Links for Keyword: Genes & Behavior

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Christie Wilcox Adult horsehair worms look about how you’d expect given their name: They’re long, noodlelike creatures that resemble wiggling horse hairs. They live and reproduce in water, but their young only develop inside the bodies of other animals—usually terrestrial insects such as praying mantises. Once they’ve finished growing inside their unwitting vessel, the worms must convince their hosts to drown themselves to complete their life cycle. How these parasites manage to lethally manipulate their hosts has long puzzled scientists. Researchers behind a new study published today in Current Biology suggest horsehair worms possess hundreds of genes that allow them to hijack a mantis’ movement—and they may have acquired these genes directly from their ill-fated hosts. “The results are amazing,” says Clément Gilbert, an evolutionary biologist at the University of Paris-Saclay who wasn’t involved in the work. If it turns out to be true that so many of the mantises’ genes jumped over to the parasitic worms—a process known as horizontal gene transfer—then “this is by far the highest number of horizontally transferred genes that have been reported between two species of animals,” he adds. The phenomenon of parasites mind-controlling their hosts to an early grave has always intrigued Tappei Mishina, an evolutionary biologist at Kyushu University and the RIKEN Center for Biosystems Dynamics Research. “For more than 100 years, there have been horrifying observations of terrestrial insects jumping into water right before our eyes all over the world,” he says. He teamed up with ecologist Takuya Sato of the Center for Ecological Research at Kyoto University to investigate the genetic basis of their parasitism. They focused on horsehair or gordian worms, a group of parasitic animals related to nematodes. Many have complex life cycles involving multiple hosts, and the ones that live in freshwater must generally find their way into an insect to finish developing into adults. The genus Mishina, Sato, and their colleagues specialize in, known as Chordodes, infect mantises and can grow to nearly 1 meter long inside the palm-size insects’ abdomens.

Related chapters from BN: Chapter 6: Evolution of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28971 - Posted: 10.25.2023

By Emily Anthes In creating modern dog breeds, humans sculpted canines into physical specimens perfectly suited for a wide variety of tasks. Bernese mountain dogs have solid, muscular bodies capable of pulling heavy loads, while greyhounds have lean, aerodynamic frames, ideal for chasing down deer. The compact Jack Russell terrier can easily shimmy into fox or badger dens. Now, a large study, published in Cell on Thursday, suggests that behavior, not just appearance, has helped qualify these dogs for their jobs. Breeds that were created for similar roles — whether rounding up sheep or flushing birds into the air — tend to cluster into distinct genetic lineages, which can be characterized by different combinations of behavioral tendencies, the researchers found. “Much of modern breeding has been focused predominantly on what dogs look like,” Evan MacLean, an expert on canine cognition at the University of Arizona who was not involved in the study, said in an email. But, he emphasized, “Long before we were breeding dogs for their appearances, we were breeding them for behavioral traits.” The study also found that many of the genetic variants that set these lineages apart from each other appear to regulate brain development, and many seem to predate modern breeds. Together, the results suggest that people may have created today’s stunning assortment of breeds, in part, by harnessing and preserving desirable behavioral traits that already existed in ancient dogs, the researchers said. “Dogs have fundamentally the same blueprint, but now you’ve got to emphasize certain things to get particular tasks done,” said Elaine Ostrander, a dog genomics expert at the National Human Genome Research Institute and the senior author of the study. “You’re going to tweak a gene up, you’re going to tweak it down.” In an email, Bridgett vonHoldt, an evolutionary biologist at Princeton University who was not involved in the research, called the new paper “a major landmark in the field of dog genomics and behavior. We know it is complicated. This study not only gives us hope, it will be viewed as an inspiration for all in the field.” © 2022 The New York Times Company

Related chapters from BN: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28589 - Posted: 12.10.2022

By James Gorman Don’t judge a book by its cover. Don’t judge a dog by its breed. After conducting owner surveys for 18,385 dogs and sequencing the genomes of 2,155 dogs, a group of researchers reported a variety of findings in the journal Science on Thursday, including that for predicting some dog behaviors, breed is essentially useless, and for most, not very good. For instance, one of the clearest findings in the massive, multifaceted study is that breed has no discernible effect on a dog’s reactions to something it finds new or strange. This behavior is related to what the nonscientist might call aggression and would seem to cast doubt on breed stereotypes of aggressive dogs, like pit bulls. One thing pit bulls did score high on was human sociability, no surprise to anyone who has seen internet videos of lap-loving pit bulls. Labrador retriever ancestry, on the other hand, didn’t seem to have any significant correlation with human sociability. This is not to say that there are no differences among breeds, or that breed can’t predict some things. If you adopt a Border collie, said Elinor Karlsson of the Broad Institute and the University of Massachusetts Chan Medical School, an expert in dog genomics and an author of the report, the probability that it will be easier to train and interested in toys “is going to be higher than if you adopt a Great Pyrenees.” But for any given dog you just don’t know — on average, breed accounts for only about 9 percent of the variations in any given dog’s behavior. And no behaviors were restricted to any one breed, even howling, though the study found that behavior was more strongly associated with breeds like Siberian huskies than with other dogs. And yet, in what might seem paradoxical at first, the researchers also found that behavior patterns are strongly inherited. The behaviors they studied had a 25 percent heritability, a complex measure which indicates the influence of genes, but depends on the group of animals studied. But with enough dogs, heritability is a good measure of what’s inherited. In comparing whole genomes, they found several genes that clearly influence behavior, including one for how friendly dogs are. © 2022 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory and Learning
Link ID: 28309 - Posted: 04.30.2022

By Jonathan Lambert Identical siblings are used to sharing a lot with their twin, including their DNA. But new research suggests all identical twins share a common signature of twinhood, not in their DNA, but on it. This signature is part of the epigenome, chemical markers that dot many spots along DNA and influence the activity of genes without altering their sequence. Identical twins everywhere largely share a specific set of these marks that persists from birth to adulthood, researchers report September 28 in Nature Communications. These shared epigenetic tags could be used to identify people who were conceived as identical twins but lost their sibling in the womb or were separated at birth. “This paper is absolutely fascinating,” says Nancy Segal, a developmental psychologist at California State University, Fullerton who has researched twins but wasn’t involved in the study. The research sets the groundwork for scientists to better understand “what might cause a fertilized egg to split and form monozygotic [identical] twins,” she says. Despite humans’ age-old fascination with identical twins, the biological process that generates them, known as monozygotic twinning, “is an enigma,” says Jenny van Dongen, an epigeneticist at Vrije Universiteit Amsterdam. Researchers know that identical twins form after a fertilized egg, called a zygote, somehow splits into two embryos during development. But why this cleavage happens remains unknown, van Dongen says. For the most part, identical twins don’t run in families, and they occur at roughly the same rate worldwide — about 3 to 4 per 1,000 births. With no clear genetic or environmental cause, the prevailing hypothesis is that identical twins arise at random, she says. © Society for Science & the Public 2000–2021.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28008 - Posted: 09.29.2021

Abby Olena Delivering anything therapeutic to the brain has long been a challenge, largely due to the blood-brain barrier, a layer of cells that separates the vessels that supply the brain with blood from the brain itself. Now, in a study published August 12 in Nature Biotechnology, researchers have found that double-stranded RNA-DNA duplexes with attached cholesterol can enter the brains of both mice and rats and change the levels of targeted proteins. The results suggest a possible route to developing drugs that could target the genes implicated in disorders such as muscular dystrophy and amyotrophic lateral sclerosis (ALS). “It’s really exciting to have a study that’s focused on delivery to the central nervous system” with antisense oligonucleotides given systemically, says Michelle Hastings, who investigates genetic disease at the Rosalind Franklin University of Medicine and Science in Chicago and was not involved in the study. The authors “showed that it works for multiple targets, some clinically relevant.” In 2015, Takanori Yokota of Tokyo Medical and Dental University and colleagues published a study showing that a so-called heteroduplex oligonucleotide (HDO)—consisting of a short chain of both DNA and an oligonucleotide with modified bases paired with complementary RNA bound to a lipid on one end—was successful at decreasing target mRNA expression in the liver. Yokota’s team later joined forces with researchers at Ionis Pharmaceuticals to determine whether HDOs could cross the blood-brain barrier and target mRNA in the central nervous system. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: The Sensorimotor System
Link ID: 27998 - Posted: 09.18.2021

Diana Kwon Susan was still a child when she first suspected something might be wrong with her mother. A cup or plate would often crash to the floor by accident when her mother was serving dinner or washing up dishes. “She was, she would have said, ‘clumsy’, but she wasn’t really clumsy,” says Susan. “Her hands had beautiful, glamorous movements, which I now recognize as early HD.” Huntington’s disease (HD) is an inherited condition that causes widespread deterioration in the brain and disrupts thinking, behaviour, emotion and movement. The disease usually begins in midlife, with subtle changes such as mood swings and difficulty in staying focused. As it progresses, people develop dementia and an inability to speak or move. Susan, who requested that her last name be withheld to protect her privacy, vividly remembers the day she learnt that her mother had the disease. It was the spring of 1982, and her mother had been admitted to a hospital because of her extreme exhaustion, frequent falls and irregular movements. There was no genetic test for the condition at the time, so she underwent a series of assessments. Her neurologist gathered the entire family into a room to break the news. “He told us that our mother had Huntington’s disease,” recalls Susan. “And that there’s no treatment and it can be wiped out in a generation if you just don’t breed.” Those blunt words had a profound impact on the lives of Susan and her siblings: her brother decided never to get married, and her sister chose to be sterilized. For Susan, however, those options were out of reach: she was pregnant when she received the news. © 2021 Springer Nature Limited

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory and Learning
Link ID: 27762 - Posted: 04.08.2021

By Erin Garcia de Jesús One defective gene might turn some bunnies’ hops into handstands, a new study suggests. To move quickly, a breed of domesticated rabbit called sauteur d’Alfort sends its back legs sky high and walks on its front paws. That strange gait may be the result of a gene tied to limb movement, researchers report March 25 in PLOS Genetics. Sauteur d’Alfort rabbits aren’t the only animal to adopt an odd scamper if there’s a mutation to this gene, known as RORB. Mice with a mutation to the gene also do handstands if they start to run, says Stephanie Koch, a neuroscientist at University College London who was not involved with the rabbit work. And even while walking, the mice hike their back legs up to waddle forward, almost like a duck. “I spent four years looking at these mice doing little handstands, and now I get to see a rabbit do the same handstand,” says Koch, who led a 2017 study published in Neuron that explored the mechanism behind the “duck gait” in mice. “It’s amazing.” Understanding why the rabbits move in such a strange way could help researchers learn more about how the spinal cord works. The study is “contributing to our basic knowledge about a very important function in humans and all animals — how we are able to move,” says Leif Andersson, a molecular geneticist at Uppsala University in Sweden. © Society for Science & the Public 2000–2021.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27747 - Posted: 03.27.2021

By Cara Giaimo The rooms that make up the Bloomington Drosophila Stock Center at Indiana University are lined wall to wall with identical shelves. Each shelf is filled with uniform racks, and each rack with indistinguishable glass vials. The tens of thousands of fruit fly types within the vials, though, are each magnificently different. Some have eyes that fluoresce pink. Some jump when you shine a red light on them. Some have short bodies and iridescent curly wings, and look “like little ballerinas,” said Carol Sylvester, who helps care for them. Each variety doubles as a unique research tool, and it has taken decades to introduce the traits that make them useful. If left unattended, the flies would die in a matter of weeks, marooning entire scientific disciplines. Throughout the Covid-19 pandemic, workers across industries have held the world together, taking on great personal risk to care for sick patients, maintain supply chains and keep people fed. But other essential jobs are less well-known. At the Stock Center dozens of employees have come to work each day, through a lockdown and afterward, to minister to the flies that underpin scientific research. Tiny Bug, Huge Impact To most casual observers, fruit flies are little dots with wings that hang out near old bananas. But over the course of the last century, researchers have turned the insect — known to science as Drosophila melanogaster — into a sort of genetic switchboard. Biologists regularly develop new “strains” of flies, in which particular genes are turned on or off. Studying these slight mutants can reveal how those genes function — including in humans, because we share over half of our genes with Drosophila. For instance, researchers discovered what is now called the hippo gene — which helps regulate organ size in both fruit flies and vertebrates — after flies with a defect in it grew up to be unusually large and wrinkly. Further work with the gene has indicated that such defects may contribute to the unchecked cell growth that leads to cancer in people. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 27624 - Posted: 12.15.2020

By Chris Woolston Sometimes it takes multitudes to reveal scientific truth. Researchers followed more than 7,000 subjects to show that a Mediterranean diet can lower the risk of heart disease. And the Women’s Health Initiative enlisted more than 160,000 women to show, among other findings, that postmenopausal hormone therapy put women at risk of breast cancer and stroke. But meaningful, scientifically valid insights don’t always have to come from studies of large groups. A growing number of researchers around the world are taking a singular approach to pain, nutrition, psychology and other highly personal health issues. Instead of looking for trends in many people, they’re designing studies for one person at a time. A study of one person — also called an N of 1 trial — can uncover subtle, important results that would be lost in a large-scale study, says geneticist Nicholas Schork of the Translational Genomics Research Institute in Phoenix. The results, he says, can be combined to provide insights for the population at large. But with N of 1 studies, the individual matters above all. “People differ at fundamental levels,” says Schork, who discussed the potential of N of 1 studies in a 2017 issue of the Annual Review of Nutrition. And the only way to understand individuals is to study them. Case studies of individuals in odd circumstances have a long history in medical literature. But the concept of a clinical medicine N of 1 study gathering the same level of information as a large study goes back to an article published in the New England Journal of Medicine in 1986. Hundreds of N of 1 studies have been published since then, and the approach is gaining momentum, says Suzanne McDonald, N of 1 research coordinator at the University of Queensland in Brisbane, Australia.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27027 - Posted: 02.10.2020

By Tina Hesman Saey Picking embryos based on genetics might not give prospective parents the “designer baby” they’re after. DNA predictions of height or IQ might help would-be parents select an embryo that would grow into a child who is, at most, only about three centimeters taller or about three IQ points smarter than an average embryo from the couple, researchers report November 21 in Cell. But offspring predicted by their DNA to be the tallest among siblings were actually the tallest in only seven of 28 real families, the study found. And in five of those families, the child predicted to be tallest was actually shorter than the average for the family. Even if it were ethical to select embryos based on genetic propensity for height or intelligence, “the impact of doing so is likely to be modest — so modest that it’s not likely to be practically worth it,” says Amit Khera, a physician and geneticist at the Center for Genomics Medicine at Massachusetts General Hospital in Boston who was not involved in the new study. For years, couples have been able to use genetic diagnosis to screen out embryos carrying a disease-causing DNA variant. The procedure, called preimplantation genetic diagnosis, or PGD, involves creating embryos through in vitro fertilization. Clinic staff remove a single cell from the embryo and test its DNA for genetic variants that cause cystic fibrosis, Tay-Sachs or other life-threatening diseases caused by defects in single genes. © Society for Science & the Public 2000–2019

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 26847 - Posted: 11.23.2019

Angela Saini How should we remember historical figures who we know have done terrible things? It’s a dilemma we face more often, as universities and public institutions critically examine their histories, reassessing the past with 21st-century eyes. And over the last year, University College London has been in the midst of a historical inquiry into its role as the institutional birthplace of eugenics – the debunked “science” that claimed that by selectively breeding humans we could improve racial quality. We tend to associate eugenics with Nazi Germany and the Holocaust, but it was in fact developed in London. Its founder was Francis Galton, who established a laboratory at UCL in 1904. Already, some students and staff have called on the university to rename its Galton lecture theatre. Galton’s seductive promise was of a bold new world filled only with beautiful, intelligent, productive people. The scientists in its thrall claimed this could be achieved by controlling reproduction, policing borders to prevent certain types of immigrants, and locking away “undesirables”, including disabled people. University College London is investigating its role as the birthplace of eugenics. In hindsight, it’s easy to say that only a moral abyss could have given rise to such a pseudo-scientific plan, not least because we have borne witness to its horrifying consequences through the 20th century, when it was used to justify genocide and mass sterilisations. And by the standards of today, Galton does resemble a monster. He was a brilliant statistician but also a racist (not just my assessment, but that of Veronica van Heyningen, the current president of the Galton Institute). He was obsessed with human difference, and determined to remove from British society those he considered inferior. © 2019 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 26683 - Posted: 10.09.2019

Bill Sullivan As author George R.R. Martin would attest, good writing takes time. For eons, DNA has been writing genetic scripts for “survival machines,” evolutionary biologist Richard Dawkins’s term for living organisms—their primary purpose being to live long enough to propagate their DNA. As author Samuel Butler recognized in 1877, “A hen is only an egg’s way of making another egg.” But our planet has limited resources, so survival machines that had a leg up on the competition won the DNA replication relay. Selfish genes were locked in an arms race to craft survival machines that were better, stronger, faster. About 600 million years ago, an ancestral neuron emerged that heralded a new weapon: intelligence. It took nearly 4 billion years, but DNA has finally built a survival machine intelligent enough to expose DNA’s game. We are the first species to meet our maker. The realization that we’re an apparatus for the dissemination of genes is quite different from traditional creationist narratives. It is even more humbling to reflect on the power of a related revelation: instead of passively watching genetic stories unfold, we can now become the authors. Are we ready for this awesome responsibility? In just a half century, we resolved the structure of DNA, made genome sequencing easy, and discovered ways to edit genes. Although we don’t fully understand its language, some are now eager to take a red pen to the genome. With the help of the first human genome, published in 2003, researchers have revealed genes involved in certain diseases, and this knowledge is guiding the discovery of novel therapeutics. © 1986–2019 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 26583 - Posted: 09.07.2019

By Dylan Loeb McClain Kary B. Mullis, a biochemist who won the 1993 Nobel Prize in Chemistry for discovering a way to analyze DNA easily and cheaply and thus pave the way for major advances in medical diagnostics, molecular biology and forensic science, died on Aug. 7 at his home in Newport Beach, Calif. He was 74. The cause was heart and respiratory failure brought on by pneumonia, his wife, Nancy Cosgrove Mullis, said. The process for analyzing DNA that Dr. Mullis invented is called polymerase chain reaction, or PCR. It replicates a single strand of DNA millions of times, enabling scientists to pinpoint a segment of the strand and amplify it for identification. Polymerase, an enzyme that synthesizes polymers and nucleic acids, is essential in creating DNA and RNA, the molecules that are responsible for coding DNA. Before PCR, amplifying DNA took weeks, because it had to be generated in bacteria. Once Dr. Mullis’s process was perfected, it took only hours, opening up a world of possibilities. We’ll bring you stories that capture the wonders of the human body, nature and the cosmos. Today, his method is used to detect genetic mutations that can lead to diagnoses of diseases, like sickle cell anemia; analyze ancient sources of DNA, like bones; assist in obtaining crime scene evidence; and determine paternity. It was used as well to decode and map the entire human DNA as part of the Human Genome Project, the landmark international research effort that ran from 1990 to 2003. As he told the story in his Nobel lecture, Dr. Mullis found his inspiration one night in 1983 while driving to his cabin in Mendocino, Calif. © 2019 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 26505 - Posted: 08.16.2019

By Gretchen Reynolds A need and desire to be in motion may have been bred into our DNA before we even became humans and could have helped to guide the evolution of our species, according to a fascinating new study of the genetics of physical activity. The study uses big data and sophisticated genetic analyses to determine that some of the gene variants associated with how much and whether people move seem to have joined our ancestors’ genome hundreds of thousands of years ago, making them integral to human existence and well-being and raising interesting questions about what that means today, when most humans are sedentary. There has been evidence for some time that whether and how much people and other animals move depends to some extent on family history and genetics. Past twin studies and genome-wide association studies — which scan genomes looking for snippets of DNA shared by individuals who also share certain traits — suggest that about 50 percent of physical activity behavior in people may depend on genes. Our tendency to move or not is different from our innate aerobic fitness. Someone could be born with a large inherited endurance capacity and no interest at all in leaving the couch, or vice versa. Little has been known, though, about when any of the gene variants associated with moving became integrated into the human genome, and that question matters. Many of the most common chronic illnesses and conditions in people today, including Type 2 diabetes, obesity, heart disease, osteoarthritis and others, are associated with being inactive. But some other species, including chimps, which share much of our DNA, retain robust good health even when they move relatively little. © 2019 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26234 - Posted: 05.15.2019

By Carolyn Y. Johnson For years, public health experts have been arguing that where people live matters crucially to their health and life span, even though factors such as genetics or access to health insurance typically get more attention. Health systems and governments have embarked on massive projects to decode people’s DNA, in the hopes that the information will lead to a new era of tailored treatments and personalized prevention. It’s the next chapter in the nature-nurture debate: To keep people healthy, is it better to focus on people’s Zip codes or their genetic codes? A new study in Nature Genetics examined 56,000 pairs of twins from a database of 45 million people insured through Aetna to try to answer the question, and found — as might be expected — a mixed picture. Of 560 diseases and conditions studied, 40 percent had some genetic contribution, while a quarter were influenced by shared environment. Cognitive conditions such as attention-deficit/hyperactivity disorder had the strongest genetic influence, while eye disorders and respiratory diseases such as sinusitis or hyperventilation were more influenced by the environment. The relative influence of Zip code or genetic code “is incredibly nuanced. It depends on what disease you’re interested in,” said Chirag Patel, a data scientist at Harvard Medical School who oversaw the work that was led by Chirag Lakhani, a postdoctoral researcher. © 1996-2019 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 25863 - Posted: 01.15.2019

By Elizabeth Pennisi American Kennel Club descriptions of dog breeds can read like online dating profiles: The border collie is a workaholic; the German shepherd will put its life on the line for loved ones. Now, in the most comprehensive study of its kind to date, scientists have shown that such distinct breed traits are actually rooted in a dog’s genes. The findings may shed light on human behaviors as well. “It’s a huge advance,” says Elaine Ostrander, a mammalian geneticist at the National Human Genome Research Institute in Bethesda, Maryland, who was not involved with the work. “It’s a finite number of genes, and a lot of them do make sense.” When the dog genome was sequenced in 2005, scientists thought they would quickly be able to pin down the genes that give every breed its hallmark personality. But they found so much variation even within a breed that they could never study enough dogs to get meaningful results. So in the new study, Evan MacLean, a comparative psychologist at the University of Arizona in Tucson, and colleagues began by looking at behavioral data for about 14,000 dogs from 101 breeds. The analyses come from the Canine Behavioral Assessment & Research Questionnaire (C-BARQ), a sort of pet personality quiz developed by James Serpell, an ethologist at the University of Pennsylvania. C-BARQ asks questions like, “What does your dog do when a stranger comes to the door?” to allow owners to objectively characterize 14 aspects of their pet’s personalities, including trainability, attachment, and aggression. Since the survey was developed in 2003, more than 50,000 owners have participated. © 2018 American Association for the Advancement of Science

Related chapters from BN: 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: 25852 - Posted: 01.09.2019

By Jocelyn Kaiser, Ann Gibbons In early 2017, epidemiologist Rory Collins at the University of Oxford in the United Kingdom and his team faced a test of their principles. They run the UK Biobank (UKB), a huge research project probing the health and genetics of 500,000 British people. They were planning their most sought-after data release yet: genetic profiles for all half-million participants. Three hundred research groups had signed up to download 8 terabytes of data—the equivalent of more than 5000 streamed movies. That's enough to tie up a home computer for weeks, threatening a key goal of the UKB: to give equal access to any qualified researcher in the world. "We wanted to create a level playing field" so that someone at a big center with a supercomputer was at no more of an advantage than a postdoc in Scotland with a smaller computer and slower internet link, says Oxford's Naomi Allen, the project's chief epidemiologist. They came up with a plan: They gave researchers 3 weeks to download the encrypted files. Then, on 19 July 2017, they released a final encryption key, firing the starting gun for a scientific race. Within a couple of days, one U.S. group had done quick analyses linking more than 120,000 genetic markers to more than 2000 diseases and traits, data it eventually put up on a blog. Only 60,000 markers had previously been tied to disease, says human geneticist Eric Lander, president and director of the Broad Institute in Cambridge, Massachusetts. "[They] doubled that in a week." © 2018 American Association for the Advancement of Science

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 25841 - Posted: 01.05.2019

By Amy Harmon It has been more than a decade since James D. Watson, a founder of modern genetics, landed in a kind of professional exile by suggesting that black people are intrinsically less intelligent than whites. In 2007, Dr. Watson, who shared a 1962 Nobel Prize for describing the double-helix structure of DNA, told a British journalist that he was “inherently gloomy about the prospect of Africa” because “all our social policies are based on the fact that their intelligence is the same as ours, whereas all the testing says, not really.” Moreover, he added, although he wished everyone were equal, “people who have to deal with black employees find this not true.” Dr. Watson’s comments reverberated around the world, and he was forced to retire from his job as chancellor of the Cold Spring Harbor Laboratory on Long Island, although he retains an office there. He apologized publicly and “unreservedly,’’ and in later interviews he sometimes suggested that he had been playing the provocateur — his trademark role — or had not understood that his comments would be made public. Ever since, Dr. Watson, 90, has been largely absent from the public eye. His speaking invitations evaporated. In 2014, he became the first living Nobelist to sell his medal, citing a depleted income from having been designated a “nonperson.’’ But his remarks have lingered. They have been invoked to support white supremacist views, and scientists routinely excoriate Dr. Watson when his name surfaces on social media. © 2019 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 25831 - Posted: 01.01.2019

Every August for the past 43 years, Twinsburg, Ohio, has hosted the biggest gathering of twins in the world. Two decades ago, organizers added an attraction to the lineup of parade, talent show and hot-dog dinner that drew more than 2,000 pairs this year: the chance to participate in research. Scientists vie for tent spots to test such things as twins’ exposure to the sun, their stroke risk and their taste preferences. “Every year we get more [research] requests than we can handle,” says Sandy Miller, a Twins Day Festival organizer and mother of 54-year-old twins. “We just don’t have room for all the scientists who want to come.” Since English scientist Francis Galton published a paper on the heritability of traits in 1875, researchers have been fascinated by how the behavior and health of identical twins differ throughout their lifetimes. “Twins are nature’s experiment,” says Australian neuropsychiatrist Perminder Sachdev, who runs the Older Australian Twins Study, which was started 10 years ago and has recruited more that 300 pairs of twins older than 65 to analyze how physical activity, psychological trauma, alcohol use and nutrition affects their brains, psyches, metabolisms and hearts. Because identical twins are the result of a single egg that splits into two, they share the same DNA and provide a perfect laboratory to answer age-old questions about the roles of genes and environment: Why does one twin get breast cancer and not the other? How does obesity increase one’s risk of Type 2 diabetes? Do genetics really determine whether you are more likely to own a gun or go to college? © 1996-2018 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 25509 - Posted: 10.01.2018

Nathaniel Comfort It’s never a good time for another bout of genetic determinism, but it’s hard to imagine a worse one than this. Social inequality gapes, exacerbated by climate change, driving hostility towards immigrants and flares of militant racism. At such a juncture, yet another expression of the discredited, simplistic idea that genes alone control human nature seems particularly insidious. And yet, here we are again with Blueprint, by educational psychologist Robert Plomin. Although Plomin frequently uses more civil, progressive language than did his predecessors, the book’s message is vintage genetic determinism: “DNA isn’t all that matters but it matters more than everything else put together”. “Nice parents have nice children because they are all nice genetically.” And it’s not just any nucleic acid that matters; it is human chromosomal DNA. Sorry, microbiologists, epigeneticists, RNA experts, developmental biologists: you’re not part of Plomin’s picture. Crude hereditarianism often re-emerges after major advances in biological knowledge: Darwinism begat eugenics; Mendelism begat worse eugenics. The flowering of medical genetics in the 1950s led to the notorious, now-debunked idea that men with an extra Y chromosome (XYY genotype) were prone to violence. Hereditarian books such as Charles Murray and Richard Herrnstein’s The Bell Curve (1994) and Nicholas Wade’s 2014 A Troublesome Inheritance (see N. Comfort Nature 513, 306–307; 2014) exploited their respective scientific and cultural moments, leveraging the cultural authority of science to advance a discredited, undemocratic agenda. Although Blueprint is cut from different ideological cloth, the consequences could be just as grave. © 2018 Springer Nature Limited.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 25492 - Posted: 09.26.2018