The always excellent New Scientist has an article synthesizing much of the research into same-sex sexual behavior in animals and the possible evolutionary explanations. They spoke with University of California evolutionary biologists Marlene Zuk and Nathan Bailey, who recently published a paper examining same-sex behavior in various species. Zuk and Bailey note that same-sex sexual behavior in other animals can't necessarily be equated with sexual orientation in humans, researchers have come up with similar questions as to why certain animals have evolved to include members who expend energy on same-sex liaisons.

Evolutionary biologists have come up with various hypotheses for why same-sex behavior has evolved in various animals. In some cases, same-sex behavior has emerged as a result of specific adaptations, such as to foster social bonding, or because certain genes for same-sex attraction hold another survival benefit when only one copy is present. In some cases, though, the behavior is incidental, such as in certain fish that cannot easily tell male and female members apart.

Below, New Scientist charts several of the possible evolutionary explanations for same-sex sexual behavior in various species:

Bailey believes that exploring the evolution of sexual behavior will give us a better understanding of evolution, including the development of our own species:

"Given its persistence in species in many different animal groups, including humans, viewing it as an evolutionary force in its own right promises to provide a much richer understanding of the evolution of reproductive behaviour," Bailey says. He suggests we could make some fascinating comparisons. Might male-male copulation in species as diverse as flour beetles and dolphins have similar, even predictable, evolutionary consequences? More daringly, could understanding the evolutionary consequences of same-sex interactions in animals help us understand our own evolution?

Homosexual selection: The power of same-sex liaisons [New Scientist]

Muscle disease specialists at Ohio State University have been studying myostatin, the protein that regulates and curbs muscle growth. Their research found that a second protein, follistatin, can bind to myostatin, preventing myostatin from stopping muscle growth. They decided to test whether artificially introducing follistatin to the body would lead to an increase in strength and muscle mass. Using a common cold virus as a carrier, the researchers injected the follistatin gene into the thigh muscles of six macaque monkeys. The monkeys' thigh muscles grew an average of 15 percent as a result of the treatment, and one monkey experienced an incredible 78 percent increase in strength. The researchers reported in Science Translational Medicine that, after 15 months, the increases remained and that the monkeys experienced no visible side effects.

The researchers hope to start clinical trials on humans next year, with an eye toward helping people with degenerative muscular diseases. But for healthy individuals looking to increase their strength, the treatment would come at a cost: immunosuppressant drugs are a necessary component of the therapy.

Gene therapy may be used to treat muscular dystrophy [Times Online via Next Big Future via Reddit]

It's been known for a while that the FOXP2 gene is involved in human speech - damage to the gene causes speech difficulties. But now a group of researchers in Los Angeles has investigated how FOXP2 works in humans, comparing it to the functioning of the gene in chimps. It turns out that FOXP2 functions as a gene regulator, which means that it unleashes proteins that can switch other genes, called "targets," on and off.

Said geneticist Daniel Geschwind:

We found that a significant number of the newly identified targets are expressed differently in human and chimpanzee brains. This suggests that FOXP2 drives these genes to behave differently in the two species.

In other words, human FOXP2 causes unique behaviors in other genes.

Added neurology researcher Genevieve Konopka:

Genetic changes between the human and chimp species hold the clues for how our brains developed their capacity for language. By pinpointing the genes influenced by FOXP2, we have identified a new set of tools for studying how human speech could be regulated at the molecular level.

Knowing what the FOXP2 gene does is just the first step. The question is whether tweaking the chimp FOXP2 could cause it to hit targets in the chimp genome that would lead to speaking chimps. You know, so we could turn them into perfect workers. Or into our future overlords.

via UCLA

A study at the University of California at Irvine studied the affect of a certain variant of the brain-derived neurotrophic factor (BDNF) gene on driving. The gene supports communication in the brain cells and is associated with keeping memory strong. For people with a certain variant of the BDNF gene, this process works less than optimally, and those people are less likely to recover from a stroke. Roughly 30 percent of Americans possess that less optimal variant.

The researchers had 29 participants, 22 without the less optimal variant of the gene and seven with it, take a simulated driving test. In the simulator, participants had to loop a track and gradually learn its nuances. They then had them drive the same simulated track days later. Participants with the gene variant performed worse on the driving test; they did not stay on the course as well as the participants and remembered less about the track during the second test.

But even if this genetic variant does make you a worse driver, it has certain advantages. Some studies have found that people with the variant retain greater mental sharpness when faced with neurodegenerative diseases like Parkinson's, Huntington's and multiple sclerosis.

[Physorg]

Despite the critters' 30-year lifespans, naked mole rats have never been found with tumors, and are the only known mammals that don't get cancer. Researchers at the University of Rochester in New York added cancerous cells to naked mole rat cells in order to observe the mechanism that inhibits cancerous growth. The growth of cancer cells in humans is inhibited by a gene known as p27, a gene that the naked mole rat also employs to inhibit cancer growth. But the gene primarily responsible for inhibiting cancer cell growth in naked mole rats is p16-ink4a, a gene humans also possess, but which plays no role in inhibiting cell growth in humans.

And the benefits for naked mole rats go beyond avoiding cancer. Unlike humans, naked mole rats have an active mechanism for cell division, called telomerase. Developing human cells divide using the same mechanism, but the mechanism is switched off in mature cells, likely to avoid cancer. Vera Gorbunova, who led the study, believes that because naked mole rats can inhibit cancerous cell division, the mechanism doesn't need to be switched off in mole rat cells as it does in human cells. This may grant a longer lifespan to naked mole rat stem cells, aiding in the repair and upkeep of their tissues.

We're still a long ways away from harnessing the naked mole rat's powers for human health, but Gorbunova believes that further study of unusual mammals, like the naked mole rat, will open up more doors than confining our medical studies to rats and mice.

The Life Span of a Rodent May Aid Human Health [NY Times]

Researchers at the University of Washington have been working with adult squirrel monkeys born without the ability to distinguish color. By introducing therapeutic genes for perfect color vision to the light-sensing cells at the back of the monkeys' eyes, the researchers have given the monkeys the ability to distinguish red and green. Although further research is needed, the team is optimistic that this is the first step in curing congenital color blindness, the most common form of which involves a faulty gene on the X chromosome.

But what's truly stunning about the breakthrough is that the monkeys in the study were adults. Light perception has been restored in children suffering from degenerative blindness, but researchers have long believed that adult brains are too "fixed" for sensory disorders to be treatable. That the adult monkey brains were readily receptive to perceiving color, something they had never done before, may open the door to treating a whole host of sensory conditions.

'Gene cure' for colour blindness [BBC]

BBC News explains:

One of the scientists, Dr Yali Xue from the Wellcome Trust Sanger Institute in Cambridgeshire, said: "The amount of data we generated would have been unimaginable just a few years ago.

"And finding this tiny number of mutations was more difficult than finding an ant's egg in an emperor's rice store."

New mutations can occasionally lead to severe diseases like cancer. It is hoped that the findings may lead to new ways to reduce mutations and provide insights into human evolution.

Joseph Nadeau, from the Case Western Reserve University in the US, who was not involved in this study said: "New mutations are the source of inherited variation, some of which can lead to disease and dysfunction, and some of which determine the nature and pace of evolutionary change.

"These are exciting times," he added.

I hope one of my 100 mutations includes the X-gene. I'm ready to grow wings now. Or, hey, I'd be satisfied with telekinesis.

via BBC

In a paper published in Forensic Science International, Dan Frumkin, a private forensics researcher, claims that fabricating DNA evidence has become so easy that "[a]ny biology undergraduate could perform this."

Frumkin outlines two methods for fabricating DNA evidence. The first requires access to a small sample of an individual's DNA, such as a hair or a bit of saliva. The size of the sample is then increased through a common technique known as DNA amplification. Then the hopeful framer takes blood from a different individual, centrifuges it to remove the DNA-carrying white blood cells, and leaves only the red blood cells, which contain no DNA. The person then adds the amplified DNA to the blood sample, creating a handy supply of blood that could be splashed onto a crime scene to implicate the chosen target.

The second method requires no actual sample of DNA, but a person's DNA profile, which may be stored in a law enforcement database. These profiles identify variations at 13 specific spots in an individual's genome. Frumkin claims that a scientist could keep a library of a cloned snippets of DNA representing the variants at the 13 spots (he estimates 425 samples would be needed in all), and he or she could mix the snippets to create a DNA sample matching anyone's genetic profile.

Frumkin says that, at the moment, there are ways to determine whether DNA evidence has been fabricated (and his own company, Nucleix, provides such tests), but it's a step forensic labs don't normally take. Although some respondents question whether criminals will actually use these techniques to throw suspicion off themselves and onto others, Tania Simoncelli, an American Civil Liberties Union science adviser, suggests that it's time for courts to reevaluate the reliability of DNA evidence:

"DNA is a lot easier to plant at a crime scene than fingerprints," she said. "We're creating a criminal justice system that is increasingly relying on this technology."

DNA Evidence Can Be Fabricated, Scientists Show [NY Times]

Though the domestication of dogs is still shrouded in mystery, one thing scientists agree on is that today's friendly pets are descended from the Eurasian grey wolf. About 15 to 40 thousand years ago, humans befriended these wolves, and over time these wolves branched into the diverse breeds we have today. The genetic diversity seen in Eurasian dogs led researchers to believe that these dogs were closest to their wolf foremothers, and therefore domestication had begun in the region.

But Cornell computational biologist Adam Boyko had a different theory. He believed that the DNA of African village dogs, if sequenced, would reveal a diversity comparable to the Eurasian types. So he asked his brother and sister-in-law, on honeymoon in Egypt, Uganda and Namibia, to collect DNA samples from hundreds of village dogs. Upon their return to the States, Boyko discovered that he had been right. The genetic diversity of African dogs rivaled that of their Eurasian counterparts. Now, he says, it seems likely that dog domestication started in Africa, though the grey wolves themselves are unarguably Eurasian in origin. Probably African village dogs are the descendants of Eurasian dogs that migrated to the continent tens of thousands of years ago.

Boyko told BBC News:

I think it means that the conclusion that was drawn before might have been premature. It's a consequence of having a lot of street dogs from East Asia that were sampled, compared to elsewhere.

"The reason that East Asia looked more diverse than elsewhere was not because East Asia as a continent had more diverse dogs than elsewhere but because non breed street and village dogs are more diverse than breed dogs.

He and an international team of researchers are now gathering DNA from village dogs across Europe and Asia to determine which area has the greatest genetic diversity - and is, by extension, is the most likely origin of the bond between human and canine.

via BBC News

Read the scientific paper by Boyko in PNAS.

Swazi village dog photo by Michael Tallman.

Scientists have been looking at embryonic development and experimenting with organ regrowth for years. This team was working on regrowing 3D organs in place. Their experiments were a success, and they were able to regrow teeth in laboratory rats.

To make these glowing regrown teeth happen, first the team created a "germ," or a seed from which the tooth can grow. This germ was coded with the fluorescent glowing dye to track the tooth development. Then they transplanted the tooth germ into the jawbone of a rat. Finally, they tested the regrown tooth. The team found that the teeth were essentially as strong as natural teeth and were able to grow nerves throughout, making them very similar to naturally developed teeth.

In the research team's experiments, the fluorescent glowing dye was a side point, but it isn't hard to imagine bio-luminescent add-ons catching on in the future. Imagine showing off your new glowing teeth to your friends, or even growing a full head of fluorescent pink hair. It could mean a whole bio-punk movement: body modification taken to the next glowing level!

For now, though, the medical implications are as exciting as the aesthetic. The successfully regrown tooth experiment means being able to replace more complex organs more easily in the future.

Fully functional bioengineered tooth replacement as an organ replacement therapy [Proceedings of the National Academy of Sciences]

The researchers, who worked with biotech firm Open Monoclonal Technology (OMT), wanted to create what are called "monoclonal antibodies," useful in fighting a number of human diseases. To do this, they needed to knock out certain gene sequences in rats. And they had to be sure that the mutated, antibody-producing rats that resulted would pass their mutations onto their children and grandchildren.

In a first for genetic engineering, a group of scientists from industry and academia managed to genetically engineer rats whose children carried the same engineered mutations as their parents (this has been done in other species, but not mammals). In the picture above you can see one example of the engineered rats. Two of the rats glow green under fluorescent light, but the rat on the right doesn't. He's the result of engineering that knocked out genes responsible for making the other two rats glow.

According to a release from OMT about the study:

With antibody sales expected to reach $50 billion within five years, many companies have entered the biologics market through acquiring antibody technologies or licensing/fee for service arrangements. Currently, the mouse is the only genetically engineered animal commercially available for the generation of human monoclonal antibodies, and many targets are licensed already. The expense and limitations of the mouse technology create an opportunity for OMT and its new monoclonal antibody platform with unrestricted development options . . .

Previously, it took either embryonic stem cells or nuclear transfer cloning — techniques that are not available for the genetic engineering of rats – to create a knockout, OMT used a new ZFN-mediated technique to generate immunoglobulin knockout rats. ZFNs are engineered proteins that induce double-strand breaks at specific sites in an organism's DNA. Such double-strand breaks stimulate the cell's natural DNA-repair pathways and can result in site- specific changes in the DNA sequence. Up to now, ZFNs have been used to edit specific genes in fruit flies, worms (C. elegans), cultured cells and zebrafish embryos, but this is the first example of successful, permanent, heritable gene-editing in a mammal.

My question is, how is this any different from using genetic engineering to intervene in evolution? If we can create whole families of mutants, who pass their mutations on to offspring, are we not forcing speciation?

There's also something squicky and intriguing about a new species of rat created entirely to produce drugs for humans.

via Science

Greenberg also possesses the mental capacity of an infant, and has never learned to speak or eat on her own. According to a recent report on ABC:

Brooke hasn't aged in the conventional sense. Dr. Richard Walker of the University of South Florida College of Medicine, in Tampa, says Brooke's body is not developing as a coordinated unit, but as independent parts that are out of sync. She has never been diagnosed with any known genetic syndrome or chromosomal abnormality that would help explain why.

She has also suffered from several strange maladies, including burst ulcers, a stroke and a brain tumor, which healed after Greenberg appeared on the verge of death.

It's unclear whether her capacity to heal is related to her agelessness, but researchers hope to find out. ABC reports:

Geneticist Maxine Sutcliffe chronicled a baffling range of inconsistencies in Brooke's aging process. She still has baby teeth at 16, for instance. And her bone age is estimated to be more like 10 years old.

"There've been very minimal changes in Brooke's brain," Walker said. "Various parts of her body, rather than all being at the same stage, seem to be disconnected."

Greenberg sleeps in a crib, and attends school. Her teachers and family aren't sure how much she understands, but they say she recognizes people familiar to her and likes to play and laugh.

Currently geneticists are trying to isolate the gene or set of genes responsible for her bizarre aging process. There are no other known cases like Greenberg's, and it's possible that her genome could be the key to unlocking how our bodies know when to age. If a sixteen-year-old can look like a sixteen-month-old, then why couldn't a sixty-year-old look twenty-one? Of course, treatments based on Greenberg's condition might keep people's brains stuck at the same age as their bodies. So you wouldn't have a person with the wisdom of a sixty-year-old in a youthful package. You'd just have somebody whose mind remained twenty-one for decades on end. Which sounds cool until you really think about it.

via ABC

The researchers wanted to shed light on how humans developed our language capabilities, including the intricate thought and muscle coordination which allowed us as a species to develop complex language. One gene responsible for that development is the FOXP2 gene. Its absence leads to speech disorders, and its presence is an important component of human speech. Humans and Neanderthals are known to have a specific variation on the FOXP2 gene, though versions of it appear in other mammals and birds.

To study the gene in action, scientists introduced the human version of it into a group of mice. The results were promising: The speech genes led to increased nerve presence and activity in the language centers of mice's brains. In short, the altered mice had better brains for language.

The results were published in Cell, and the researchers were careful to say that understanding the entire genetic development of language is a ways off. This experiment allowed scientists to take just a peek at how language evolved in humans, and maybe even to nudge a different species down that same evolutionary path.

But mice with increased language abilities don't seem too many ethical steps away from ape lab assistants in Planet of the Apes or dolphin commanders in the Uplift series. Maybe mouse language is just the next step in Frankie and Benjy Mouse's ten-million-year experiment from the Hitchhiker's Guide?

A Humanized Version of Foxp2 Affects Cortico-Basal Ganglia Circuits in Mice at Cell

Mouse image from sean dreilinger.

What these scientists have done could give us the first foolproof HIV vaccine. They have re-awakened the human genome's latent potential to make us all into HIV-resistant creatures. This evening in PLoS Biology, they've published their ground-breaking research.

A group of scientists led by Nitya Venkataraman and Alexander Colewhether wanted to try a new approach to fighting HIV - one that worked with the body's own immune system. They knew Old World monkeys had a built-in immunity to HIV: a protein called retrocyclin, which can prevent HIV from entering cell walls and starting an infection. So they began poring over the human genome, looking to see if humans had a latent gene that could manufacture retrocyclin too. It turned out that we did, but a "nonsense mutation" in the gene had turned it off at some point in our evolutionary history.

Nonsense mutations are caused when random DNA code shows up in the middle of a gene, preventing it from beginning the process of manufacturing proteins in the cell. Venkataraman and her team decided to investigate this gene further, doing a series of tests to see if the retrocyclin it produced would keep HIV out of human cells. It did.

At last, they knew that if they could just figure out a way to reawaken the "junk" gene that creates retrocyclin in humans, they might be able to stop HIV infections. The researchers just needed to figure out a way to remove that nonsense mutation and get the target gene to start manufacturing retrocyclin again.

Here's where things really get interesting. The team found a way to use a compound called aminoglycosides, which itself can cause errors when RNA transcribes information from DNA to make proteins. But this time, the aminoglycoside error would work in their favor: It would cause that RNA to ignore the nonsense mutation in the junk gene, and therefore start making retrocyclin again. In preliminary tests, their scheme worked. The human cells made retrocyclin, fended off HIV, and effectively became AIDS-resistant. And it was done entirely using the latent potential in the so-called junk DNA of the human genome.

After more research is done, the researchers believe this might become a viable way to make humans immune to HIV infection.

What intrigues me, beyond the amazing idea of an AIDS vaccine, is that aminoglycosides have the potential to unlock the uses for other pieces of junk DNA. Those of you who read Greg Bear's novel Darwin's Radio know that this scenario is familiar scifi territory: In that book, humans start rapidly evolving after their junk DNA re-awakens in response to stress. Could we induce instant mutations, or gain other new immunities by using aminoglycosides on our junk DNA? What would it mean to have the whole crazy, giant human genome at our command?

via PLoS Biology

Science Commons' John Wilibanks made the announcement today at O'Reilly's Etech Conference in San Jose, explaining that the data would be provided by Harvard's Personal Genome Project, a group whose goal is to sequence thousands of people's genomes over the next several years. They're committed to making all the data from these genomes public, in order to foster research into everything from disease to evolution.

The first few genomes that the Personal Genome Project has sequenced will soon be available via BitTorrent, using a system developed by ProteomeCommons. The genomes are being released under a Creative Commons Zero (CC0) agreement, which places zero restrictions on how people use the data.

Wilibanks explained that the genomes themselves would not be CC licensed, since you can't copyright genomic data - but all the notes and information about the genomes would be available to the public. And the public is welcome to use the genomic data however they wish. Ultimately, he suggested, making the data available in such an accessible manner encourages scientists to share their research findings and may discourage companies from locking up the information in dubious patents.

A group of researchers at the University of Washington have discovered that there is one area where human and ape DNA mutated very rapidly during the time that they were diverging on the evolutionary tree. Both species' genomes mutated a great deal in areas where there are a lot of repeat sequences of DNA. Humans, like most creatures, have areas of their genome where the same chunk of genetic code is repeated once or several times.

According to the University of Washington, lead researchers Tomas Marques-Bonet and Jeffrey M. Kidd said:

The new study shows big differences in the genomes of humans and great apes within duplicated sequences containing rapidly evolving genes. Most of these differences occurred at a time just prior to the speciation of chimpanzee, gorilla, and humans.

So is it possible that the reasons for such dramatic differences between human and chimp can be traced back to these quickly-mutating repeat regions?

According to the University of Washington:

Chimps and people share almost 99 percent of the non-duplicated sequences of their genomes; their proteins are virtually identical; and there are very few rearrangements that distinguish ape-human chromosomes. In contrast, the researchers noted that the duplicated sequences show much more variation than the other portions of the genetic code.

But this is such a new area of research that we need to be cautious before drawing any firm conclusions. While this looks like a promising avenue for further inquiry, the researchers explained:

There is still no final answer as to why chimps and humans are different. Maybe segmental duplications that are specific to humans are another layer to explore, or maybe the distinction between human and chimps is not found in these genetic differences. What is certain is that genetic differences contribute significantly to what makes a human and chimp different, and we know that these regions of our genetic code are changing much more rapidly than most others. The next challenge will be making sense of all these differences and the genes that are affected by them.

While previous studies have suggested that we will learn more about ourselves by studying so-called junk DNA, or DNA that doesn't seem actively involved in coding for proteins. But this new work suggests we study the parts of our genetic code that repeat themselves. These odd, repeated segments of our DNA may be the key to understanding why we mutated into the hairless, neurotic hominids we are, instead of turning into happy-go-lucky bonobos.

SOURCES:

University of Washington

Nature

Scientists have discovered that disabling series of genes in mice makes them engage in repetitive actions, similar to what humans do when they have schizophrenia, autism, or obsessive-compulsive disorder. But, as the researchers report in a paper to be published in Neuron tomorrow, medicines could be used to replicate the functions of the disabled genes, essentially switching off the craziness like a light. Is this a weapon or a cure?

Obviously the researchers are most interested in how their discovery could help bring stability into the lives of people suffering neurological distress. They hope to garget FKBP12, a key gene involved in creating the obsessive behaviors, for therapeutic techniques. NYU's Eric Klann, a researcher on the project, said:

[FKBP12] may be an ideal target for therapeutic drug development aimed at ameliorating some of the . . . related pathologies of neurological disease.

However, this research could just as easily lead to drugs that temporarily induce schizophrenic states. Exploring the cascade of effects created when tampering with FKBP12 has revealed that the gene is involved with enhanced memory as well. Would it be worth it to become temporarily OCD or autistic if it would give you an incredibly sharp memory for a few hours or days?

In twenty years, you could see rooms full of students taking tests who are hopped up on FKBP12 inhibitors, carefully regurgitating all the answers they memorized but unfortunately also feeling compelled to wash their hands every five minutes. And of course inducing schizophrenia in prisoners could become a new form of torture.

Brain deletion of FK-506 Binding Protein Enhances Repetitive Behaviors in Mice [via Neuron]

Image from Scorpions' awesome album Blackout. If you already knew that, you are an old fart like me.

The researchers found two fly genes, known as magu and hebe, that are responsible for causing older female flies to continue laying eggs. And they noticed that when those genes "over-express," or go into overdrive, that they also extend the natural lifespan of the flies by up to 30 percent. Humans have a gene, SMOC2, which is similar to the magu gene, so it's possible that these findings will be relevant to humans as well. Scientists already know of reliable ways to make genes over-express.

John Tower and Yishi Li, who conducted the research, are publishing the results this month in Molecular Genetics and Genomics. They suggest that hebe and magu genes have life-extending effects because they promote the formation of stem cells. Stem cells keep bodies young, and are also crucial to reproductive health. So when hebe and magu over-express, they stimulate the growth of new stem cells, and that has a cascade effect on the body's youthfulness.

Said Tower:

This would appear to be stimulating the stem cells to divide more in the old fly and therefore produce more offspring. It both makes females lay more eggs and live longer, so it really argues against any kind of obligatory tradeoff between reproduction and lifespan.

Add to your purses of the future a little bag of life-extension pills that will keep you fertile and lively well into your 100s.

Adult-Specific Over-Expression of the Drosophila Genes magu and hebe [via Molecular Genetics and Genomics]

When Tyrolean Iceman was defrosted in 2000, researchers took some DNA from his intestines and sequenced it. But that was only his nuclear DNA, inherited from both parents, and it revealed that he was related to a large group of Europeans who share a common ancestor. The new study, which will be published November 11 in Current Biology, allowed researchers to examine the mummy's lineage in more detail. And that's when they realized how different he was from modern populations.

Said Franco Rollo, a co-author of the study:

We have obtained evidence of a significant genetic difference between present-day Europeans and a representative prehistoric human—despite the fact that the Iceman is not so old—just about 5,000 years. This doesn't simply mean that Ötzi had some 'personal' mutations making him different from the others but that, in the past, there was a group—a branch of the phylogenetic tree—of men and women sharing the same mitochondrial DNA. Apparently, this genetic group is no longer present. We don't know whether it is extinct or it has become extremely rare.

What this reveals is that even large groups of genetically similar people can completely disappear from the gene pool in a relatively short time. This should shore up current theories that hold humans are actually evolving very rapidly.

SOURCE: The Complete Mitochondrial Genome Sequence of the Tyrolean Iceman [via Current Biology]