As I have blogged about before, a big part of sexual preference is biological. Research shows that some people are hardwired to prefer the same sex. This is true in animals as well.

What scientists haven’t had much luck at yet is finding out why this is. There have been studies that have implicated the X chromosome (although not convincingly). And others that have pointed to brain structure. But none of these studies really gets at what is going on in these folks’ brains that makes them prefer relationships with the same sex.

A new study out suggests that, at least in mice, the neurotransmitter serotonin may play a big role. Scientists created a strain of mice that lacked most of a certain kind of serotonin receptors in the brain (central serotonin receptors). These mice were healthy and happy. And the males were not at all fussy about whom they hooked up with.

When scientists put wild type* male mice in a cage with other males, they mostly ignored the other mice. The male mice lacking their central serotonin receptors reacted differently. They got busy with the male mice almost every time.

These mice aren’t homosexual though. Given a choice of a male or female, they didn’t really care; they went after both at about the same rate. The genetically altered mice were more bisexual than homosexual.

The researchers did lots of other experiments as well that showed that these mice were not oversexed or lacking anything in particular. They just liked the boys as much as the girls.

What this study tells us is that in mice, serotonin plays a big role in sexual preference through these particular brain neurons. What it doesn’t tell us is if the same thing is true in people. After all, picking a mate is very different in mice as compared to people.

But there are hints that serotonin works differently in the brains of bisexual and homosexual men. For example, certain selective serotonin reuptake inhibitors (or SSRIs) have different effects in bisexual and homosexual men compared to heterosexual men. Still, this isn’t yet enough to finger serotonin use as the main driver of sexual preference in people.

What it does do though is provide scientists some direction for their research. Instead of wading through all 20,000+ genes, they can start out focusing on those that deal with serotonin. This will greatly simplify the research and if serotonin does play a role, then scientists will find the genetic variations involved sooner rather than later.

And frankly, given the slow progress thus far, focusing on serotonin genes won’t set the field back too far. It is probably worth taking the research in this direction.

* Wild type just means a mouse (or any living thing) that hasn’t been tampered with. In this case, it is a run of the mill lab mouse.

A more in depth look at the story from blogger Ed Yong at Not Exactly Rocket Science.

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It will probably take more than a human FOXP2 gene to reach this future.

People with a certain version of this gene have trouble forming words and speaking but are otherwise OK.  This is exactly what you would expect if a gene were primarily involved in speech.

One way to test this idea would be to put the human version of the gene into an animal and see what happens to that animal's speech.  A natural candidate would be the chimpanzee.  Humans and chimps are around 98.8% similar at the DNA level* and their FOXP2 gene has only two differences.

Unfortunately (or fortunately…), we can't yet do this experiment because we aren't very good at changing a chimp's genes.  But what we are good at is changing a mouse's gene.  And this is exactly what scientists did in a new study.

The scientists changed a mouse's FOXP2 gene into a human's.  Now no one expected that we'd have a Mickey Mouse on our hands.  Mice just don't have all the equipment for speech and it is really unlikely that the only difference between mice and people in terms of speech is this gene.

But by putting a human FOXP2 gene in mice, we can learn some things about how the gene influences human speech.  Does it change the vocalization part of the brain?  Does it change something with mouth anatomy?  Something with breathing?

The results with these mice were interesting.  They weren't suddenly chatty but changing the gene definitely caused the mice to emit different squeaks than their natural cousins.  The vocalization part of the mouse's brain also changed.

These results suggest that FOXP2 affects human speech at least partly through changes in the brain.  And that if you give a mouse a human Foxp2 gene, you change the way it communicates.

The next steps are a little harder to figure out.  We do know that Neanderthals had the same FOXP2 gene that we do.  Perhaps by comparing human, chimp and Neanderthal DNA we'll be able to find other genes involved in speech too.  We'll have to wait a few months for this kind of analysis as the Neanderthal genome isn't quite done yet.

*When we include extra copies of some DNA and missing DNA, the similarity goes down to 96%.

Here is a video discussing the results of the study.

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Maybe a clone of this guy will wander the Earth one day.A new study shows that scientists can clone a mouse that has been dead and frozen for 16 years. If they can apply what they've learned to a mammoth that has been dead and frozen for over 10,000 years, then maybe my kids can ride a mammoth one day. Or at least my grandkids can.

You Need More than DNA to Clone

Cloning isn't as simple as was shown in Jurassic Park. You can't take DNA and make a clone from it. Instead, you need an intact nucleus. And ideally, an intact nucleus in an intact cell.

The nucleus is where DNA is kept in our cells. The DNA is stored and packaged there in a way that only Mother Nature can do (for now). We can’t take our 6 feet of DNA and cram it into the tiny space of the nucleus.

Cloning 101.As I said, right now cloning uses intact cells. Here's how it works:

1) Take a cell from the animal to be cloned
2) Remove the nucleus from an egg (this is called an enucleated egg)
3) Fuse the two cells and let it divide a few times in a Petri dish
4) Implant the growing embryo into a surrogate mother
5) If everything goes well, a clone is born

This procedure requires living intact cells to be used. The problem with a frozen animal cell is that it is dead and ice crystals have torn it apart. It is not possible to fuse a beat up dead cell with an enucleated egg.

Cloning Using Frozen Cells

What the researchers in this new study did was change the protocol a bit. Instead of fusing two cells, they harvested nuclei from the frozen cells and injected them directly into the enucleated egg.

When they tried to clone the mouse that had been frozen for 16 years this way, it didn't work. But they managed to get 4 clones by adding an extra step. What they did was to make embryonic stem (ES) cells from the frozen mouse and use those cells to make a clone.

Basically they cloned the mouse but then instead of putting the embryo into a surrogate mother, they harvested its ES cells. Then they used the nuclei from these cells to create a clone in the usual way.

So we can now clone a long frozen mouse. The next step will be to try to clone an extinct animal like a mammoth.

Cloning a Mammoth is Trickier than a Mouse

Mammoth cloning will be no walk in the park. First off, we don’t have any mammoth eggs or cells to use. We'll have to use elephant ones. Hopefully, elephant eggs and/or cells will be compatible with a mammoth's nucleus. ( But there is some concern they they might not be compatible.)

Second, elephants are a lot harder to work with than mice. The experiments in this study used thousands of eggs to get a few clones. I don’t know enough about elephant biology but it seems like you'd need a lot of elephants to get that many eggs.

But this is definitely the first step in resurrecting long dead animals. For now we'll have to focus on the frozen ones. Maybe in the future researchers can figure out how to clone animals stored in formaldehyde. Or from pelts. Then we can start reviving species we humans have managed to kill off over the years.

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