QUEST Community Science Blog Author: Dr. Barry Starr

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Chromosome Fusion: Chance or Design?

May 12th, 2008 by Dr. Barry Starr

Human and chimpanzee chromosomes are very similar.
Note that human chromosome 2 is very similar to a
fusion of two chimpanzee chromosomes.

For the last few weeks I have been corresponding with someone about intelligent design (ID). More specifically, we have been chatting about why humans have 46 chromosomes and most of the great apes have 48.

To me, this is great evidence for evolution. Why? Because if you look at the chromosomes closely, you can see that human chromosome 2 is really just a fusion of two great ape chromosomes.

The idea is that a few million years ago, a common human-chimpanzee ancestor of ours had two of his or her chromosomes fused together. This sort of thing happens all the time even today. Around 1 in 1000 live births has one of these kinds of fusions.

Then, probably through chance,this ancestor with the fused chromosomes went on to found the human race. Now people have 46 chromosomes and chimpanzees have 48.

An alternative explanation is that the designers fused the two chromosomes together when they created humans. The idea would be that the designer wouldn’t create every plant, animal, bacteria, and virus from scratch–why reinvent the wheel every time? Instead the designers would mix and match parts that worked.

So as part of the process of designing a human, the designer fused two ape chromosomes together. This would presumably be simpler than creating a human chromosome 2 the way the other chromosomes were made.

The difficulty with this idea is that there is no obvious advantage to having 46 chromosomes instead of 48. What matters is our DNA, not how it happens to be packaged.

It is possible that there was some advantage to fusing the chromosomes together. For example, maybe a new gene was created at the fusion point. Or maybe genes that were shut off before were now turned on in the new fused chromosomes.

There isn’t any evidence of these kinds of things. And even if there were, a designer who can easily put in the 60 million or so differences between humans and chimpanzees should be able to accomplish whatever results a chromosome fusion gives more elegantly than sticking two ape chromosomes together.

Also, when you look at the fusion point, you can see that the DNA isn’t exactly what you would expect if a fusion happened in the last 10,000 or even 100,000 years. The results look more like an event that happened millions of years ago.

The ends of a chromosome have a defined sequence of DNA repeats called a telomere. The DNA at the fusion point looks very similar to a string of telomeres (as we would expect from a fusion) but it isn’t perfect. This is just what you would expect if the fusion happened millions of years ago. Because our DNA gets changed a little all of the time.

The environment or even our own cells can cause the wrong letter to end up in our DNA. Our cells are pretty good at fixing these mistakes but they don’t catch them all. What this means is that our DNA builds up mutations over time.

When an unfixed change happens in a sperm or egg, then it is passed down to the next generation. If the changes that aren’t fixed happen somewhere important, then they are selected for or against. But if they’re neutral, then they just build up over time. Scientists can even use these sorts of errors to predict how long ago something happened. Or to trace human migration patterns.

These DNA changes at the fusion point do not fit with ID if they don’t serve a purpose. Otherwise, why put them there? It will be interesting to see the results of experiments that might show if these sequences matter or not.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.





Tags: chimpanzee, chromosomes, dna, genetics, intelligent design, KQED, mutations, Science



37.332, -121.903




Posted in Biology, KQED, Partners | Please Comment

Fish and SNPs: What fish are teaching us about human skin color

April 28th, 2008 by Dr. Barry Starr

These fish can tell us a lot about ourselves.

Species often end up a different color when their environment changes. And humans are no exception.

When people moved out of Africa tens of thousands of years ago, they were dark-skinned. Now when we look around Northern Europe or parts of Asia, we see much lighter people. What happened?

A common explanation has to do with sunlight and vitamin D. When people moved north, they got less sun. Less sun means less vitamin D and awful diseases like rickets.

Anyone who moved north and had lighter skin ended up getting more vitamin D and did better than their darker neighbors. After awhile, most of the population had light skin.

This is all well and good, but what happened at the gene level to cause this transformation? One way scientists are learning about how humans ended up with lighter skin is by studying fish. For example, the zebrafish has taught us a lot about why Europeans are often so pale.

The zebrafish is an important model system that scientists use to study vertebrate development, human disease, and lots of other things. A common mutant fish that scientists use in these studies is called “golden.” These fish have lighter, yellowish stripes instead of black ones.

Scientists discovered that these mutant fish had yellow stripes because of a single DNA difference (or SNP*) in their SLC24A5 gene. When fish have this DNA difference, they have yellow stripes.

These scientists next looked for this gene in people. What they found was that most of the people they looked at had two copies of the “black stripe” version of the gene. Except for Europeans. They tended to share a common SNP in their SLC24A5 gene that the scientists went on to show is a big part of why many Europeans have lighter skin.

Another group of researchers decided to dig a bit deeper and find out when this transformation happened. By looking at the DNA around SLC24A5, they found that lighter skin came to dominate Europe around 6,000-12,000 years ago. At first this result is a bit confusing because humans moved into Europe around 40,000 years ago. Why did it take so long for lighter skin to become the norm?

Scientists can’t know for sure but one idea is diet. Around this time, Europeans started to grow their own food. And a farmer’s diet has less vitamin D than does a hunter-gatherer’s diet. Maybe the lack of sun only started to affect Europeans after they started growing their own food. Then, after a relatively brief time, most Europeans ended up fair-skinned to get enough vitamin D.

This gene doesn’t explain all of skin color. For example, it doesn’t explain the difference in color between Northern and Southern Europeans. Or why some Asians have fair skin. But it does explain a good deal of European coloration. Thanks, zebrafish!

*SNP=single nucleotide polymorphism

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.



Tags: dna, evolution, genetics, KQED, model systems, single nucleotide polymorphismm vitamin D, skin color, SNP, zebrafish



37.332, -121.903




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Hug-a-helix: celebrate DNA Day, April 25th

April 14th, 2008 by Dr. Barry Starr

DNA magnified 850,000 times through a scanning electron
microscope
DNA day is coming up on Friday April 25th. This annual celebration of genetics and genomics was set up in 2003 to commemorate the sequencing of the human genome and the 50th anniversary of the solving of the structure of DNA.DNA day was thought of as an opportunity for teachers, students, and the general public to learn about DNA. And to have fun with it.

This should be a chance to pull DNA out of beef, strawberries, kumquats or even yourself and learn that you have around 100 billion miles* of DNA inside of you. In case you’re interested, that’ll reach from the Earth to Pluto and back when Pluto is farthest from Earth. And that is one person’s DNA.

Add up everyone’s DNA in the world and you get 125 million light years of DNA. (At least I think you do… these numbers are getting ridiculous!) That’ll get us to the galaxy Andromeda and back 25 times. Add up all the DNA on Earth and… OK, that’s probably enough of that.

There isn’t just a lot of the stuff but it is amazing to me how similar all human DNA is. The latest estimates are that people are around 99.5% the same at the DNA level. That means that all those light years of DNA are mostly the same old thing just copied over and over.

Notice the mostly. With 6 billion letters of code in every person, a 0.5% difference means 30 million differences between you and me. It is these differences that make me look different than you. And to a varying degree, make me act differently than you.

This code doesn’t work in a vacuum either. The environment can change how it works which is a big reason identical twins aren’t really identical. And one of the reasons why it is so hard to figure out the genetics of complicated diseases like diabetes or heart disease.

Our DNA also changes with time. Things in the environment might damage it. Or our own cells can make mistakes when they make copies of themselves. What this means is that today’s light years of human DNA will be different than the same stretched out DNA in 100 years.

This also means that you have some cells in your body have different DNA than the rest of your cells. And if a DNA change happens in sperm or egg cells, then they are passed on to the next generation. Which is where all the wonderful diversity around us originally came from.

As you can see, there is a lot about DNA to celebrate. It is huge and mysterious and we’re just starting to get a good grasp on what it is all about.

I plan to spend the morning of DNA day at The Tech Museum in San Jose exciting kids (and hopefully some adults) about DNA by running five different hands on genetics programs all at once. It’ll be a blast!

I have searched high and low for a list of DNA day activities here in the bay area but I haven’t come across any. Does anyone know about other DNA day celebrations here in the bay area?

* Each cell has 6 feet of DNA and we are made up of around 50-100 trillion cells.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.




Tags: dna, genetics, holiday, KQED, pbs, QUEST, techmuseum, twins



37.332, -121.903




Posted in Biology, Health, Partners | 1 Comment

Redheads are here to stay

March 31st, 2008 by Dr. Barry Starr

Red hair genes will be diluted but will not go away.I got a call last week from a reporter in Virginia. Someone had come up to her in a bookstore to offer her condolences about her kind dying out. She is a redhead.

The guy from the bookstore must have read one of the stories about the imminent demise of redheads that flashes across the media landscape every few months. People with red hair have to deal with headlines like:

“Redheads Set for Extinction.”
‘Will rare redheads be extinct by 2100?’
“Gingers Extinct in 100 Years.”

The reporter suspected these stories weren’t right and wanted to write a story about it. She called me to get some science to back her up. I was able to reassure her that redheads weren’t going the way of the dodo. They’ll become much less common, but there will probably always be red haired people around.

To understand why redheads will fade but not disappear, we need to dig a bit deeper into how red hair works. Red hair happens when both copies of the MC1R gene do not work properly. (Remember we have two copies of almost all of our genes–one from mom and one from dad.)

So if you’re a redhead, you inherited a nonworking copy of MC1R from both your mom and your dad. If you get a non-working copy from only one of them, then you won’t have red hair. You’ll be a carrier.

Right now redheads are at an artificially high level in the human population because their recessive red hair genes are concentrated in North America, Europe, and Australia. For example, 10% of Ireland and 2-6% of the U.S. has red hair.

These numbers are maintained because carriers and redheads keep making new redheads with each other. But as barriers go down, their red hair genes will flow out of these populations and into the human gene pool.

Red hair genes will become diluted in this pool but they won’t be completely swamped out. Even as redheads decline in numbers, their genes will remain constant. It will just be less likely that two carriers and/or redheads will meet and have babies with red hair.

This is all interesting but it got me to wondering about how many redheads there will be in the distant future when all the mixing is said and done. We can use something called the Hardy Weinberg equation to figure this out.

This equation works great for simple dominant/recessive traits like red hair if we know how many of each gene version there is. To do this, we need to figure out how many redheads and how many carriers there are in the world.

It is easy to figure out how many redheads there are–you can tell who they are just by looking at them. But figuring out carriers is a lot harder. We can make guesses based on the number of redheads (again using Hardy Weinberg) but until we sequence a lot more MC1R genes, they’ll only be guesses.

The numbers I have seen floating around are that around 1% of the world’s population has red hair and that around 4% carry the red hair version of MC1R. This means that there are around 65 million or so redheads in the world and 260 million carriers. (This sounds high to me but these are the numbers out there.)

When we use these numbers and apply the Hardy Weinberg equation, we end up with a final percentage of redheads of 0.1% or 6.5 million. This is quite a fall from current levels but they are hardly wiped out!

There are lots of assumptions* in these calculations that might cause the number of redheads to actually be more or less than 0.1%. But unless there is some red hair specific catastrophe or people start burning them as witches again, redheads are here to stay.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.

*Some assumptions used:

1) There are no barriers to finding partners
2) The 4% carrier number is an accurate one
3) Two non-workingMC1R genes produce red hair in all genetic backgrounds
4) Other assumptions described here


Tags: gene, genetics, hardy weinberg equation, KQED, kqedquest, mc1r, pbs, red hair, redhead, Science, techmuseum



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Explosive hypothesis about humans’ lack of genetic diversity

March 17th, 2008 by Dr. Barry Starr

Genetically, we’re all pretty much the same. A massive volcanic eruption 75,000 years ago may be why.

Lake Toba is all that is left of the volcano
that nearly wiped out mankind.Last blog I talked about how East Africans are genetically more diverse than Asians. Who are genetically more diverse than Native Americans.

From all of this you might have concluded that people are pretty different from each other. They aren’t.

People are surprisingly similar at a genetic level. For example, any two people from anywhere on Earth are more similar than two chimps from the same troop. Why are we all so alike?

One possible explanation is that something in our collective past nearly wiped us all out. And we all come from the few survivors who were left.

A likely candidate for this near annihilation event is the Toba volcanic eruption that happened in Indonesia 75,000 or so years ago. This eruption was huge.

It was equivalent to around 1 billion tons of dynamite and was about 3000 times more powerful than the Mount Saint Helens eruption in 1980. It also may have reduced the average global temperature by 5 degrees Celsius, darkened the world for 5 or 6 years, and plunged the world into a new Ice Age.

As you might imagine, this eruption had dramatic effects on species around the world including our own. Estimates of how many people were left range from around 1000-10,000 breeding pairs. The theory is that we are all so alike because we share these survivors’ DNA.

Whether true or not, a bottleneck in our past would not make us unique. Lots of species go through these near death experiences.

Scientists think cheetahs went through one around 10,000 years ago. Cheetahs are all so similar genetically that veterinarians can do skin grafts with “unrelated” cheetahs.

And of course, people have created bottlenecks in species too. For example, in the late 1890’s there may have only been 20-100 elephant seals left in the world because of hunting. Now there are at least 150,000 spread across the west coast.

Species are in danger long after they go through a bottleneck. They have a pretty limited gene pool which means they may not be particularly healthy and are in danger of being wiped out by, for example, a single disease. Humans are probably OK in this regard (consider natural resistance to HIV for example) but elephant seals, bison, and cheetahs, and many other species may not be.

Fortunately for us we successfully came through our bottleneck. Hopefully, the animals that we’ve nearly wiped out will too.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.




Tags: bottleneck, eruption, evolution, genetics, KQED, kqedquest, QUEST, techmuseum, toba, volcano



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Posted in Environment, Geology, Partners, Weather | 1 Comment

Tracing the Travels of the Human Race

March 3rd, 2008 by Dr. Barry Starr

We are all Africans in our DNA.

We all originally came from Africa. At least that is what a couple of new studies have claimed.

Now this isn’t breaking news. Other studies have looked at people’s DNA and proposed the “Out of Africa” hypothesis. What is different with these studies is how many people they looked at. And how much of their DNA.

One study looked at over 500,000 DNA differences in 438 people from 29 different populations. The other looked at over 600,000 differences in 938 people from 51 different populations. This dwarfs any other previous study.

All of this data showed that East Africans had the most diverse DNA. And that the further away a population got from East Africa, the less diverse their DNA was. So how does this show that we are all Africans at heart (or at least in our DNA)?

It has to do with the fact that DNA changes over time. Everyone’s DNA is a little different from when they were a fertilized egg because of DNA mutations.

If a change happens in the DNA of an egg or sperm cell, then it will be passed to the next generation. So the group that stays longer in one place will build up more of these changes. Their DNA will be more genetically diverse.

Imagine it is 50,000 years ago and our ancestors are all in Africa. These folks have been there for hundreds of thousands or even millions of years. Over this time, there were lots of individuals all mixing their DNA. And their DNA was changing slightly generation to generation.

Now imagine that a few people develop a bit of wanderlust. They’re tired of Africa and want to see what the Arabian Peninsula looks like. So a small group takes off and heads over there. And doesn’t return.



This group, which will go on to found Asia’s population, is not nearly so diverse as the group they left behind. And the smaller the founding group, the less diverse their DNA will be.

Now 50,000 years later, here we are. East Africans have continued to mix and change from their big diverse starting population. Asians have mixed and changed too but from a smaller, less diverse starting population. So the East Africans are more genetically diverse than the Asians.

Now imagine it is 10,000 years ago. A small group of Asians heads over to Alaska and doesn’t return. This starting group is even less diverse than the original group of East Africans. Which helps explain why Native Americans are genetically less diverse than Asians.

The studies were so big that they were able to make even finer distinctions (see the tree to the right). And as data continues to pour in (especially from companies like 23andMe and DeCODEme),
scientists will be able to refine ancestry even further.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.




latitude: 0.213671, longitude: 16.9849


Tags: dna, KQED, kqedquest, out of africa, QUEST, Science



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Posted in Biology, KQED, Partners | 4 Comments

The Tech Museum’s Tech Challenge goes global

February 18th, 2008 by Dr. Barry Starr

Guest blogger Lisa Croel of The Tech Museum in San Jose, CA sits in for Dr. Barry Starr this week.


I remember loving science class as a kid. The paper-maché messes, the bubbling baking soda, all of the wonderful experiments… I loved it all. Now, many grammar school kids are lucky to get 15 minutes of science education a week. Hardly enough time to get them imagining future careers as scientists, engineers and inventors.

Between the lack of time given to science education, and the structure imposed by curriculum standards, museums need to be part of the education equation. My boss has a saying: “Give random a chance.” I love this quote because it speaks to the role informal educational resources like science museums need to be playing. By exposing young people to the experiences and programs in a museum, who knows what might really resonate and inspire?

For over 20 years, The Tech’s Tech Challenge program has presented kids with an open-ended problem for which there is no one right answer. It forces participants to use their knowledge and ingenuity to solve the problem. For example, this year the Challenge (called Water Works) is all about moving water from a stream up to a village without electricity. There is no one right answer, and there are lots of ways to solve this problem.

Participants are 5^th to 12^th graders who will work in teams of 2-6 to explore solutions to solving this real world problem. Along the way, they will hit some roadblocks and come up with some duds. And that’s OK because it is here that kids will learn that failure is an important part of problem solving. We have a great quote etched into a wall on the outside of The Tech from Intel co-founder and philanthropist Gordon Moore that says, “If everything you try works, you are not trying hard enough.” Through failure, many of the Tech Challenge teams will come up with a far superior solution.

This year we’re going international for the first time by partnering with the City of San Jose’s Sister City program. On the final event day, where all of the teams come together to present and demonstrate their solutions, we’ll be webcasting in teams from far-away locations, and look forward to seeing and hearing how kids from other countries have tackled the challenge. Hopefully the involvement of other cultures will drive home how important it is to be inclusive to come up with better ways to solve problems.

I just looked at the U.S. Census Bureau web site for the latest world population number, and today there are 6,650,846,379 people on Planet Earth. One in five people on Earth don’t have access to safe, clean drinking water, which means that 1.3 billion people are suffering from lack of water. As this year’s Tech Challenge participants work on solutions to a global water problem, I hope they get excited (or more excited) about science and remain engaged, even they don’t get to study it much in the classroom.

Lisa Croel is the Marketing Director at The Tech Museum of Innovation in San Jose, Calif.


Tags: k-12 education, KQED, kqedquest, robotics, san jose, Science, science education, tech challenge, tech museum of innovation, techmuseum, water



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Posted in Education, Engineering, Partners | 1 Comment

How to get away with murder

February 4th, 2008 by Dr. Barry Starr



ABC, Yahoo! and others ran a story about a woman who had a liver transplant whose blood type ended up changing. I love stories like this.

Not because of the change itself. Most likely, stem cells traveled from the new liver to the patient’s bone marrow. There, the stem cells set up shop and gave her a new blood type.

What intrigues me is what these types of stories mean for solving crimes. Because changed blood type usually means changed blood DNA. In other words, her blood cells now have different DNA from the other cells in her body. This can really confound an investigation if the police aren’t careful.

Of course this was a very rare event. But bone marrow transplants aren’t. And every bone marrow transplant results in blood cells with different DNA compared to the rest of the recipient’s cells.

Imagine that someone who has had a bone marrow transplant does something wrong and leaves blood behind at the crime scene. The police do a cheek swab to gather DNA evidence and check it against the police DNA database as well as likely suspects (including our bone marrow recipient).

The police don’t catch our bone marrow recipient because his cheek DNA is different than his new blood DNA. So he is off the hook (as long as the police don’t check the blood too). But they do get a match and arrest someone—the donor.

Sounds weird but something almost like this complicated a case in Alaska a few years ago. There was a serious crime and a semen sample from the crime scene matched a known criminal’s DNA. But the person whose DNA matched the DNA from the crime scene had a strong alibi…he was in jail at the time! So what happened?

A little further investigation showed that the guy in jail had received a bone marrow transplant from his brother. And his brother was the one who committed the crime.

This one worked out all right in the end. But what would have happened to the brother if he weren’t in jail at the time? Would an overworked public defender have figured something like this out? The guy was lucky he was already in jail!

So people with bone marrow transplants need to be careful. And the police need to be careful about what sample they take from suspects.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.




latitude: -33.8027, longitude: 150.988


Tags: bone marrow transplant, crime, dna, forensics, KQED, kqedquest, QUEST, Science, stem cell, transplant



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Curing mouse sickle cell anemia with stem cells

January 21st, 2008 by Dr. Barry Starr

Last blog I talked about how scientists turned skin cells into embryonic stem (ES) cells. This was big news because scientists can now make an ES-like cell without destroying an embryo.

This blog I thought I’d talk about how scientists have used these cells to cure a mouse’s sickle cell anemia. If the mouse stays cured, this is a hugely important finding.

First some terminology so I don’t have to keep saying, “skin cell turned ES cell.” Scientists are now starting to call these cells iPS for induced pluripotent stem cells and I figured I’d jump on the bandwagon too. (Pluripotent is just a way to say that a cell can turn into lots of other kinds of cells).

Now as you probably know, sickle cell anemia is a genetic disease that is more common in people whose ancestors came from areas where there was lots of malaria. In sickle cell anemia, the red blood cells “sickle up,” forming crescent shapes. These shapes can’t fit in the smallest blood vessels causing the problems associated with the disease. Right now there are treatments but no cure.

The way to cure the disease is to fix the broken hemoglobin gene in the cells that make red blood cells. Since red blood cells are all replaced within a few months, this would lead to a cure pretty quickly.

Unfortunately, fixing a gene is not like falling off a log–it is really hard to do. The scientists in this study decided to try it with iPS cells. Basically they replaced the mouse’s blood stem cells with newly repaired ones so that the new blood stem cells made healthy new red blood cells. The mouse has not shown signs of sickle cell anemia for 12 weeks so far.

I don’t want you to come away thinking that it was an easy thing to do. It wasn’t (see below). But it does show that it is possible to treat and possibly cure sickle cell anemia in mice using iPS cells.

To move it to humans, we need to make sure that the treatment sticks. When these kinds of things have been tried with gene therapy, the cure almost always wears off over time. It shouldn’t happen at the DNA level with the way they did their experiment, but we need to wait and see.

The scientists also need to find genes that can turn a skin cell into an iPS with less risk of causing cancer. And to find better ways to get these genes into the skin cell so that, again, the treatment doesn’t cause cancer.

Even taking all of this into account, this is a very promising first step. Curing a genetic disease with stem cells that do not get rejected by the recipient’s body is one of the big goals of stem cell research. And these researchers may have accomplished this in mice.



More details on how to cure a mouse’s sickle cell anemia:

1. Add four genes to turn the skin cell into an iPS cell.

See the previous blogto see how to do this. To decrease the risk of the mouse developing cancer from these cells, the researchers chopped out one of the genes they used, the myc gene.

2. Use the ES cell to fix the gene using a process called homologous recombination.

Homologous recombination is a way to swap out one DNA for another. It is incredibly inefficient and we can really only get it to work at all in ES cells. Out of 72 cells, they managed to get one where one copy of the gene was repaired.* This result showed that homologous recombination would work in iPS cells which was an open question.

3. Turn the ES cell into a blood-like stem cell by adding the HoxB4 gene.

4.Destroy the mouse’s bone marrow and replace the cells with the new blood stem cells.

This is really just a bone marrow transplant using the newly created cells as the blood stem cells.

*In the end they had a mouse with one of its copies of the hemoglobin gene repaired in its blood cells. (All the rest of the cells including its sperm cells still carried the disease version of the hemoglobin gene.) The mouse exhibited no sickle cell anemia symptoms similar to most human carriers of the disease who have a single broken copy.

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.



latitude 37.3316, longitude -121.89


Tags: gene therapy, genetics, HoxB4, induced pluripotent stem cells, KQED, kqedquest, myc, pbs, QUEST, Science, sickle cell anemia



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Posted in Biology, Partners | 3 Comments

Stemming the tide of disease

January 7th, 2008 by Dr. Barry Starr

Scientists can now turn skin cells into embryonic
stem cells like these.(Image: Nissim Benvenisty)It is amazing how fast stem cell research is accelerating. Six months ago, we had to destroy embryos to get at their precious embryonic stem (ES) cells. Or we had to at least steal them.

Now, as 2008 begins, we can turn skin cells into ES cells in mice and humans. This is huge and here’s why:

1) No embryos need to be destroyed
2) No one needs to be cloned
3) ES cells derived from skin cells won’t be rejected by the body

So how’d the researchers do it? As with any important new finding, this one started out as basic research. And like many other findings, this one also started out not in humans but in an animal model system.

A Japanese group had been studying how a mouse ES cell eventually gets turned into a skin cell. In the end, they identified around 20 genes that were turned on to reprogram a skin cell into an ES cell.

The 20 genes the Japanese group identified are really master control genes. They are responsible for affecting how lots of other genes work. So, all a scientist would have to do is turn on these 20 genes in a skin cell and you’d get back to an ES cell. Sounds simple, right?

Unfortunately, scientists aren’t very good at all at turning on a specific gene in a cell let alone 20. To get around this limitation, the scientists decided to add the genes to a skin cell using gene therapy.

Unfortunately, scientists can’t easily add 20 genes to a cell with gene therapy either. This meant they had to find the bare minimum that might work. After much research, the group settled on four genes that could turn a skin cell into an ES cell.

Remember, this was all in mice. Now this same group (and another from the U.S.) has accomplished the same thing with a human cell. Both groups have taken a human skin cell, added four genes, and changed it into an ES cell.

We aren’t going to be curing diseases with these cells quite yet though. When the Japanese group put the mouse cells back into a mouse, 20% of them developed cancer. This is probably due to one of the genes they used (myc), as well as the way they did their gene therapy (viral mediated).

The U.S. researchers who converted the human skin cell were able to do it without the myc gene. This tells us there are different sets of genes that can work in this process. Hopefully scientists can discover a set of genes and a way to get them into cells that won’t cause cancer.

All this work got me to thinking. I wonder if scientists would have worked this hard to make ES cells from skin cells without George Bush’s ban on ES cell research. They certainly would have got there eventually but would they have gotten there so quickly?

Dr. Barry Starr is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA.



latitude 37.3316, longitude -121.89


Tags: gene therapy, genetics, KQED, kqedquest, myc, pbs stem cells, QUEST, Science



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Posted in Biology, Health, Partners | 2 Comments
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