture of some of the, this would be the x-ray crystallography of DNA.
So they were looking at DNA and trying to figure out its structure. If you know anything
about crystallography you’d know that this is a helix. Or it suggests the structure of
a helix. Actually James Watson sat in on one of Rosalind Franklin’s secret meetings and
took notes on it. And it actually helped them to figure the structure a lot. Next we’ve
got Erwin Chargaff. Erwin Chargaff was looking at different organisms and studying the amount
of As, Ts, Cs and Gs. And so A, G, C and T are the four different bases that are found
in DNA. And he found something unique. If you look at for example an octopus, the amount
of A, 33.2 and the amount of T is exactly the same, about the same. And if you look
at the amount of G, 17.6 and 17.1, that’s about the same as well. In other words the amount of
A and the amount of T is always the same. And the amount of G and the amount of C is
always the same. We sometimes call this Chargaff’s Rule. So as you look all the way down here,
like in humans, we have 29.3% A and 30% T. Likewise we have 20% G and C. And so he didn’t
know what that meant, but Crick and Watson knew that. They knew the structure of a helix
coming from the work the Franklin and Wilkins. And so they used models to figure out the
structure of DNA. Why do we always have the A and the T equal? And the G and C equal?
Well if you look at the structure of DNA, you have a backbone. This is actually a model
of, this is the model that Watson and Crick were working on. So you’ve got a backbone
that looks like this. But then on the inside you have your bases. And if you have an A
on this side, a T will be on the other side. And if you have a C on this side a G will
be on the other side. And so the amount of As and the amount of Ts are always equal because
they bond to each other. And so this that double helix. So Watson and Crick are given
the credit for that. They actually share the Noble prize with Maurice Wilkins. Rosalind
Franklin doesn’t get the Nobel Prize because sadly she had died before then of cancer.
And it was probably as a result of the x-rays that she was using in her lab. And you can’t
get a Nobel prize if you die. Okay. So let’s now go to the structure. Structure of DNA.
DNA doesn’t just sit loose inside the nucleus. It’s organized into something called a chromosome.
And so in us, in eukaryotic cells, we have this characteristic shape of a chromosome.
If you actually look at how the DNA is organized, the DNA is wrapped around these proteins called
histone proteins. And those are swirled around other proteins and other proteins and eventually
you get to the structure of the chromosome that looks like this. Now the reason it characteristically
looks like an X is that when we take a picture of our chromosomes, this would be a picture
of our chromosomes, they’re usually in metaphase. And so they usually have this characteristic
X structure. What does that mean? That means that the left side is a mirror copy of the
right side. And so in a lot of my diagrams, you’ll see me drawing it, a chromosome just
looking like this. With a centromere in the middle. And that’s because that’s what a chromes
usually looks like. It’s a linear stretch. And so in eukaryotic cells we have this long
stretch of DNA wrapped around proteins and that’s where the genetic material is found.
And it’s really really really long compared to the size of the actual cell itself. If
we look at prokaryotic chromosomes it’s different. In a prokaryotic chromosome, the chromosome
is simply loose here. It’s not in a nucleus at all. And it’s also a loop. And so in us,
we have a linear chromosome. In other words it’s a length with a definite end of either
side. But in prokaryotics they’ve got just a loop. Now the loop is wrapped around itself
so it can fit in what’s called the nucleoid region of the bacteria. But it’s a loop none
the less. They also have extra little tiny loops called plasmids. And those have DNA
in them as well. And they carry genetic information. And these can actually be swapped between
bacteria. So it’s like an extra set of genes. Another important difference between us and
bacteria is that a lot of our chromosomes is what’s called junk DNA. In other words
it’s DNA that’s not actual genes. It’s between genes. And if you look at the DNA of a prokaryotic
cell, each of those little stretches is going to be one gene after gene after gene after
gene. Now we’re starting to figure out that it’s not really junk DNA. That it actually
has an important function. We’ll talk about that in a different podcast.

100 Comments

Add a Comment

Your email address will not be published. Required fields are marked *