Links for Keyword: Genes & Behavior

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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

Jennifer Couzin-Frankel In the fall of 2008, Stephen Kingsmore, a longtime gene hunter, was approached by two biotech entrepreneurs. One of them, Craig Benson, had just learned that his 5-year-old daughter had juvenile Batten disease, a rare, fatal, inherited, neurological disorder. The pair had a question for Kingsmore: Could he develop a cheap, reliable genetic test for Batten and other equally horrible diseases, available to all parents to prevent the conception or birth of affected children? Their goal was simple: Do everything possible to eradicate these diseases, because, knowing now which genes cause them, we can. At the time this kind of screening, called carrier testing, was relatively uncommon. Both parents need to carry the same mutated gene for their child to develop a disease like Batten, and many of these recessive diseases are vanishingly rare. The number of affected children born each year can be in the single digits. Given that, it hasn't made fiscal sense to offer tests for dozens of diseases to everyone when so few couples will be carriers of any given one. In communities in which certain mutated genes pop up more often, such as Ashkenazi Jews, carrier testing has been common for years and has drastically reduced the number of babies born with diseases like Tay-Sachs. But DNA sequencing technology was moving fast and costs were dropping. What the two men proposed might now be doable, Kingsmore thought. He took on the project. © 2011 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: 14877 - Posted: 01.17.2011

By Tina Hesman Saey Standing over Darwin’s grave in Westminster Abbey, Andrew Feinberg had a realization. Feinberg, a genetics researcher at Johns Hopkins University in Baltimore, looked to the left and saw Newton’s grave. Just above Newton is a plaque honoring physicist Paul Dirac, a pioneer of quantum theory. Inherent in quantum theory is the idea of uncertainty in the interaction of subatomic particles. “So I look back at Darwin’s grave and it hits me; there’s nothing like that in biology,” Feinberg says. Nothing that deals with uncertainty. Yet there is uncertainty in biology. Genes that run in families explain only some of the wide variety of physical appearances among people and their susceptibility to diseases. Much uncertainty in what causes these differences remains. But biologists don’t just accept this seeming randomness as a fundamental part of reality. Instead, they are seeking an explanation for unknown sources of variation in heritable traits, the way physicists are searching for a mysterious substance dubbed dark matter that could explain puzzling aspects of the cosmos. And biologists have proposed some solutions. Feinberg’s, scribbled down at a pub in the shadow of the Tower of London, is that chemical modifications to DNA could be the genetic dark matter. Feinberg is in the minority, though; others have their own favorite theories about what the missing ingredient might be. Some think that researchers just need to hunt harder and longer for common changes in the sequence of genetic letters that make up DNA. But a growing number of researchers are turning to rare genetic changes or absent or duplicated chunks of DNA as important contributors. Others say that interactions among genes deserve more attention. © Society for Science & the Public 2000 - 2010

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: 14735 - Posted: 12.04.2010

by Bob Holmes, Eugene, Oregon EXTROVERTS are born not made - or at least, that's what they say. But what if it's more subtle than that? What if we tailor our personalities to our surroundings to make the most of our genes? Conventional comparisons between identical and fraternal twins indicate that nearly half of individual differences in personality traits have some underlying genetic cause. So people have tended to think of personality traits as largely determined by genes, says evolutionary psychologist Aaron Lukaszewski of the University of California at Santa Barbara. He felt there was a flaw in this thinking: if personality were rigidly determined, individuals could end up with the "wrong" personality type for their circumstances. Being extrovert, for instance, exposes people to social conflict. Wimpy men are more likely to suffer in such encounters, while hunkier men may benefit from putting good genes on display. To avoid mismatches, Lukaszewski reasoned, evolution must have favoured a more flexible system. To test this idea, he measured the strength of 85 male and 89 female students and asked them to rate their own attractiveness relative to their peers. Then he gave each a standard personality test to measure how extrovert they were. Sure enough, stronger and more attractive men, and more attractive women, were more extrovert, Lukaszewski reported at a June meeting of the Human Behavior and Evolution Society in Eugene, Oregon. © Copyright Reed Business Information Ltd.

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: 14230 - Posted: 07.06.2010

Greg Miller Michael Meaney and Moshe Szyf work in the same Canadian city, but it took a chance meeting at a Spanish pub more than 15 years ago to jump-start a collaboration that helped create a new discipline. Meaney, a neuroscientist at the Douglas Mental Health University Institute in Montreal, studies how early life experiences shape behavior later in life. Across town at McGill University, Szyf is a leading expert on chemical alterations to DNA that affect gene activity. Sometime in the mid-1990s, both men attended the same meeting in Madrid and ended up at a bar talking and drinking beer. "A lot of it," Szyf recalls. Meaney told Szyf about his findings that rat pups raised by inattentive mothers tend to be more anxious as adults than pups raised by more nurturing mothers. He also described how the activity of stress-related genes was altered in the undernurtured pups. At some point in the conversation, Szyf had a flash of insight: This difference must be due to DNA methylation—the chemical alteration he had been studying in stem cells and tumor cells. The idea cut against the conventional thinking in both fields. In neuroscience, the prevailing wisdom held that long-term changes in behavior result from physical changes in neural circuits—such as when neurons build new synapses and become more sensitive to messages from their neighbors. And most scientists who studied DNA methylation thought the process was restricted to embryonic development or cancer cells. © 2010 American Association for the Advancement of Science. All Rights Reserved.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 14221 - Posted: 07.03.2010

By NICHOLAS WADE Researchers studying the social behavior of ants have found that a single gene underlies both the aggressive behavior of the ant colony’s soldiers and the food gathering behavior of its foraging caste. The gene is active in soldier ants, particularly in five neurons in the front of their brain, where it generates large amounts of its product, a protein known as PKG. The exact amount of the protein in the ants’ brains is critical to their behavior. Low levels of PKG predispose both castes of ant to foraging; high levels make the soldiers fight and the foraging caste less interested in food gathering, Christophe Lucas and Marla B. Sokolowski report in the current issue of The Proceedings of the National Academy of Sciences. The soldier and foraging castes in the species of ant under study, known as Pheidole pallidula, have their career choices settled in infancy when they start to be fed different diets. The soldiers develop large heads and jaws, and go on to guard the colony and kill invaders. The foragers, who remain small, specialize in looking for food and bringing back prey to the nest. Copyright 2009 The New York Times Company

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: 12705 - Posted: 06.24.2010

By Jeff Wheelwright Pecos Road runs due west along the southern boundary of Phoenix. On the city side of the road, new subdivisions of retirement homes are pushing up their tile roofs like mushrooms that sprout with no rain. On the other side of the road lies the flat scrub of the Gila River Indian Community, some 600 square miles, most of it empty. The reservation shimmers out of the reach of the builders like a desert mirage. This land was no good to anyone in 1859, when it was allocated to the Pima Indians. Today it has 13,000 Native American residents, living in squat cinder-block houses in scattered, dusty hamlets; three casinos that have boosted the tribal income to $100 million annually from $4 million; irrigated cotton, alfalfa, and citrus, for Pimas were always farmers; and a hospital and two kidney-dialysis clinics, with another medical clinic in the planning stage. Kidney failure is a deadly complication of diabetes, and Pimas, so far as scientists can tell, have the world’s highest rate of type 2 diabetes. The Pimas have grown to hate this superlative perhaps more than the disease itself. Mary Thomas, the 60-year-old ex-governor of the tribe and presently its lieutenant governor, drove me around the community. A few miles south of Pecos Road, we came to the St. Johns Mission, a quiet, whitewashed church. There was once a Catholic boarding school for Indian children on the grounds. Thomas said that when she was 17 and in school here, she went for an eye test and was told she had diabetes. © 2004 The Walt Disney Company. All rights reserved

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 7226 - Posted: 06.24.2010

Heidi Ledford Networks of genes linked to obesity have been uncovered.GettyResearchers have used a new technique to identify networks of genes linked to obesity in both mice and humans. The procedure is more comprehensive than the traditional method of hunting for genes associated with disease, and is already being used to identify new drug targets. Over the past year, a flurry of studies have revealed genetic variations associated with disease. These ‘genome-wide association studies’ have been used to find variants associated with everything from heart disease to diabetes (See Genome studies: Genetics by numbers). Traditionally, single genes are linked with particular diseases by locating genetic variants present in people who have the disease and identifying the part of a chromosome associated with that disease. Then researchers have to track down the gene on the chromosome, without knowing what it does or why it would be involved. Eric Schadt of Rosetta Inpharmatics, a subsidiary of Merck Pharmaceuticals in Seattle, Washington, lead one of the research teams involved in the new work. He likens the traditional approach to finding a simple light switch for a disease: flipping this single gene switch on or off may produce a higher or lower risk of disease. The new approach looks at changes in expression of already-known genes, and finds networks of genes associated with disease, rather than single switches. “Instead of the simple ‘turn the light on or off’ analogy, we would view this as a network of these switches,” says Schadt. © 2008 Nature Publishing Group

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 11421 - Posted: 06.24.2010

— By studying gene mutations in patients with the complex set of behavioral and neurological symptoms that accompany Rett syndrome, Howard Hughes Medical Institute investigator Huda Zoghbi and her colleagues at Baylor College of Medicine have designed a mouse model that faithfully recapitulates the disease down to its distinctive hand-wringing behavior. The development of the mouse, reported in the July 18, 2002 issue of the journal Neuron, provides a springboard into the study of Rett syndrome, the leading cause of mental retardation in girls. First recognized as a syndrome in the 1980s, the disorder affects one in 10,000-15,000 girls. It is particularly devastating for families with affected children because infants are seemingly normal at birth and achieve the usual developmental milestones for the first few months of life. Then, as the infant reaches toddlerhood, a sudden and dramatic decline in physical and mental capabilities takes hold, accompanied by onset of seizures, irregular breathing, awkward gait, and hand-wringing. “I know of no other neurological disease that gives this distinctive stereotypic behavior — this hand-wringing these girls do basically all the time they are awake,” said Zoghbi. “With this mouse model we can now ask, ‘Why is that?’” ©2002 Howard Hughes Medical Institute

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: 2332 - Posted: 06.24.2010

First fruits of the genome project identify genes in flies bred for a behavioral preference SAN DIEGO – From Triple Crown winner Seattle Slew to Yorkshire ‘lowfat' pigs, people have been breeding animals and plants for desirable traits since prehistoric times. But there has been no easy way of telling which genes have been favored by the selective breeding. Until now. By making use of the new technique of DNA microarrays ("chips"), a team of scientists lead by Ralph J. Greenspan at The Neurosciences Institute has discovered a way of solving the conundrum of identifying which genes have changed when breeding for a particular trait. In their study of two strains of the common fruit fly (Drosophila melanogaster), selected for differences in their response to gravity ("geotaxis”), they have found that the difference is due to small contributions from many genes, and they have identified several of the genes, two of which have human genetic counterparts.

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: 2196 - Posted: 06.24.2010

Ewen Callaway A handful of genes could mark the difference between high-strung Chihuahuas and unflappable basset hounds. A comparison of 148 dog breeds has uncovered genes for size, lifespan, and even complex behaviours such as pointing and herding. Geneticists have previously uncovered genes for dog traits such as coat colour and narcolepsy, but these searches tended to focus on a single breed, comparing pooches with variations in a single trait – for example, boxers with and without white spots. This strategy does not work for rooting out the genetic basis of behaviours because certain breeds either display these behaviours or they don't, says Gordon Lark at the University of Utah in Salt Lake City, US. So with the help of a dog show judge, Lark's team scored dogs from 148 breeds for traits including herding, pointing, boldness, excitability and trainability. Then they scoured their genomes for similarities and differences. Dogs were also scored for size, body proportions and longevity. The search implicated several genes in stereotypical dog behaviours. For example, herding behaviour typical of collies and shepherds may be linked to a gene that is similar to one associated with schizophrenia in humans. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 11729 - Posted: 06.24.2010

BETHESDA, Md. – Researchers have identified a novel gene mutation that causes X-linked mental retardation for which there was no previously known molecular diagnosis, according to an article to be published electronically on Tuesday, March 20, 2007 in The American Journal of Human Genetics. Investigators F. Lucy Raymond (Cambridge Institute of Medical Research, University of Cambridge, Cambridge, UK) and Patrick S. Tarpey (Wellcome Trust Sanger Institute, Hixton, UK) describe the ZDHHC9 gene found in those with severe retardation as being mutated to the point of entirely losing function. "ZDHHC9 is a novel gene," explains Dr. Raymond. "This gene would not have been predicted to play a role in mental retardation based on the previous genetics work. It was found only because we were systematically looking at all the genes on the X chromosome irrespective of what they do." X-linked mental retardation is severe. Some patients require total care and may not have language ability. The condition runs in families and only affects the male offspring. So far only a few of these genes have been identified. Working through a large, international collaboration, the researchers collected genetic samples from 250 families in which at least two boys have mental retardation to help identify novel genes that cause X-linked mental retardation. The investigators systematically analyzed the X chromosome for gene mutations.

Related chapters from BP7e: Chapter 1: Biological Psychology: Scope and Outlook; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior; Chapter 13: Memory, Learning, and Development
Link ID: 10116 - Posted: 06.24.2010

By comparing foxes selected for tameness with others that have not been selected in this way, researchers have found evidence that dramatic behavioral and physiological changes accompanying tameness may be associated with only limited changes in gene activity in the brain. The work is reported by Elena Jazin and colleagues at Uppsala University, the Swedish University of Agricultural Sciences, and the Norwegian University of Life Science. The first step in the process of domestication in mammals is the selection for tame individuals that can adapt to life with humans and to frequent handling. To investigate the changes in gene activity that accompany tameness, in the present study the authors compared two groups of farm-raised silver foxes (Vulpes vulpes). One group derived from a long-standing domestication process in which farm-raised silver foxes have been selected for more than 40 generations for non-aggressive behavior toward men (see the related work of Brian Hare and colleagues, Current Biology 15:226–230). Another group of foxes was also farm raised but was not selected for tameness. The foxes selected for tameness were docile and friendly and showed developmental, morphological, and neurochemical changes similar to those observed in other domestic animals.

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 0:
Link ID: 8212 - Posted: 06.24.2010

SEATTLE – One teenager likes to snowboard off a cliff. Another prefers to read a book and wouldn't think of trading places. Why these differences exist is a mystery, but for the first time researchers have identified a possible genetic explanation behind risk-seeking behavior. Scientists at Fred Hutchinson Cancer Research Center have found that a specific neurodevelopmental gene, called neuroD2, is related to the development of an almond-shaped area of the brain called the amygdala, the brain's emotional seat. This gene also controls emotional-memory formation and development of the fear response, according to research led by James Olson, M.D., Ph.D., associate member of the Clinical Research Division at the Hutchinson Center. The findings will be published in the early online edition of the Proceedings of the National Academy of Sciences the week of Sept. 26. Olson and colleagues studied mice with a single copy of the neuroD2 gene and found they had an impaired ability to form emotional memories and conditioned fear. "Most of us are familiar with the fact that we can remember things better if those memories are formed at a time when there is a strong emotional impact – times when we are frightened, angry or falling in love," he said. "That's called emotional-memory formation. The amygdala is the part of the brain that is responsible for formation of emotional memory."

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 7956 - Posted: 06.24.2010

Antwerp, Belgium – Neuralgic Amyotrophy is a painful disorder of the peripheral nervous system. This heritable disease causes prolonged acute attacks of pain in the shoulder or arm, followed by temporary paralysis. Researchers from the Flanders Interuniversity Institute for Biotechnology (VIB) connected to the University of Antwerp, have uncovered a small piece of the molecular puzzle of this disease by identifying the defects in the gene responsible for this disorder. Hereditary Neuralgic Amyotrophy (HNA) is characterized by repeated attacks of pain in a shoulder, arm, and/or hand, followed by total or partial paralysis of the affected area. The pain and the loss of movement usually disappear within a couple of weeks, but sometimes recovery can take months or even several years. Many HNA patients also have particular facial features, such as eyes that are somewhat closer together, a fold in the upper eyelid that covers the inside corner of the eye, and sometimes a cleft palate. HNA is a relatively rare disorder: the disease appears in some 200 families worldwide. There is also a non-hereditary form of HNA, called the Parsonage-Turner Syndrome. The clinical picture of this more frequently occurring form - 2 to 4 cases per 100,000 persons - is not distinguishable from that of the heritable form. The attacks of pain are usually provoked by external factors such as vaccination, infection, operation, and even pregnancy or childbirth. By virtue of their genetic predisposition, carriers of the hereditary form of HNA run greater risk of having an attack.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7947 - Posted: 06.24.2010

CAMBRIDGE, Mass., –- Scientists working with salmon have found that gene expression in the brain can differ significantly among members of a species with different life histories. Their study indicates that roughly 15 percent of Atlantic salmon genes show differential expression in males who migrate from their freshwater birthplaces to mature in oceans versus those who do not leave the freshwater environment to mature. The researchers, at Harvard University, the University of Massachusetts and the US Geological Survey, report the finding in the current issue of Proceedings of the Royal Society B. They compared female salmon, male salmon that will eventually undertake the well-known journey from their river birthplaces to oceans –- and then migrate heroically back upstream one to three years later to spawn –- and males of the same age known as "sneakers" that mature at greatly reduced size without leaving freshwater. "The finding that hundreds of the nearly 3,000 genes we studied were expressed differently in the brains of sneakers and other male salmon came as a surprise," says Nadia Aubin-Horth, a postdoctoral researcher in the Bauer Center for Genomics Research in Harvard's Faculty of Arts and Sciences. "Since these males of the same species in the same wild environment differed only in their life history, we did not expect the expression of so many of their genes to differ." Aubin-Horth and her colleagues were also surprised by some of the 17 separate classes of genes demonstrating differing activity levels.

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: 7667 - Posted: 06.24.2010

Durham, N.C. – A gene that plays many fundamental roles in cells throughout the body has, for the first time, been implicated in human disease, according to researchers at the Duke Center for Human Genetics. A defect in the ubiquitous gene dynamin 2 underlies one form of the prevalent, familial nerve disorder, known as Charcot-Marie-Tooth disease (CMT). The disorder affects approximately 1 in every 2,500 people, making it one of the most common of all hereditary disorders, said the researchers. Their findings also reveal a previously unknown link between CMT and a deficiency of white blood cells, suggesting that defects in dynamin 2 might underlie both conditions, the researchers reported in the Jan. 30, 2005, issue of Nature Genetics. The discovery -- together with earlier findings of genes that can also cause the genetically heterogeneous and debilitating disease -- is providing new insight into the nervous system, said first author of the study Stephan Zchner, M.D., assistant professor of psychiatry and member of the Duke Center for Human Genetics. Also, he said, the findings bring a better understanding of the types of defects that might, in general, lead to peripheral nerve disorders. © 2001-2005 Duke University Medical Center

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: 6791 - Posted: 06.24.2010

BOSTON- Researchers at Dana-Farber Cancer Institute have compiled the first atlas showing the locations of crucial gene regulators, or switches that determine how different parts of the brain develop – and, in some cases, develop abnormally or malfunction. The scientists say the map will accelerate research on brain tumors and neurological diseases that result from mutations in these switch genes – called "transcription factors." When these genes are altered, the genes they control can go awry, causing abnormalities in the development or function of nerves and related structures. Although the gene regulators were pinpointed using mouse brains, the map applies to the human brain as well. "This is the first systematic mapping of all of the major brain areas that shows what regulatory genes are expressed in those specific locations," said Quifu Ma, PhD, of Dana-Farber's Cancer Biology Department. He is senior author of a paper appearing in today's online issue of the journal Science, along with Charles D. Stiles, PhD, also of Dana-Farber. Transcription factors are genes that control the expression, or activity, of "target" genes. These factors play a pivotal role in brain development by direction the formation of neurons and supporting cells called glia from uncommitted progenitor cells. Until now, brain transcription factors had not been systematically isolated and their locations within different parts of the brain pinned down.

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: 6617 - Posted: 06.24.2010

Female mice that are abnormally small due to gene "knockout" technology are also bad mothers whose poor parenting skills cause their young to die within a day or two of birth, scientists report this week in the on-line edition of the Proceedings of the National Academy of Sciences. Since Chawnshang Chang, Ph.D., cloned the gene for testicular orphan receptor 4 (TR4) 10 years ago, he and other scientists have tried to learn its function – scientists call it an "orphan" receptor because they don't know what protein links up with it. So a team led by Chang, director of George Whipple Laboratory for Cancer Research at the University of Rochester Medical Center, knocked out the gene in mice, then watched what happened. They found that many of the mice died before birth. Those that lived are markedly smaller than their normal counterparts: They're born far smaller and then make up some of the difference as they grow, but generally they are about 20 to 30 percent smaller by the time they reach adulthood. The miniature mice are not as fertile as normal mice, having only about half the offspring as other mice. Most visibly, the females have very bad parenting skills: They don't build nests, nurse their young, or tend to their offspring, which die within a day or two as a result.

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 8: Hormones and Sex
Link ID: 6255 - Posted: 06.24.2010