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Monster Mutants lurk in the midst of many cultures.
And we're fascinated, yet fearful of nature's mutants.
But mutants are closer to home that we think, often invisible, mutations are
happening all around us in every living thing.
They're crucial path of evolution.
Now research is uncovering how mutations actually work.
And it may help us find cures for life threatening diseases.
As we understand more about mutation, we may discover more secrets of the
history and future of life on this planet.
In 19th century America, people flock to dime museums to view the odd, the
elite and the unexplained.
We're recreation of a 19th century American Dime Museum.
And Dime Museums when they sprung up in this country were full of anything
the American public would pay 10 cents to see.
People have always been interested in the weird, the strange, the bizarre,
the exotic and the unusual.
For just 10 cents they came to see the worst that nature had on offer.
Some creatures were patently fake, products of an entrepreneur's
imagination, but others brought us face to face with real mutations.
It is friendly, but it is look at it.
Across the Atlantic and Great Britain was a celebrated sideshow freak,
Joseph Merrick, the famed elephant man.
A tragic mutation within his genes gave rise to a disease called Proteus
syndrome.
Large boney growths covered the right side of his entire body.
A mutation is a change in our genes.
Deep within every cell, our chromosomes hold the instructions for
life.
These are our genes and they held on long delicate strands of DNA.
They read like a recipe book.
But sometimes there's an unexpected change in part of the recipe, the
result is an altered or damaged gene that we call a mutation.
For Joseph Merrick, the mutation was so severe, he could never lead a
normal life.
He spent his adult years as a sideshow freak, until he was rescued and
offered shelter at the Royal London Hospital.
His short life ended at the age of 28.
Today such human tragedies are no longer a source of entertainment, but
many of us are still fascinated by creatures that are one in a million.
In West Fork, Arkansas, Fred Lally has spent 50 years collecting some most
unusual reptiles.
This is Zip and his better half pet.
With this member of Fred's menagerie, it's not clear if the left head knows
what the right is doing.
They are both equally perfect head, perfectly aware of everything, but one
of them is more of a mild disposition and the other one is a little grouch.
And every now and then they like me fill with it, it nips me.
Fred has been fascinated by reptilian oddities all his life and he now makes
a living, taking his mutant pets on tour to summer county fairs.
It's not the most lucrative business, but I do make a living at it and I'm a
free person.
But of all the animal anomalies he's encountered in his long career, one
stands head and shoulders above the rest.
Meet golden girls.
She's no ordinary snake and came with no ordinary price tag.
Fred paid $20,000 for one of the rarest reptiles in the world.
But this isn't a case where two heads are really better than one.
Sometimes when she crawls you will see one head want to one way and one's
another, that's very natural.
It shows that both heads--and I would say that they are near equal, but it
seems like the head on the right usually gets its way.
The main thing I watch for is that they don't breach an object.
Their heads are formed into the body, somewhat like a Y.
And it's easy for them to become impaled I guess you could say on a
twig or small shrub or something and they can injure themselves.
Golden girls wouldn't survive in the wild.
She depends on Fred's care and attention.
But what causes a two headed mutation?
At the University of Pennsylvania Dr. Margret Casal studies genetic diseases
in young animals.
What I can show you here is a one headed, two bodied conjoint pig twin.
You can see it has one head here clearly and it has--it has all arms
two on this side, two on the backside and it has all of its legs, its hind
legs you can see down here.
So it's actually a pig that has a complete separate spine from each
other, so it's twins but just one head, typical conjoint twins.
In nature conjoint twins are rear, but they nearly always make the slot at
the end of the evening news bulletin.
This is Rudy, the two headed pig.
He's got two noses, two mouths, three eyes and a personality.
Normally what you have is one egg gets fertilized by one single ***.
The cells didn't start to divide.
Sometimes you will get a split in those cells and two separate
individuals will form twins.
But sometimes that split doesn't quite make it, depending on where they are
joint is two heads or two bodies, four limbs, five limbs.
You get a variety of different malformations caused by this not quite
complete split.
In humans, if the embryo hasn't divided by the third week of pregnancy
than Siamese or conjoined twins may result.
They are among the rarest of human beings.
Only a few hundred pairs are born each year.
More than half are still born and may live for only a few days, but are
conjoint twins actually caused by mutation.
We think it's a combination of both genetics and environment but nobody
actually knows.
We geneticists tend to be a little more careful and say, we call it a
malformation at this point because we haven't been able to locate any genes
to this day that actually cause conjoint twins.
But whether conjoint twins are mutations or not, they are only the
tip of the mutation iceberg.
Mutations are happening everyday to all of us, but most of the time they
are invisible.
For me a mutation is something that occurs all the time.
It's a natural process.
Many times a mutation has no consequence.
There's a change in the DNA, but that DNA is not important for the
development of the embryo or the physiology of the organs.
When the cells in our body divide, they must replicate their DNA.
Sometimes that's when a copy error can take place.
But usually it's fixed up by our bodies own correction system.
So we have proofreading enzymes if you will, that actually zip along the DNA
and they go and find a mistake and they get rid of it.
They are quite efficient, they work in general.
I mean, we'd be long dead if we didn't have these.
Proofreading enzymes fix up small mutations on a daily basis.
But when they failed to do their job, that's when a mutation occurs.
A mutation can occur in any cell in the body, but if it occurs in a cell
that gives rise to an egg or *** and those egg or *** are used to make a
child, then that mutation is inherited and passed on to generations.
Thos mutations could be detrimental and could cause things like birth
defects or they could be beneficial and cause for instance stronger bones
or wider teeth or a change in your hair or eye color, or sometimes a
mutation just make me different from you.
The town's folk of Olney, Illinois know only too well about color
mutations.
Their parks are filled with some of the cutest mutants on the planet and
every evening they come out to play.
A population of albino squirrels has settled here and made the town their
home.
According to local folk law, the first pair of white squirrels appeared in
1902, when William Stroup found them in woods outside the city.
Stroup captured the pair and displayed them in the local saloon.
Later they were released into City Park where they started to breed.
In their heyday in the 1940s the population of albino squirrels reached
almost 800.
The town's folk of Olney have given the squirrels pride of place and they
have helped shake the very identity of the town.
Olney is not alone in treasuring its albinos.
Whenever one of these rare white creatures are discovered, its
strangeness captivate us.
Thought to be about 40 years old, the crocodile's creamy skin and pale
whitish eyes erratically different from the coloring of normal crocs.
And according to researchers the syndrome is extremely rare.
But at least they have named the rare creature.
From today, he will be simply Snowy.
And two headedness isn't golden girls only claim to fame.
Normal rat snakes are black with a black tongue and eyes.
Golden girls is also an albino.
A case of being doubly blessed or doubly cursed.
But whether it's an albino snake or an albino squirrel, the course of their
albinism is the same.
Within every cell in the body, our genes hold the DNA instructions for
how that body grows and functions.
Amongst the thousands of genes in every cell, there are those that
determine eye and hand color.
In grey squirrels these genes code for a pigment called melanin which gives
them grey fur and black eyes.
But a mutation in these genes means little or no melanin is produced.
So there's no color at all on the fur or the eyes.
The result is an albino animal.
Genes comes in pairs and every baby squirrel receives one from mom and one
from dad.
It's only when both parents pass on a mutated gene that the baby is an
albino.
The citizens have only pampered their squirrels.
But dogs, cats and other predators find the albinos easy pickings.
Their eye sight is poor and without any color for camouflage they stand
out.
So these special creatures are at risk.
To help more albinos survive, Olney has risen to the challenge.
Police officers here are perhaps the only ones in the world charged with
protecting albino animals.
White squirrels have the right away on city streets and it's an offense to
harm them in any way.
The latest squirrel senses shows that the population is now stable.
It's the same the world over.
Albino animals carry a slight disadvantage in the struggle for
survival.
This small mutation makes life just a little bit harder.
But sometimes a small mutation may be an advantage giving some animals the
edge over their competitors.
Mutations have allowed the whole animal plan, human world to actually
survive and make it in this world.
Without mutations we would probably die out when we encounter the first
virus for example we wouldn't be able to survive.
Seven hundred years ago, a genetic mutation enabled a small group of
human beings to survive a deadly disease.
In the middle of the 14th century the plague swept rapidly through Europe
killing 25 million people, that's a third of the population in just 4
years.
But a small group of people managed to survive the deadly virus.
There was a small subset of people less than 1% who did not get plague
and they would survive no matter how bad the plague outbreaks were.
About 300 years later, the number of these people had actually increased to
about 10%.
These people actually had a mutation that made them resistant to the plague
bacteria.
And later, so many years later of course these people increase because
they were often times the only survivors of the plague outbreaks.
The last great outbreak of plague occurred in the 17th century.
In 1665, the Black Death struck London taking 75,000 victims in its wake.
In September of that year George Viccars a tailor in the small village
of Eyam received a parcel of clothes from London.
It was returned with plague infected flees.
Four days later Viccars was dead.
After many villagers succumbed at an alarming rate, the rector of the
village made the momentous decision to quarantine the whole community.
It was a heroic and radical act and prevented disease spreading to the
surrounding district.
But a year later, when the first outsiders ventured into Eyam, they
were surprised to find that nearly half the town's folk had actually
survived.
Now descendents of these survivors are helping researchers battle a modern
day plague.
From previous work undertaken on *** Aids, researchers had isolated a gene
known as CCR5.
When this gene is active, it allows the *** virus to penetrate white blood
cells thus spreading the virus through the body.
But in people who have the mutation, the *** virus just can't get into the
white blood cells.
When researchers analyzed the blood samples from Eyam descendants, they
found an unusually high number of people carrying the mutated version of
the gene.
This mutation may be the reason so many town's folk survived in 1665 and
could hold a key to preventing AIDS.
But positive mutations aren't always a matter of life and death.
A remarkable mutation arose after human beings first domesticated the
cow.
Our ancestors were quick to discover that cow's milk was similar to human
milk and so was a good source of nutrition, but there was just one
hitch, only babies could digest it without problems.
Once people grew up, they found drinking milk gave them stomach cramps
and nausea.
They had lactose intolerance, which means they could no longer breakdown
the sugars in milk.
This was the norm for the majority of the population.
But a lucky few are able to carry on enjoying milk as they grew up.
They had a new advantage.
A helpful mutation which meant their lactose tolerance gene didn't switch
off after childhood.
Those with the new mutation thrived and may have been healthier than the
rest.
They certainly would have had stronger bones and teeth.
They may have made more attractive mates and may even have had more
children.
So in populations where dairy became established, the new mutation slowly
spread enabling most people to enjoy drinking milk throughout their lives.
And this new taste for cow's milk wasn't just confine to human beings.
Cats probably developed the ability to breakdown lactose along with humans as
we domesticated cattle and started using milk as a food source.
Cats that could breakdown lactose probably did lot better than the cats
that couldn't.
But this mutation was mainly helpful in northern European cultures where
dairy had became the norm.
But in cultures that didn't drink a lot of milk, the mutation simply
didn't take hold.
And even today the majority of Africans and Asians are still lactose
intolerant.
They carry the original version of the gene.
Ever since life began, mutations have enabled species to adapt to changing
conditions.
But mutations are actually random events and can occur for better or for
worst.
But there's another natural force that determines which mutations catch on
and which fall by the wayside.
Charles Darwin called it natural selection.
If there's a disadvantage to a mutation, then it would probably die
out.
But if there's positive advantage, then natural selection will ensure
that it eventually spreads through the community.
Working together mutation and natural selection are the engines of
evolution.
Paleontologist can trace millions of years of evolutionary changed packed
into just a few centimeters of rock.
If we consider the history of life which stretches back more than 500
million years and the history have changed and that change is governed by
mutation.
We do find that some lineages shifted fairly dramatically, perhaps in
response to say change in climate or change in food resources or maybe some
sort of change in the type of predator that was after it.
When environments begin to change, mutations offer random solutions.
And that contagious mutation might help the species survive the new
situation while another species maybe faced with extinction.
In fact extinctions really the bread and butter of, the history of life
strange to say.
And if we think about the groups that went extinct, our normal explanation
is that extinction meant inability to adapt.
That particular lineages of fossils just haven't been able to change
enough to keep pace with the changing earth.
And so those organisms weren't mutating enough, they weren't changing
enough.
While the fossil record gives us a condensed history of evolutionary
change.
We can see living examples of evolution in action on many of the
world's islands.
Island populations offer a unique glimpse of how mutation and natural
selection can work very quickly under the right conditions.
So when you think about a population of--sort of species that population
contains a large amount of variation.
Genetic variation which is mutation has produced over millennia.
But when you take two organisms and you put them on an island isolated
from the main population where they come from, they are only taking a
small part of the variation that they came from and that may lead to
differences in that population arising very, very rapidly and that's where
you tend to see evolution change, because when you have small
populations, natural selection acts much more strongly.
On his famed visit to the Galapagos Islands in 1835, Charles Darwin was
fascinated to find so many unique species found nowhere else on earth.
His hunch was that the ancestors of these unique animals has somehow
hitchhiked their way from the mainland.
And once on the islands that evolved in isolation, each adapting to the new
environments they encountered.
On the islands he counted 13 different species of finches.
Some lived in the trees, others lived on the ground.
Some ate insects and others ate plants and berries.
He concluded that one original founding species had overtime evolved
into 13.
Each one taking on new roles of the island environment.
It was the same everywhere he looked.
Even the tortoises had evolved so that you could tell which island they came
from just by looking at the shape of their shells.
Had Darwin ever visited the island of Sulawesi in Southeast Asia, he would
have found much the same story.
Here the island's early arrivals have evolved into a hundred unique species
that exists nowhere else.
This grey macaque monkey lives on the south coast.
And is probably closest to the original macaques that rafted here
nearly 2 million years ago.
Compare that to the black crested macaque that lives on the northern tip
of the island.
It's hard to believe that both have descended from common ancestors.
But it's the humble monitor lizard that provides the most remarkable
example of island evolution.
This hardy traveler has colonized many islands in Indonesia.
And depending on the situation has evolved into some strikingly different
forms.
On an island to the east of Sulawesi, the omnivorous monitor lizard has
evolved into the emerald tree monitor, a small and gentle leaf eater which
uses its tail to balance delicately in the canopy.
But on the island of Komodo where there were no large mammal predators,
the descendants of the monitor lizard have filled the gap in a most
impressive way.
They have evolved into the largest and most fierce lizard in the world, the
Komodo dragon.
Since life began on earth, mutation and natural selection had been the
twin driving forces behind evolution.
But now, a relative new comer on the scene, *** sapiens has begun
engineering evolution to suit himself.
By selecting mutations and breeding from them, we humans are changing the
world to the way we wanted.
Around 2000 BC, natives of north India took the wild Red Junglefowl, gallus
gallus into their farmyards.
And so the domestic chicken was born.
Ever since they have been selectively bred for their eggs, tasty flesh and
even fanciful decoration.
Eventually mutation pops up somewhere these happen randomly, this is a
normal occurrence.
So if somebody finds a individual that has the qualities that they are
looking for.
And then they pick that and breed it to one that's most similar.
So this is an old, old process that's been known for thousands of years.
You breed similar to similar and you will get similar.
Wild roses which grew on the planet some 50 million years before humans
have now being selectively bred over the centuries to produce the sensuous
array of blooms we enjoy today.
Koi carp had been glittering jewels in the ponds of their admirers for over
400 years.
Originally domesticated as a food source by peasant farmers at northern
Japan, they then became living works of art.
By virtue of the terrain that they lived in along these long winding
narrow ravines and gullies just dotted with thousands of ponds.
They were able to notice some of the mutations in their fish.
So they put them in different ponds and starting developing them.
The result of that was that instead of having one or two people that were
experimenting immutations, you had hundreds of geneticist so to speak
that were really evolving these fish.
We've even engineered evolution to produce man's best friend.
The dog was in fact our first domesticated animal.
Wait, wait. Go.
Whether big or small, bread for working or bread to be the family
pooch, that all descendant from one common ancestor, the wolf.
What happened was that certain people found that there were certain
subgroups of wolfs that seem to be more tame than others and these they
made then to their companions and then by selective breeding.
Breeding together what they thought was appropriate for their needs or
uses, that's how then the modern day dog most likely evolved.
Many believe that wolves adopted humans rather than the other way
around.
Perhaps wolves scavenge for scraps around early human campsites and
puppies were taking into cave dwellings to be tamed and kept as
pets.
Whatever the scenario, it's clear that the partnership between dogs and
humans was of mutual benefit.
Dogs are social animals and they enjoy the protection, shelter and easy
access to food that humans provided.
As pack animals they soon came to recognize the human as the alpha dog
or leader.
In turn humans found that the dog, a loyal protector and devoted companion.
Hunting became easier and life was safer with an animal that could guard
the campsite at night.
Perhaps different groups of people domesticated different breeds of dog.
And by the time of the Roman Empire, most of the breeds we know today were
already established.
Humans use the genetic variability of early dogs to breed for specific
characteristics.
Intelligent and confident dogs were bred together to produce sheep dogs.
Today the heading dog can hunt in a pack the way its ancestors did.
It instinctively rounds up its prey animal,
Its uncanny ability to steer down the sheep is like its wolf ancestor.
But generations of selective breeding means these dogs will only hunt, they
won't kill.
But some breeds have strayed far from their original purpose and clearly
would not survive without us.
Brenda Heinsohn owns a most unusual dog.
When Brenda's daughter was born allergic to dog hair, she searched for
dog that wouldn't trigger reactions, they discovered the Xolo or Mexican
hairless dog.
No one knows when this hairless mutation first occurred.
But it's not the breed originated in the warm climate of northern Africa,
but extreme artificial selection has its downsides.
Associated with the hairless gene is a lack of the premolar teeth.
And you also will see either very stunted or a total absence of the
canine teeth.
And it doesn't pose any problem for them because they eat just as well.
I mean, it's--they don't have a problem with food.
Hairlessness maybe a bonus for Brenda and her family but for Xolo the lack
of protective fur isn't.
Too much sun and he will get sunburn.
If you leave him to expose to the sun too long just like with the person,
they can be prone to skin cancer.
You have to be very careful with that.
Like hairless dogs, we humans are also prone to sunburn which can lead to
skin cancer, another type of cell mutation.
Probably one of the most well known is UV radiation from the sunlight.
Everybody knows you expose yourself too much to the sunlight, you may get
cancer.
Because it will change the DNA, the genetic makeup of the skin cells.
So each cell has a little blueprint.
So if you change that, you get uncontrolled growth which is basically
cancer.
Ultraviolet radiation can have devastating effects on our DNA,
causing replicating cells to lose the ability to switch off.
Cells grow randomly and cancerous tumors can develop.
Radiation from sunlight is a mutagen.
An outside force that can cause a mutation in our DNA.
But we're also affected by chemical mutagens and they pop up in some
surprising places.
The humble barbeque can create a deadly weapon against the human body.
Fat drippings from meat can burn.
In the resulting smoke a chemicals called PAHs.
It's all just part of that barbecue flavor, but once eaten PAHs can pass
into your cells and damage your DNA.
Different mutagens cause their damage in different ways.
They can scramble your DNA completely.
They can take large chunks of your DNA out, invert them or put them on the
other strand or you can have just huge deletions meaning that whole sections
of DNA will be missing completely, just zap gone.
The whole world witnessed the affects of the most powerful mutagen during
the Second World War.
When America unleashed the terrifying specter of atomic warfare.
In August 1945, they detonated two atomic bombs, the first on the city of
Hiroshima, the second on Nagasaki.
The bombs caused widespread devastation and left a lethal legacy
of radiation.
After the atomic bomb it was noticed that there were many defects that were
inherited in the offspring of the survivors.
And so a lot of research started in trying to determine how radiation
affected DNA and how strongly it affected DNA.
When Watson and Crick discovered the structure of DNA in 1953, the science
of genetics was coming of age.
We now knew that all genes were made up of the series of three laser codes.
And that even one tiny error in the code could cause a mutation.
But the genesis of genetic research began much earlier in the century.
One of its unsung heroes is the humble fruit fly.
Fruit flies have been critical to genetic research for almost a hundred
years now.
And the real reasons behind it is that fruit flies are excellent model
organisms.
They're really easy to grow in the laboratory.
They don't have many diseases.
They're very robust, so it's quite difficult to make fruit fly sick.
So we can produce mutations in fruit flies and the fruit flies will still
survive
Another good reason for using fruit flies is that they only have four
chromosomes which makes analyzing their genetics very, very easy.
Early in the 20th century, Thomas Morgan bred fruit flies to track how
certain characteristics could be passed on from generation to
generation.
Long before the discovery of the structure of DNA, his research on
fruit flies proved that our genes are contained in chromosomes within every
living cell.
Later, people added to this original knowledge so that in genetic research,
the fruit fly became the most studied living creature of all time.
The one of the fantastic things about fruit flies is that they're very, very
cheap to work with.
And that meant that they were tended to be given to students.
So those are young community researchers.
And they had a philosophy that everything should be shared amongst
them.
So if one person produced a mutant line of flies, that line of flies had
to be available to the rest of the community.
And that meant that fruit fly research really rocketed because everyone was
sharing information, they're sharing ideas.
More recently, the scientists had discovered a group of genes which
determined body shape and body pattern.
If you alter these genes in fruit flies, you get some very interesting
mutation such as stumpy wings, curly wings and even legs coming out of
their head in place of antenna.
But does any of this research relate to human beings?
We find the same genes which are doing similar jobs in fruit flies and doing
the same jobs in humans.
What that means is that fruit fly research is incredibly useful because
it enables us in a simple system to understand how genes work.
Once we have that information from a simple organism, we can try and use
that to understand what's happening in more complex organisms like humans.
Using fruit flies, scientists have just found that so called chaperone
protein maybe able hide or paper over small mutations in the gene code.
It's a discovery that has major implications.
Over the generations, a family of flies can accumulate many mutations
that are hidden harmlessly away.
When this protein is working, these mutations never see the light of day.
But if it stops doing its job, then mutations that were invisible suddenly
appear.
And you find that, that the fruit fly strain that you've been looking at
actually has a mutation you never knew about.
This is incredibly important for evolution in your research.
Because it means that organisms can build up inside their own genes, a
degree of variation which is never seen in the environment.
But under stressful circumstances change in the environment, change in
temperature, those mutations can pop out here in the environment and
perhaps be selected by natural selection.
If the study of genetics was a major motion picture, then the fruit fly
would take the leading role.
But to learn more about human genetics, scientists have turned to
animals that are a little closer to us on the evolutionary tree.
Mice, a fast becoming the new superheroes of genetic research.
At Baylor College of Medicine in Houston, Texas, geneticist, Monica
Justice is researching mutation in mice.
Monica's work involves studying genetic diseases in mouse's
populations with the goal of applying that knowledge to the same diseases in
humans.
Monica and her team use a powerful chemical mutagen to cause mutations in
her mouse population which mimics similar conditions in humans.
They introduce this chemical mutagen directly into mouse *** cells.
From the offspring she identifies mutant mice that show signs of a
health defect.
She then breeds these mutants to create whole families of mice with the
same condition.
Right now I have approximately 30,000 mice.
And these mice all have different mutations.
So some of the mutations cause birth defects, some of them cause changes in
their skin or coat.
The mice have almost the same profile of genetic diseases as you would find
in the human population.
Whole families of mutant mice are then treated for their various conditions.
And that's one of the advantages of mice over humans.
They usually--if we have a disease in humans, we may choose not to have more
children or something.
We can produce lines of mice that produce this disease.
And then we can determine how that disease might be treated.
Research in this area has highlighted new knowledge about genetic diseases.
If you take a disease such as osteoporosis, you might predict that
this certain gene causes osteoporosis and in fact it might.
But what we're learning is that this gene can cause osteoporosis if
mutated.
But so can another gene on this chromosome and a different gene on
this chromosome and yet another gene.
So we're find that mutations in many different genes could contribute to a
single disease.
Across the street at the MD Anderson Cancer Centre, researchers are
creating mouse mutations in different ways.
They are targeting individual genes and altering them with pinpoint
accuracy.
It's a fiddly business but it's actually possible to insert new genes
into a mouse by microinjecting foreign DNA directly into a fertilized mouse
egg.
So you have a very, very fine needle.
And that pierces the egg and goes into the nucleus and a solution of DNA is
pumped in.
Then you can transfer them back into a surrogate mother and she will give
birth to babies.
And some of those babies will have incorporated this DNA into their
genomes.
Then we can breed these mice and see in the progeny of these animals that
carry this DNA.
What is the impact of this gene on the animal?
It's incredible that within only 50 years of discovering the structure of
DNA, we now have the tools to cut and paste it so precisely.
Richard's latest research is on human ovarian cancer.
This is a very serious cancer for woman.
It's usually detected very late.
And because it's detected very late, the treatment options are not great.
So we decided to use our technologies to model this disease in mice.
The team is targeting a mutant gene that's strongly associated with
ovarian cancer.
They've even constructed this mutant gene in the lab.
The next step is to insert the mutant gene into developing mouse embryos.
The mutant gene replaces the normal one slotting itself into the exact
same position in the mouse gene.
The results are preliminary, but they think that normally this gene
regulates cell division.
And so the mutant diversion may cause cells to divide abnormally.
So this is interesting to us because cancer is really abnormal cell
proliferation.
Further tests suggest that this mutant gene may also play a part in others
forms of cancer.
So these are very basic steps, very basic findings.
We're hoping by pursuing this gene and creating other models in mice of
ovarian cancer that we can contribute to the therapies that might be used
for this very serious cancer.
Molecular biology works on such a minute scale, that it's difficult to
keep track of which mice are carrying which mutations.
After all, these genetic changes are taking place on the scale that's
invisible to the human eye.
So researchers have come up with a clever method of keeping track of all
their mice mutants.
They add a florescent jellyfish gene alongside the gene of medical
interest.
Now the mice that have an active mutant gene are easy to find because
they glow under blue light.
In nature, mutations are slow and random.
In the lab, researchers are stepping in to make them fast and surgically
precise.
It's really remarkable the pace that mouse genetic technology is moving.
At this point in time we can almost do anything we want to the genome of the
mouse.
We can add genes, we can take away genes.
We can clone mice, we can freeze embryos and store them for decades.
I think in 50 years we'll look back on mouse genetics and say that they--that
the mouse was one of the most powerful genetic organisms.
So they will join the ranks of bacteria, yeast, worms, flies in
showing us how we develop, how disease develops, what types of mutations can
cause diseases.
And even better how we can treat them.
Of all nature's forces, it's mutation that's been the most misunderstood.
While freakish mutations grab the headlines.
Few of us realize that mutation is a natural part of the ongoing cycle of
life.
In the evolutionary big picture, it provides the variation species need to
adapt to an ever changing world.
Under the microscope, understanding how it really works may hold the key
to conquering life threatening diseases.
Mutation is change.
Some changes are for better, some for worse.
But change will always be with us so long as there is life on earth.