Sex would be a very different proposition for humans if — like some animals including chimpanzees, macaques and mice — men had penises studded with small, hard spines.

Now researchers at Stanford University in California have found a molecular mechanism for how the human penis could have evolved to be so distinctly spine-free. They have pinpointed it as the loss of a particular chunk of non-coding DNA that influences the expression of the androgen receptor gene involved in hormone signalling.

The research also suggests a molecular mechanism for how we evolved bigger brains than chimpanzees and lost the small sensory whiskers that the apes — who are amongst our closest relatives and with whom it has been estimated we share 96% of our DNA — have on their face.

{ Nature | Continue reading }

artwork { Tom Gallant, Japanese Iris, 2010 | Cut paper, glass, wood }

In January, the shooting of Gabrielle Giffords produced a half dozen bona fide heroes, including Patricia Maisch, a 61-year-old woman who snatched ammunition out of alleged gunman Jared Loughner’s hands as he tried to reload. For good reason, people like these earn our respect and adulation; their grace under pressure strikes us as almost superhuman. Yet as we marvel at their deeds, we’re always left wondering about where, exactly, this composure comes from. Do these people emerge from the womb with sanguine looks on their faces, ready to perform life-saving surgery in the next room if necessary? Or is their coolness something they picked up through life experience? (…)

Let’s start with the “nature” side of the equation. For every one of us, the starting point for cool-headedness comes bundled within our DNA: our innate disposition toward anxiety. It’s never been a secret that anxiousness is partially inherited, but no one knew how much influence our genes threw around until psychiatrist Kenneth Kendler came along. In a 2001 study, Kendler and his colleagues examined 1,200 pairs of male twins, some identical and some fraternal, probing into each brother’s individual phobias. Because all of the twins shared the same upbringing, yet only the identical twins shared the same DNA, Kendler could filter out environmental factors altogether and calculate a pure figure for our genetic susceptibility to anxiety. The answer? Genes account for around 30 percent of our anxiousness.

{ Slate | Continue reading }

When it comes to genes, evolutionary biologists have traditionally favored seniority. Genes thought to be most essential to life must be ancient and conserved, the assumption goes, handed down from species to species as the basic instructions of life. That sharing is evident in early developmental stages, which 19th-century biologist Ernst Haeckel observed to be very similar between different organisms in his famed recapitulation theory. The genes that drive those early stages of development are also shared by creatures as different as flies, mice, and humans, lending support to the idea that the most important genes for life go a long way back on the evolutionary tree.

By comparison, new genes haven’t gotten nearly as much credit. Arising more recently in evolution’s history, rookies that only count their age in tens of millions of years were thought to be less important - providing new functions and features that were nice, but not essential. If old genes were the bread and butter of life…

“Maybe the new genes serve a function like vinegar or soy sauce,” said Manyuan Long, professor of ecology & evolution at the University of Chicago. “They make your life better, change behavior, help a male find females more efficiently, but that’s all.”

But that ageist perspective is shaken in this week’s Science, courtesy of an exciting new study from Long’s laboratory. Using the fly species Drosophila melanogaster, Long, graduate student Sidi Chen, and postdoctoral researcher Yong Zhang tested whether silencing a new gene would be as fatal as silencing an old one. (…)

Another surprise implication of the data is the speed with which new genes can become an indispensable part of a species’ genome. When a new gene appears in a species due to evolution, one would not expect it to be immediately crucial - otherwise, how did the species survive before its arrival? But like a new employee in an office, a new gene can make itself essential by forming relationships with older, essential genes through what are called gene-gene interactions. Before long, the new gene has become a key part of the species’ survival…and there’s no turning back.

{ University of Chicago | Continue reading }

photo { Jeremy Liebman }

Like to sleep around? Blame your genes.

People’s predilections for promiscuity lie partially in their DNA, according to a new study.

A particular version of a dopamine receptor gene called DRD4 is linked to people’s tendency toward both infidelity and uncommitted one-night stands, the researchers reported Nov. 30 in the online open-access journal PloS One.

The same gene has already been linked to alcoholism and gambling addiction, as well as less destructive thrills like a love of horror films. One study linked the gene to an openness to new social situations, which in turn correlated with political liberalism.

{ LiveScience | Continue reading }

photo { Logan White }

…an essential difference between genetics, the study of a fixed inheritance in DNA, and epigenetics, which is the study of how the environment affects those genes, causing different ones to be active at different rates, times and places in the body.

Evolutionary approaches to human behavior have often been framed in terms of “good” and “bad”: Why did homosexuality evolve if it’s “bad” for the genes, because it reduces the chance that they’ll be passed on to a new generation? Why wouldn’t an impulsive temperament be “selected against,” seeing as its possessors would be more likely to fall off cliffs? Some thinkers have twisted themselves into pretzels trying to explain why a “maladaptive” behavior hasn’t disappeared. (…)

When we focus on particular genes in your particular cortex turning “on” and “off,” the selective forces of evolution aren’t our concern. They’ve done their work; they’re history. But your genes, all “winners” in that eons-long Darwinian process of elimination, still permit a range of human behavior. That range runs from a sober, quiet conscientious life at one extreme to, say, playing for the Rolling Stones at the other. From the long-term genetic point of view, everything on that range, no matter how extreme, is as adaptive as any other. Because the same genes make them all possible.

In other words, the epigenetic idea is that your DNA could support many different versions of you; so the particular you that exists is the result of your experiences, which turned your genes “on” and “off” in patterns that would have been different if you’d lived under different conditions.

{ Big Think | Continue reading }

photo { Hiroshi Watanabe }

Researchers create ‘lesbian’ mice by deleting a single gene.

Deletion of a single gene switches the sexual orientation of female mice, causing them to engage in sexual behaviour that is typical of males. Korean researchers found that deleting the appropriately named FucM gene causes masculinization of the mouse brain, so that female mice lacking the gene avoid the advances of males and try to mate with other females instead. The findings probably have little relavence to human sexual orientation, however.

{ ScienceBlogs/Neurophilosophy | Continue reading }

painting { Atilla Adorján }

Cars kill a lot more people than spiders, bats, snakes and wolves, but why don’t we fear them in the same visceral way? (…)

Although some of us fear snakes more than others, all baby humans, chimps and monkeys are equally jumpy when confronted with a black plastic snake. That aversion probably grew out of the pressures of life in the jungle eons ago. Back then, encounters with certain snakes were a matter of life and death, and a healthy fear of snakes kept our ancestors alive long enough to procreate.

In the field of evolutionary psychology, the belief is that instinctive fears became hard-wired in our biology, through genes or other inheritance, during the time (the Stone Age) and place (the African jungle and savannah) of our development into the Homo sapiens we are today.

But some new thinking suggests that these adaptations might date back before the Stone Age, and some, perhaps, to more recent times. (…)

Fear of heights is so widespread and understandable that psychologists consider it a normal fear. (…) Other phobias that persist into modern times may have been fixed much more recently than snakes and spiders, say in the late Paleolithic age, about 100,000 years ago, or even more recently.

Take fainting in response to seeing blood or surgical instruments. Fainting, Bracha posits, might have been an adaptive female response to the frequent raiding bands in the early hunting-and-gathering societies. You might have been less likely to be murdered if you fainted at the sight of a sharp stick.

Then there are the fears that point to inherently dangerous things and that no doubt have an “adaptive” function, except that they’ve gotten out of hand. Fears of dirt, rats, mice and insects are obviously self-protective, since all these carry diseases. But most vermin-spread diseases probably were not a serious problem before people began creating cities several thousand years ago.

Instinctual repulsion to some of these critters, Bracha hypothesizes, might have arisen in the Neolithic period, which started about 10,000 years ago.

So why do some of us appear to be addicted to fear, as evidenced by the popularity of increasingly horrifying horror movies? (…)

“They are people who need strong feelings of arousal, and they get those from horror movies as well as sexy movies. Low-sensation-seekers don’t like to be aroused by unpleasant things. High-sensation-seekers can enjoy any vicarious experience if it’s strong enough.”

{ Washington Post | Continue reading }

photo { Helmut Newton }

{ 1. Linnea Strid | 2. Amanda Lepore by David LaChapelle }

quote { When the Key to Good Genetics Research Isn’t in the Genes | Newsweek | full story }

Humans are a social species, we interact with other people – aided by language- and exchange information on daily basis. The effects of social isolation have been demonstrated and predicted to be very severe and “de-humanising” in many cases with a long list of adverse effects on cognitive abilities and emotional stability. The question often posed when considering this feature of mankind is whether it is an adaptation to the presence of others in our environment, a simple product of proximity; or it is a function developmentally wired into our genes and is ,thus, needed for proper growth and development. The latter also would imply the evolutionary advantage of cooperation and living in a group.

In a recent study, researchers tackled the question of whether we are genetically wired to be social, and they did so by finding one of the most controlled environments in human developmental studies, and chose the ideal subjects for most genetic questions. Twins in utero! (…)

The intentional nature of movements directed towards the other twin is an important observation from this study; it suggests that we are , in fact, genetically wired to be social.

{ Glial Dance | Continue reading }

In new research published in Psychological Science, scientists analyzed genes in the dopamine system and found a group of mutations that help predict whether someone is inclined toward sensation seeking.

Jaime Derringer and coauthors wanted to use a new technique to find out more about the genetics of sensation seeking. Most obvious connections with genes have already been found, Derringer says. Now new methods are letting scientists look for more subtle associations between genes and all kinds of traits, including behavior and personality.

{ APS | Continue reading }

Billions of brain cells are communicating at any given moment. Like an organic supercomputer they keep everything going, from breathing to solving riddles, and “programming errors” can lead to serious conditions such as schizophrenia, Parkinson’s Disease and Attention-Deficit Hyperactivity Disorder.

{ University of Copenhagen | Continue reading }

One of the great puzzles of cell biology is how information is stored, processed and passed from generation to generation at the biochemical level.

By far the most famous mechanism is the sequence of nucleotides in DNA. However, in recent years a number other data storage mechanisms have emerged, so-called epigenetic processes, and their role is under fierce debate. For example, the pattern of methyl groups attached to DNA seems to be an important data storage system as do modifications to the proteins that control how DNA is packaged.

Today, Georg Fritz at the University of Cologne and a few buddies put forward a new idea. They say that a simple network of genes can act as a conditional memory, that either stores or ignores information when it is told to do so. “The circuit behaves similarly to a “data latch” in an electronic circuit, i.e. it reads and stores an input signal only when conditioned to do so by a “read command,” say the group.

{ The Physics arXiv Blog | Continue reading }

Tracking your internal clock may be as easy as plucking a few strands of hair, according to a new study.

The research found that hair follicles hold a record of the gene activity that influences when we wake and when we sleep. The results could be used to diagnose and study sleep disorders and conditions like jet lag.

Whether you’re a night owl or a morning lark, your sleep-wake cycle is controlled in large part by genes called clock genes. These genes vary their activity throughout the day, setting the internal clock that drives our circadian rhythms.

The first human clock gene was discovered almost 10 years ago, but isolating the genes efficiently enough to study sleep-wake cycles in real time has proved difficult. When the genes are active, they transcribe their DNA into RNA, the first step in producing various proteins that essentially carry out a gene’s instructions and, in this case, influence circadian rhythms. The RNA can be found in cells all over the body, from white blood cells to the lining of the mouth, but techniques for extracting it from these cells proved unreliable.

{ LiveScience | Continue reading }

Why human lifespan is rapidly increasing: solving “longevity riddle” with “revealed-slow-aging” hypothesis.

Healthy life span is rapidly increasing and human aging seems to be postponed. … To explain current increase in longevity, I discuss that certain genetic variants such as hyper-active mTOR (mTarget of Rapamycin) may increase survival early in life at the expense of accelerated aging. In other words, robustness and fast aging may be associated and slow-aging individuals died prematurely in the past. Therefore, until recently, mostly fast-aging individuals managed to survive into old age. The progress of civilization (especially 60 years ago) allowed slow-aging individuals to survive until old age, emerging as healthy centenarians now.

{ fightaging | Continue reading }

A foreign language can sound so unintelligible that it’s hard to believe what linguists have been saying for years: Languages from around the world all follow the same rules. No language will ever require placing a particular word at a fixed point in a sentence (e.g., “da” must always be in the fifth position). No language forms questions by simply reversing the words in a statement. The reasons for this lie in the brain’s wiring, which dictates the possible patterns languages can follow. Anything that breaks the mold will be impossible to learn or pass down to a new generation.

Similarly, biologists say there are limits to what forms of life can possibly exist, because all new species must evolve from existing genetic material and because the external environment places constraints on which variations survive.

If evolution limits what creatures can look like and neurobiology dictates how languages work, perhaps our genes constrain the range of possible human cultures. “Some cultural forms will never be considered. … These can be thought of as impossible cultures,” writes Marc D. Hauser, a professor of psychology and human evolutionary biology at Harvard.

{ The Wilson Quarterly | Continue reading }

artwork { Ana Bagayan }

The perception and recognition of faces is crucial for the social situations we encounter every day. From the moment we are born, we prefer looking at faces than at inanimate objects, because the brain is geared to perceive them, and has specialized mechanisms for doing so. Such is the importance of the face to everyday life, that we see faces everywhere, even when they are not there.

We know that the ability to recognize faces varies among individuals. Some people are born with prosopagnosia, the inability to recognize faces, and others acquire the condition as a result of brain damage. At the other end of the scale are people who never forget a face - the so-called “super-recognizers”. Two independent studies published recently now provide strong evidence that the ability to recognize faces is largely inherited, and that it is passed on independently from intelligence and other cognitive functions.

{ Neurophilosophy/ScienceBlogs | Continue reading }

photo { Diane Arbus, NYC, 1960 }

Over the past quarter century, DNA evidence has transformed criminal justice, freeing hundreds of innocent people and helping unravel countless crimes that might otherwise have gone unsolved. It has also captivated the public imagination: the plots of popular TV crime shows often hinge on the power of DNA to crack impossible cases, which has helped to give this forensic tool an air of infallibility—a phenomenon known in criminal justice circles as “the CSI effect.” This failsafe image is not entirely unfounded, especially when it comes to traditional applications of DNA evidence.

But increasingly DNA is being used for a new purpose: to target the culprits in cold cases, where other investigative options have been exhausted. All told, U.S. law enforcement agencies have conducted more than 100,000 so-called cold-hit investigations using the federal DNA database and its state-level counterparts, which hold upward of 7.6 million offender profiles. In these instances, where the DNA is often incomplete or degraded and there are few other clues to go on, the reliability of DNA evidence plummets—a fact that jurors weighing such cases are almost never told. As a result, DNA, a tool renowned for exonerating the innocent, may actually be putting a growing number of them behind bars.

{ Washington Monthly | Continue reading }

The promise—and the hype—of changing your DNA through behavior.

Studies showing how experience alters genes have been few and far between—which is why a new one on smoking and diet caught my eye.

The study of these kinds of changes in genes is called epigenetics. Crucially, the changes do not involve alterations of gene sequences, those famous A’s, T’s, C’s, and G’s that the Human Genome Project figured out. (…)

Scientists are now making specific, actionable discoveries in epigenetics. This week, for instance, researchers are reporting that eating leafy green vegetables, folate (found in these veggies as well as in some fruits and in dried beans and peas), and multivitamins can affect the epigenetics of genes involved in lung cancer in a way that could reduce the risk of getting the disease, especially from smoking.

{ Sharon Begley/Newsweek | Continue reading }

A new way of using the genetic code has been created, allowing proteins to be made with properties that have never been seen in the natural world. The breakthrough could eventually lead to the creation of new or “improved” life forms incorporating these new materials into their tissue.

In all existing life forms, the four “letters” of the genetic code, called nucleotides, are read in triplets, so that every three nucleotides encode a single amino acid.

Not any more. Jason Chin at the University of Cambridge and his colleagues have now redesigned the cell’s machinery so that it reads the genetic code in quadruplets.

In the genetic code that life has used up to now, there are 64 possible triplet combinations of the four nucleotide letters; these genetic “words” are called codons. Each codon either codes for an amino acid or tells the cell to stop making a protein chain. Now Chin’s team have created 256 blank four-letter codons that can be assigned to amino acids that don’t even exist yet.

{ NewScientist | Continue reading }

photo { Maria Petschnig, Born to Perform, 2009 }

You can’t buy happiness, but you can at least inherit it, said British and Australian researchers, after studying a thousand pairs of identical and non-identical twins. Their Eureka! on happiness is: Genes control half the personality traits that make people happy, while factors such as relationships, health and careers are responsible for the rest of our well-being.

The researchers identified common genes in identical twins that result in certain personality traits and predispose people to happiness. Sociable, active, stable, hardworking and conscientious people tend to be happier, the researchers reported in Psychological Science.

{ The Hindu | Continue reading }

More than a century ago, an Irish economist named Francis Edgeworth imagined a futuristic device that he called a hedonimeter. It would be, Edgeworth speculated, “an ideally perfect instrument, a psychophysical machine.” His hedonimeter would measure happiness by “continually registering the height of pleasure experienced by an individual.”

This may sound more like something out of science fiction than an idea from the annals of economic history. But Edgeworth’s fantasy grew out of his utilitarian approach to economics, with its assumption that the best way to make choices and allocate resources was to aim to maximize happiness in society. Today, the idea that happiness can indeed be measured and quantified remains at the heart of a new science of happiness.

Over the last few decades, psychologists, neuroscientists, sociologists, behavioral economists and other social scientists have been busy using cold, hard data to try to fill in some of the blank spaces on the map of human happiness. It turns out that no hedonimeter is necessary. Much of the latest data on happiness is generated simply by asking people how they feel. (…)

As historian of happiness Darrin McMahon said in a paper he presented at a 2006 Notre Dame conference on the subject, people “have never been as preoccupied, never been as obsessed, I would argue, with happiness as they are right now.”

{ University of Notre Dame | Continue reading }

read more { Happiness: Cognition, Experience, Language | Collegium, Volume 3, 2008 }

If there’s one thing that’s certain, it’s that humans, like other living things, will continue to evolve. “Evolution is unstoppable,” says Lawrence Moran of the University of Toronto in Canada. But that doesn’t mean that humans are marching on a path toward becoming giant-brained, telepathic creatures out of Star Trek. All it means is that the human genome will continue to change from generation to generation.

Each baby’s DNA carries about 130 new mutations. Most of them have no effect on our well-being. People can pass these neutral mutations down to their offspring without harm, and over time, a small fraction of them will end up spreading across entire populations, or even the entire species, thanks to random luck.

{ Carl Zimmer | Continue reading }

photo { Shooting the ‘Decade From Hell’ cover photo. }

related { If Darwin didn’t rock your world, this should. }