Links for Keyword: Genes & Behavior

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by Kai Kupferschmidt Those palm readers predicting your age from your lifeline are making it up. But now scientists say they have found a true lifeline in the cells of Zebra finches. The birds with the longest telomeres—the protective caps at the ends of chromosomes—live the longest, according to a new study. "It is the first time this has been shown for any species," says María Blasco, a telomere researcher at the Spanish National Cancer Research Centre in Madrid, who was not involved in the work. Telomeres are repetitive DNA sequences that, together with some proteins, sit at the ends of chromosomes to keep them from fraying. They have long been known to shorten with age, and when they reach a critical length, cells stop dividing. While abnormally short telomeres have been implicated in some diseases, studies investigating whether longer telomeres lead to a longer life have shown mixed results. Now biologist Pat Monaghan and her colleagues at the University of Glasgow in the United Kingdom have come up with the best evidence yet that telomere length correlates with life span. The scientists measured telomere length in red blood cells of 99 captive zebra finches (Taeniopygia guttata). The birds resemble long-lived animals in that there is little restoration of telomeres in body cells as they age. The first measurement was taken at 25 days; the researchers then followed the birds over their natural life span, ranging from less than a year to nearly 9 years, and measured telomeres again at various time points. They found a highly significant correlation between telomere length at 25 days and life span; birds with longer telomeres lived longer. Length measured at 1 year also predicted life span, but the relationship was weaker, whereas at later time points (after 3, 4, 6, and 7 years) there was no correlation, the team reports online today in the Proceedings of the National Academy of Sciences. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16239 - Posted: 01.10.2012

By Virginia Hughes Among the bloodletting boxes, ether inhalers, kangaroo-tendon sutures and other artifacts stored at the Indiana Medical History Museum in Indianapolis are hundreds of scuffed-up canning jars full of dingy yellow liquid and chunks of human brains. Until the late 1960s the museum was the pathology department of the Central Indiana Hospital for the Insane. The bits of brain in the jars were collected during patient autopsies performed between 1896 and 1938. Most of the jars sat on a shelf until the summer of 2010, when Indiana University School of Medicine pathologist George Sandusky began popping off the lids. Frustrated by a dearth of postmortem brain donations from people with mental illness, Sandusky—who is on the board of directors at the museum—seized the chance to search this neglected collection for genes that contribute to mental disorders. Sandusky is not alone. Several research groups are now seeking ways to mine genetic and other information hidden in old, often forgotten tissue archives—a handful of which can be found in the U.S., along with many more in Europe. Several technical hurdles stand in the way, but if these can be overcome, the archives would offer several advantages. Beyond supplying tissues that can be hard to acquire at a time when autopsies are on the decline, the vintage brains are untainted by modern psychiatric drugs and are often paired with detailed clinical notes that help researchers make more accurate post hoc diagnoses. © 2012 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 16234 - Posted: 01.10.2012

Heidi Ledford Protective caps known as telomeres that help to preserve the integrity of chromosomes can also predict lifespan in young zebra finches (Taeniopygia guttata), researchers have found. Telomeres are stretches of repetitive DNA sequence that are found at the ends of chromosomes, where they help to maintain cell viability by preventing the fraying of DNA and the fusion of one chromosome to another. The relationship between normal ageing and telomere decline has long been suspected — and even asserted by some companies that measure customers’ telomere length — but the link remains unproven in humans (see 'Spit test offers guide to health'). Most studies of longevity and telomere length have relied on only one or two measurements from an individual during their lifespan. But population ecologist Pat Monaghan of the University of Glasgow, UK, and her colleagues found that measuring telomere length periodically over the course of a zebra finch’s life revealed a tight association between length and lifespan — particularly when those measurements were taken when the birds were only 25 days old. The results are reported online this week in Proceedings of the National Academy of Sciences1. “This study is important,” says María Blasco, a telomere researcher at the Spanish National Cancer Research Centre in Madrid. “It’s the first time that normal differences in telomere length have been shown to be predictive of longevity.” Blasco was not involved in the current study, but serves as chief scientific adviser for Madrid-based company Life Length, which advertises telomere length measurements as a service for determining an individual’s "biological age". © 2012 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16233 - Posted: 01.10.2012

By Tina Hesman Saey By kick-starting a gene that is naturally inactivated, chemotherapy drugs could help reverse a genetic brain disorder that is sometimes mistaken for autism or cerebral palsy. The unexpected finding may also spark a new avenue of research on a type of gene regulation known as imprinting. The genetic disorder, Angelman syndrome, occurs in about one in 15,000 live births. It is caused when the copy of a gene called UBE3A inherited from the mother goes missing or is damaged by a mutation. That’s a problem because the copy of the gene inherited from the father is already turned off in brain cells, leaving no way to make UBE3A protein. Genes such as UBE3A that turn off one parent’s copy are called imprinted genes. Until now, researchers knew of no way short of gene therapy to override the imprinting and restore gene activity. Now, researchers from the University of North Carolina at Chapel Hill have discovered that a type of chemotherapy drug called topoisomerase inhibitors can turn on the father’s inactive copy of the gene in brain cells of mice with a version of Angelman syndrome. The team reports the achievement online December 21 in Nature. The prospect that a drug could correct the underlying defect responsible for Angelman syndrome is exciting, says Stormy Chamberlain, a geneticist at the University of Connecticut Health Center in Farmington. “There’s every reason to have hope that it will help our Angelman syndrome kids,” she says. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16179 - Posted: 12.23.2011

By NICHOLAS WADE Social behavior among primates — including humans — has a substantial genetic basis, a team of scientists has concluded from a new survey of social structure across the primate family tree. The scientists, at the University of Oxford in England, looked at the evolutionary family tree of 217 primate species whose social organization is known. Their findings, published in the journal Nature, challenge some of the leading theories of social behavior, including: ¶ That social structure is shaped by environment — for instance, a species whose food is widely dispersed may need to live in large groups. ¶ That complex societies evolve step by step from simple ones. ¶ And the so-called social brain hypothesis: that intelligence and brain volume increase with group size because individuals must manage more social relationships. By contrast, the new survey emphasizes the major role of genetics in shaping sociality. Being rooted in genetics, social structure is hard to change, and a species has to operate with whatever social structure it inherits. If social behavior were mostly shaped by ecology, then related species living in different environments should display a variety of social structures. But the Oxford biologists — Susanne Shultz, Christopher Opie and Quentin Atkinson — found the opposite was true: Primate species tended to have the same social structure as their close relatives, regardless of how and where they live. © 2011 The New York Times Company

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 16172 - Posted: 12.20.2011

By Tina Hesman Saey Nearly everybody knows that Frank Lloyd Wright designed Fallingwater, the house in Pennsylvania that sits above and appears to cascade into a waterfall. I.M. Pei’s glass pyramid at the Louvre in Paris is similarly famous. And Frank Gehry is widely known for the curvi­linear shining steel Walt Disney Concert Hall in Los Angeles. But most people couldn’t name the contractors and subcontractors responsible for translating those great architects’ blueprints into solid structures. Geneticists have the same problem. Details for erecting an organism’s structure are encoded within DNA, written in chemical subunits designated by the letters A, T, C and G. But it has been hard to say exactly who takes those details and oversees the construction of the organism from proteins and other molecular materials. Only now have scientists begun identifying the previously invisible contractors who make sure that materials get where they are supposed to be and in the right order to build a human being or any other creature. Some of these little-known workers belong to a class of molecules called long intergenic noncoding RNAs. Scientists used to think that these “linc­RNAs” were worthless. As their name suggests, these molecules — at least 200 chemical letters long — do not encode information that the body’s manufacturing machinery can use to cobble together proteins. And the lincRNAs originate in what scientists used to view as barren wastelands between protein-coding genes. But new research is showing that these formerly underappreciated workers have important roles in projects both large and microscopic. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16107 - Posted: 12.03.2011

By Tina Hesman Saey WASHINGTON — Separation anxiety in some children may be due to extra doses of a particular gene. The gene, GTF2I, is located on human chromosome 7. People missing part of the chromosome that contains GTF2I have a condition called Williams syndrome and are generally extra social. On the other hand, people who have extra copies of that part of chromosome 7 may have social and other types of anxiety: About 26 percent of children with an extra copy the region containing GTF2I have been diagnosed by a doctor as having separation anxiety, human geneticist Lucy Osborne of the University of Toronto said November 15 at a press conference at the Society for Neuroscience’s annual meeting. Osborne and colleagues genetically engineered mice to have a duplicate copy or two of GTF2I, or to be missing one copy of the gene, then tested the effect of the gene dosage on separation anxiety with a squeak test. Week-old baby mice separated from their mothers send out ultrasonic distress calls. “It’s a ‘come get me’ signal,” Osborne said. Baby mice with a normal two copies of GTF2I squeaked an average of 192 times over four minutes when removed briefly from their nests. Mice with three or four copies squeaked nearly twice as much, indicating greater anxiety at being separated from their mothers. Mice missing one copy of the gene were a little bit less vocal. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 16051 - Posted: 11.19.2011

By Laura Sanders Human brains all work pretty much the same and use roughly the same genes in the same way to build and maintain the infrastructure that makes people who they are, two new studies show. And by charting the brain’s genetic activity from before birth to old age, the studies reveal that the brain continually remodels itself in predictable ways throughout life. In addition to uncovering details of how the brain grows and ages, the results may help scientists better understand what goes awry in brain disorders such as schizophrenia and autism. “The complexity is mind-numbing,” says neuroscientist Stephen Ginsberg of the Nathan Kline Institute and New York University Langone Medical Center, who wasn’t involved in the studies. “It puts the brain in rarefied air.” In the studies, published in the Oct. 27 Nature, researchers focused not on DNA — virtually every cell’s raw genetic material is identical — but on when, where and for how long each gene is turned on over the course of a person’s life. To do this, the researchers measured levels of mRNA, a molecule whose appearance marks one of the first steps in executing the orders contained in a gene, in postmortem samples of donated brains that ranged in age from weeks after conception to old age. These different patterns of mRNA levels distinguish the brain from a heart, for instance, and a human from a mouse, too, says Nenad Šestan of Yale University School of Medicine and coauthor of one of the studies. “Essentially, we carry the same genes as mice,” he says. “However, in us, these genes are up to something quite different.” © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15961 - Posted: 10.29.2011

Despite vast differences in the genetic code across individuals and ethnicities, the human brain shows a "consistent molecular architecture," say researchers supported by the National Institutes of Health. The finding is from a pair of studies that have created databases revealing when and where genes turn on and off in multiple brain regions through development. "Our study shows how 650,000 common genetic variations that make each of us a unique person may influence the ebb and flow of 24,000 genes in the most distinctly human part of our brain as we grow and age," explained Joel Kleinman, M.D., Ph.D., of the National Institute of Mental Health (NIMH) Clinical Brain Disorders Branch. Kleinman and NIMH grantee Nenad Sestan, M.D., Ph.D. of Yale University, New Haven, Conn., led the sister studies in the Oct. 27, 2011 issue of the journal Nature. genetic difference vs. transcriptional distance colored by race comparison. Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture. For example, overall differences in the genetic code (“genetic distance”) between African -Americans (AA) and caucasians (cauc) showed no effect on their overall difference in expressed transcripts (“transcriptional distance”). The vertical span of color-coded areas is about the same, indicating that our brains all share the same tissue at a molecular level, despite distinct DNA differences on the horizontal axis. Each dot represents a comparison between two individuals. The AA::AA comparisons (blue) generally show more genetic diversity than cauc::cauc comparisons (yellow), because caucasians are descended from a relatively small subset of ancestors who migrated from Africa, while African Americans are descended from a more diverse gene pool among the much larger population that remained in Africa. AA::cauc comparisons (green) differed most across their genomes as a whole, but this had no effect on their transcriptomes as a whole. Source: Joel Kleinman, M.D., Ph.D., NIMH Clinical Brain Disorders Branch

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15960 - Posted: 10.29.2011

By Tina Hesman Saey A genetic variant that makes small tweaks in an important brain protein may cause aging to hit some people’s brains harder than others. Pilots’ performance on a flight simulator test generally declines slightly with age. But a new study shows that pilots with a particular version of a gene called BDNF have a faster drop than others. Researchers also observed a decline in the size of an important learning and memory center in the brains of those with the variant, Ahmad Salehi of the Department of Veterans Affairs Palo Alto Health Care System and Stanford University, and colleagues report online October 25 in Translational Psychiatry. About 38 percent of pilots in the new study carried the variant in either one or both of their copies of the BDNF gene. Over the course of two years the flight simulator scores of all the pilots in the study declined a little with age. But scores of pilots carrying the variant dropped about three times faster than scores of pilots who have the normal version of the gene. The drop in scores was not so dramatic that pilots should be removed from the cockpit, says Salehi. “It certainly did not disable them at all,” he says. But the score drop did reflect a slightly faster decline in factors like reaction time, navigation skills, plane positioning and performance in emergency situations. For some of the pilots, the researchers measured the size of the hippocampus, a structure in the brain that is important for learning and memory. After age 65, men who had the alternate version of the gene also lost more hippocampus volume than men with the normal version of the gene, the researchers found. The size of the hippocampus did not correlate with scores on flight simulator tests, probably because flying a plane requires much more of the brain than just the hippocampus, Salehi says. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 15953 - Posted: 10.27.2011

Jonathan Weitzman As an identical twin, I have always been fascinated by what determines who we are. Nature's clones are never truly identical, so what explains the differences between my brother and myself? How much of our identity is inherited; how much acquired by interacting with the environment? The field of epigenetics, standing at the interface between our environment and our genes, is beginning to offer answers. Epigenetics explores how genetically identical entities, whether cells or whole organisms, display different characteristics, and how these are inherited. The past century witnessed amazing advances in our understanding of genetics, but secrets remain hidden within the genome. Epigenetics research is now blossoming, offering a potential panacea for these post-genome blues. Two timely books open up this emergent field: Epigenetics by Richard Francis and The Epigenetics Revolution by Nessa Carey offer very different takes. Francis's thoughtful and succinct book focuses on the narrative and the excitement of discovery, rather than on the nitty-gritty details at the molecular level. His personal tour includes anecdotes from his travels around the world and allusions to popular culture. Carey's book is more DNA-centric, focusing on epigenetic mechanisms and the chemistry of chromatin, which defines how DNA is packaged around proteins in the nucleus. Her book combines an easy style with a textbook's thoroughness. © 2011 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15857 - Posted: 09.29.2011

By Lauren Ware In a clear Plexiglas laboratory cage, a mouse sleeps. A thin fiber optic cable projects upward from the top of its head and out through the cage’s lid. The cable lights with a pulse of blue light. The mouse continues to sleep; the light continues to pulse. After a few more pulses, the mouse wakes up. It rubs its face, stretches its legs and runs over to its food cup and begins to eat voraciously, as though it were starving. It keeps eating as the blue light pulses. The optical fiber that carries the blue light goes directly into the mouse’s brain. It targets a specific group of brain cells that have been modified to react to light. The experiment uses a technique called optogenetics, developed seven years ago, which can selectively activate or silence groups of nerve cells, or neurons, in real time. And it allows scientists to interact with the brain and begin to map how it works with a degree of detail that was previously unimaginable. That’s what Scott Sternson has done with the apparently starving mouse at Janelia Farm in Ashburn, Va., an interdisciplinary biomedical research center that is part of the Howard Hughes Medical Institute. In fact, this mouse was well fed and should not have been hungry. Sternson’s research group targeted a type of cell called the agouti-related peptide (AGRP) neuron. AGRP cells live in the hypothalamus and have been linked to feeding behavior in other studies. The scientists used a virus to insert the DNA of a light-sensitive protein from bacteria, channelrhodopsin-2, into the AGRP neurons. Some of the AGRP neurons take up the DNA and begin to produce the protein and send it to the cell membrane. When the blue light is flashed into the mouse’s brain via the optical fiber, the protein causes the neurons to move ions across the cell membrane, effectively stimulating them to fire an electrical signal, the action potential, which neurons use to communicate with each other. Sternson found that the more AGRP neurons are stimulated, the more the mouse eats. And as soon as the light stops, so does the feeding. Miller-McCune © 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 15792 - Posted: 09.13.2011

McMaster University researchers have discovered that a key gene may explain why some people are energetic and others find it hard to get moving. The team was working with mice, some of which had two genes removed. The genes control the AMP-activated protein kinase (or AMPK), an enzyme that is released during exercise. While mice like to run, the mice without the genes were not as active as mice with the genes. "While the normal mice could run for miles, those without the genes in their muscle could only run the same distance as down the hall and back," Gregory Steinberg, associate professor of medicine in the Michael G. DeGroote School of Medicine and Canada Research Chair in Metabolism and Obesity, said in a release Monday. "The mice looked identical to their brothers or sisters, but within seconds we knew which ones had the genes and which one didn't." The researchers found the mice without the AMPK genes had lower levels of mitochondria — sometimes described as cellular power plants — and their muscles were less able to take up glucose while they exercised. By removing the genes, the researchers found that AMPK is the key regulator of the mitochondria, said Steinberg. The research is in the current issue of the Proceedings of the National Academy of Sciences. © CBC 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15768 - Posted: 09.06.2011

A new atlas of gene expression in the mouse brain provides insight into how genes work in the outer part of the brain called the cerebral cortex. In humans, the cerebral cortex is the largest part of the brain, and the region responsible for memory, sensory perception and language. Mice and people share 90 percent of their genes so the atlas, which is based on the study of normal mice, lays a foundation for future studies of mouse models for human diseases and, eventually, the development of treatments. Researchers from the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, and from Oxford University in the United Kingdom, published a description of the new atlas in the Aug. 25, 2011, journal Neuron. The study describes the activity of more than 11,000 genes in the six layers of brain cells that make up the cerebral cortex. To map gene activity in all six layers of the mouse cerebral cortex, the research team first micro-dissected the brains of eight adult mice, separating the layers of the cortex. They then purified processed RNAs, including messenger RNA, from each cortical layer. The international collaborators have made the new atlas freely available at http://genserv.anat.ox.ac.uk/layers.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15717 - Posted: 08.25.2011

by Sarah C.P. Williams Lab mice usually take only an occasional jaunt on their exercise wheels. But mice missing a gene called IL-15Rα run for hours each night, a new study reveals. And the gene doesn't just make a difference to mice—it might also be linked to the ability of long-distance athletes to outperform the rest of us. Previous studies had suggested that IL-15Rα is important for muscle strength. In experiments on cells grown in a Petri dish, the gene seemed to control the accumulation of proteins necessary for muscle contraction. But IL-15Rα had never been studied in a living animal. In the new research, physiologist Tejvir Khurana of the University of Pennsylvania and his colleagues genetically engineered mice to lack the IL-15Rα gene. The changes were dramatic. Each night, according to sensors on the wheels in the mice's cages, the modified mice ran six times farther than normal mice. But these behavioral quirks weren't quite enough to convince Khurana of the effect on muscles. Lack of the IL-15Rα gene could just be making the mice jittery or giving them extra energy. So the researchers dissected muscles from the longer-running mice. The muscles sported increased numbers of energy-generating mitochondria and more muscle fibers, indicating that they tired less easily. And when the researchers stimulated them with electricity, the muscles continued to contract for longer than normal, taking longer to use up their energy stores, the team reports today in The Journal of Clinical Investigation. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15572 - Posted: 07.19.2011

Erika Check Hayden Two years ago, 13-year-old Alexis Beery developed a cough and a breathing problem so severe that her parents placed a baby monitor in her room just to make sure she would survive the night. Alexis would often cough so hard and so long that she would throw up, and had to take daily injections of adrenaline just to keep breathing. Yet doctors weren't sure what was wrong. In a paper published today in Science Translational Medicine1, researchers led by Richard Gibbs, head of the Baylor College of Medicine Human Genome Sequencing Center in Houston, Texas, describe how they sequenced the genomes of Alexis and her twin brother, Noah, to diagnose the cause of her cough — a discovery that led to a treatment. Today, Alexis is playing soccer and running, and her breathing problem has gone, says Alexis's mother, Retta. "We honestly didn't know if Alexis was going to make it through this," Retta Beery says. "Sequencing has brought her life back." At age 5, the Beery twins had already been diagnosed with a genetic disorder called dopa-responsive dystonia, which causes abnormal movements, and had been taking a medication that was apparently successfully treating the condition. When Alexis developed a worsening cough and breathing problem, the twins' neurologists did not think it was related to her dystonia. © 2011 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 15433 - Posted: 06.16.2011

By Steve Connor, Science Editor Women have a stronger genetic predisposition to help other people compared with men, according to a study that has found a significant link between genes and the tendency to be "nice". The research, based on an analysis of nearly 1,000 pairs of identical and non-identical twins, found that about half of "prosocial" traits – the willingness to help others – identified in women could be linked with genes rather than environmental upbringing, whereas the figure was just 20 per cent in men. Scientists believe the findings lend further support to the idea that prosocial behaviour has a strong heritable component with some people displaying an innate tendency from childhood. One conclusion from the study, published in the journal Biology Letters, is that some women, and rather fewer men, find it easier than the rest of the population to be generous and helpful towards others, given the right sort of upbringing. "There is a very big debate at the moment about whether humans are altruistic or not," said Gary Lewis, a psychologist at the University of Edinburgh who carried out the research. "There are some people who argue that we have evolved to be altruistic independently of external interventions, and others who argue that we are rather selfish and need a rather conducive external environment for us to be nice to others. ©independent.co.uk

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 14980 - Posted: 02.10.2011

A tiny, translucent water flea that can reproduce without sex and lives in ponds and lakes has more genes than any other creature, said scientists who have sequenced the crustacean's genome. Daphnia pulex, named after the nymph in Greek mythology who transforms into a tree in order to escape the lovestruck Apollo, has 31,000 genes compared to humans who have about 23,000, said the research in the journal Science. Often studied by scientists who want to learn about the effects of pollution and environmental changes on water creatures, the almost-microscopic freshwater Daphnia is the first crustacean to have its genome sequenced. But just because this creature -- viewed as the canary in the gold mine of the world's waters -- has more genes doesn't necessarily mean they are all unique, explained project leader John Colbourne. "Daphnia's high gene number is largely because its genes are multiplying, by creating copies at a higher rate than other species," said Colbourne, genomics director at the Center for Genomics and Bioinformatics. Daphnia has a large number of never-before seen genes, as well as a big chunk of the same genes found in humans, the most of any insects or crustacean so far known to scientists. "More than one-third of Daphnia's genes are undocumented in any other organism -- in other words, they are completely new to science," said Don Gilbert, coauthor and Department of Biology scientist at IU Bloomington. © 2011 Discovery Communications, LLC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14963 - Posted: 02.07.2011

By Neil Bowdler Science reporter, BBC News Researchers in the United States say they have uncovered tentative evidence of a genetic component to friendship. Using data from two independent studies, they found carriers of one gene associated with alcoholism tended to stick together. However, people with another gene linked with metabolism and openness, stayed apart. Details are published in the journal Proceedings of the National Academy of Sciences. The researchers looked at six genetic markers in two long-running US studies, the National Longitudinal Study of Adolescent Health and the Framingham Heart Study, which contain both genetic data and information on friends. With one gene, called DRD2, which has been associated with alcoholism, they found clusters of friends with the very same marker. Another gene called CYP2A6, which has a suspected role in the metabolism of foreign bodies including nicotine, appeared more divisive. People with this gene seemed to steer clear of those who also carry the gene. Why, the researchers don't know, but they speculate it could form part of a defensive ploy. They say similar patterns have been observed among couples, with individuals avoiding prospective partners who are susceptible to the same diseases. BBC © MMXI

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14900 - Posted: 01.21.2011

A person's friends tend to share certain genes in common with each other — but not always with the individual, a new study suggests. "People’s friends may not only have similar traits, but actually resemble each other on a genotypic level," said the study led by James Fowler, a geneticist at the University of California at San Diego. The findings were published Friday in the Proceedings of the National Academy of Sciences. Researchers noticed two distinct patterns within social networks when it came to the genes DRD2, which has been linked to alcoholism, and CYP2AP, which is linked with the character trait of openness. In the case of DRD2, people with the marker tend to make friends with those who also have that marker. People without it tend to make friends with other DRD2-negative individuals. In the case of CYP2A6, the person who has the gene tends to be the hub of a social network made up of people who don't have it and instead share the opposite genotype. Four other genes examined by the researchers did not show such patterns among groups of friends. The analysis found that this gene clustering within social networks was apparent even when the researchers took into account the fact that people are more likely to make friends with people who live near them. The findings suggest that studies linking certain traits to genes may be biased in ways that were not previously anticipated. © CBC 2011

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 0: ; Chapter 13: Memory, Learning, and Development
Link ID: 14885 - Posted: 01.18.2011