Links for Keyword: Epigenetics

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By Rachel Yehuda Rachel Yehuda is a professor of psychiatry and neuroscience and director of the Center for Psychedelic Psychotherapy and Trauma Research at the Icahn School of Medicine at Mount Sinai. She is also director of mental health at the James J. Peters Veterans Affairs Medical Center. Credit: Nick Higgins After the twin towers of the World Trade Center collapsed on September 11, 2001, in a haze of horror and smoke, clinicians at the Icahn School of Medicine at Mount Sinai in Manhattan offered to check anyone who'd been in the area for exposure to toxins. Among those who came in for evaluation were 187 pregnant women. Many were in shock, and a colleague asked if I could help diagnose and monitor them. They were at risk of developing post-traumatic stress disorder, or PTSD—experiencing flashbacks, nightmares, emotional numbness or other psychiatric symptoms for years afterward. And were the fetuses at risk? My trauma research team quickly trained health professionals to evaluate and, if needed, treat the women. We monitored them through their pregnancies and beyond. When the babies were born, they were smaller than usual—the first sign that the trauma of the World Trade Center attack had reached the womb. Nine months later we examined 38 women and their infants when they came in for a wellness visit. Psychological evaluations revealed that many of the mothers had developed PTSD. And those with PTSD had unusually low levels of the stress-related hormone cortisol, a feature that researchers were coming to associate with the disorder. Surprisingly and disturbingly, the saliva of the nine-month-old babies of the women with PTSD also showed low cortisol. The effect was most prominent in babies whose mothers had been in their third trimester on that fateful day. Just a year earlier a team I led had reported low cortisol levels in adult children of Holocaust survivors, but we'd assumed that it had something to do with being raised by parents who were suffering from the long-term emotional consequences of severe trauma. Now it looked like trauma leaves a trace in offspring even before they are born. © 2022 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28378 - Posted: 06.25.2022

Jennifer Hellmann Parents who are exposed to predators pass on information about risky environments to their offspring through changes in gene expression – but how that information affects offspring differs depending on the sex of the parent. My colleagues and I showed this using sticklebacks – a small species of freshwater fish whose brightly colored males care for developing eggs – in a series of papers recently published in the Journal of Animal Ecology. First, we exposed mothers and fathers to predators. Then we looked at their offspring and measured behavior as well as how genes were expressed in their brains. We found that the sex of the parent exposed to predators matters, but surprisingly, the sex of the offspring also changed how the information influenced behavior. Predator‐exposed fathers produced bolder sons that took more risks, but the father’s experiences had no effect on the boldness of daughters. Predator‐exposed mothers, on the other hand, produced more anxious daughters and also more anxious sons. These sons and daughters had different patterns of gene expression, matching our behavioral results. We also studied whether these changes persisted into a second generation. In grandkids, we again found complicated patterns of sex-specific inheritance. So how does this work? It’s not that experiences have changed what genes the parents pass on. Rather, what changes is how those genes are expressed in the offspring. This variability in gene expression is called epigenetics. Stickleback eggs showing embryos growing inside. Through epigenetics, a parent can pass down information to the next generation of sticklebacks like the ones growing in these eggs. Jennifer Hellman, CC BY-ND © 2010–2021, The Conversation US, Inc.

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: 27750 - Posted: 03.31.2021

Researchers at the National Institutes of Health (NIH) have discovered specific regions within the DNA of neurons that accumulate a certain type of damage (called single-strand breaks or SSBs). This accumulation of SSBs appears to be unique to neurons, and it challenges what is generally understood about the cause of DNA damage and its potential implications in neurodegenerative diseases. Because neurons require considerable amounts of oxygen to function properly, they are exposed to high levels of free radicals—toxic compounds that can damage DNA within cells. Normally, this damage occurs randomly. However, in this study, damage within neurons was often found within specific regions of DNA called “enhancers” that control the activity of nearby genes. Fully mature cells like neurons do not need all of their genes to be active at any one time. One way that cells can control gene activity involves the presence or absence of a chemical tag called a methyl group on a specific building block of DNA. Closer inspection of the neurons revealed that a significant number of SSBs occurred when methyl groups were removed, which typically makes that gene available to be activated. An explanation proposed by the researchers is that the removal of the methyl group from DNA itself creates an SSB, and neurons have multiple repair mechanisms at the ready to repair that damage as soon as it occurs. This challenges the common wisdom that DNA damage is inherently a process to be prevented. Instead, at least in neurons, it is part of the normal process of switching genes on and off. Furthermore, it implies that defects in the repair process, not the DNA damage itself, can potentially lead to developmental or neurodegenerative diseases.

Related chapters from BN: 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: The Biology of Behavioral Disorders; Chapter 13: Memory and Learning
Link ID: 27744 - Posted: 03.27.2021

By Andrew Curry ZURICH, SWITZERLAND—The children living in SOS Children's Villages orphanages in Pakistan have had a rough start in life. Many have lost their fathers, which in conservative Pakistani society can effectively mean losing their mothers, too: Destitute widows often struggle to find enough work to support their families and may have to give up their children. The orphanages, in Multan, Lahore, and Islamabad, provide shelter and health care and send kids to local schools, trying to provide "the best possible support," says University of Zurich (UZH) physician and neuroscientist Ali Jawaid. "But despite that, these children experience symptoms similar to PTSD [post-traumatic stress disorder]," including anxiety and depression. Beyond these psychological burdens, Jawaid wonders about a potential hidden consequence of the children's experience. He has set up a study with the orphanages to probe the disturbing possibility that the emotional trauma of separation from their parents also triggers subtle biological alterations—changes so lasting that the children might even pass them to their own offspring. That idea would have been laughed at 20 years ago. But today the hypothesis that an individual's experience might alter the cells and behavior of their children and grandchildren has become widely accepted. In animals, exposure to stress, cold, or high-fat diets has been shown to trigger metabolic changes in later generations. And small studies in humans exposed to traumatic conditions—among them the children of Holocaust survivors—suggest subtle biological and health changes in their children. © 2019 American Association for the Advancement of Science.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26432 - Posted: 07.19.2019

By Ken Garber The idea that chemical tags on genes can affect their expression without altering the DNA sequence, once surprising, is the stuff of textbooks. The phenomenon, epigenetics, has now come to messenger RNA (mRNA), the molecule that carries genetic information from DNA to a cell’s proteinmaking factories. At a conference here last month, researchers discussed evidence that RNA epigenetics is also critical for gene expression and disease, and they described a new chemical modification linked to leukemia. Research has found that epigenetic marks decorate mRNAs like Christmas lights on a fence. The cell uses the marks “to determine where, when, and how much of the [associated] protein should be generated,” RNA biologist Pedro Batista of the National Cancer Institute (NCI) in Bethesda, Maryland, said at the conference. What’s more, says Michael Kharas of Memorial Sloan Kettering Cancer Center in New York City, mRNA modifications “can affect the viability of cells, whether cells divide, cancer, neurologic diseases.” They are providing promising leads for drug developers. And, he adds, “There’s so many [more] diseases these things could be important in, ones people aren’t even looking at.” Modified mRNAs had been reported in the 1970s, but by 2008 they were largely forgotten. Then, Chuan He at the University of Chicago, Samie Jaffrey at Cornell University, and Gideon Rechavi at Tel Aviv University in Israel took a fresh look. Their teams focused on one mRNA modification called m6A: a methyl group—a simple chemical unit—attached to some of an RNA molecule’s adenine bases. He’s group showed that a well-known enzyme removes this mRNA modification, indicating that m6A has an important biological role, and Jaffrey’s and Rechavi’s groups developed mapping tools that showed it is widespread. Before the work, researchers knew mRNA epigenetic marks were there, but “they just didn’t know how to actually look for them,” says NCI researcher Shalini Oberdoerffer. © 2019 American Association for the Advancement of Science

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: 26377 - Posted: 07.02.2019

Katarina Zimmer Occasionally, as the nematode worm C. elegans meanders across rotten fruit on the prowl for bacteria to eat, it comes across ones it shouldn’t dine on. Some bacteria are lethal to the animals when ingested, and unfortunately, the worms can’t always distinguish them from the nutritious kind until it’s too late. Nevertheless, this doesn’t stop them from teaching their young not to make the same mistake, researchers recently realized when watching the nematodes in the lab. Before the animals die from the pathogen, they often lay eggs. These offspring, researchers at Princeton University observed, consistently avoid that particular bacterial species. Evidently, pathogen avoidance—a behavioral habit the mothers learned towards the end of their lifetime—can be transmitted to the next generation, aiding their survival. But it’s not a hard-wired trait; instead, an epigenetic mechanism involving small RNAs appears to be responsible. That’s the finding of a paper published in Cell yesterday (June 6). Alongside it in the journal, a group at Tel Aviv University also reports on transgenerational inheritance of behavior traits in C. elegans. This team took a different approach, demonstrating how a small RNA–based mechanism allows information from the nervous system to be transmitted to germline cells and into future generations. While it’s known that traits involved in immunity and stress can be inherited across generations in C. elegans, the two papers are among the first to show that complex behaviors can be transmitted in the same way. © 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: 26322 - Posted: 06.11.2019

Ashley Yeager Brown and yellow mice nestle side by side in their cages in Anne Ferguson-Smith’s molecular genetics lab at the University of Cambridge. The mice are Agouti Viable Yellow, naturally occurring mutants, which, though genetically identical, have coats that vary in color—a phenomenon that researchers have long studied as an example of epigenetic inheritance. All of the mutant mice have a gene, Agouti, that influences coat color, and an adjacent transposable element—a DNA sequence that can move about the genome, creating or reversing mutations—that promotes the gene’s expression. In the brown mice, this element is methylated and, therefore, silenced. But in the yellow mice, it isn’t methylated, meaning that these animals overexpress Agouti signaling protein in many tissues, leading to their yellow hue. Importantly, Ferguson-Smith says, yellow mother mice tend to have yellow baby mice and brown mother mice tend to have brown baby mice, suggesting that the methylation mark—or lack of it—is passed down from generation to generation. This phenomenon has sparked scientists to hypothesize that other methylation marks on transposable elements can also be passed directly from parent to child, raising the possibility that parents’ diet, behavior, and experiences might affect future generations via this route. © 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: 26035 - Posted: 03.15.2019

Diana Kwon The effects of antidepressant exposure during early development can pass down through three generations of offspring—at least in zebrafish. A new study, published today (December 10) in PNAS, reveals that fluoxetine, a commonly used antidepressant that goes by the brand name Prozac, can alter hormone levels and blunt stress responses in an exposed embryo and its descendants. “The paper is very intriguing,” says Tim Oberlander, a developmental pediatrician at the British Columbia Children’s Hospital who was not involved in this work. The question of whether these medications have a transgenerational effect is “a really important one that requires further study in other animal models, and ultimately, when we have the data, we need to figure out whether it’s also true in humans.” Fluoxetine is a selective serotonin reuptake inhibitor (SSRI), a class of drugs widely used to treat depression as well as other conditions such as obsessive-compulsive disorder and anxiety disorders. Recent data from the US National Health and Nutrition Survey show increasing antidepressant use, from approximately 7.7 percent of the population in 1999–2002 to 12.7 percent from 2011–2014. SSRIs are often prescribed as the first-line treatment for pregnant women with depression, and prior studies in humans suggest infants exposed to SSRIs while in the womb may experience developmental disturbances such as delayed motor development and increased levels of anxiety later in childhood. Oberlander, whose research is focused on the influence of prenatal exposure to these medications, notes that it has been unclear whether those correlations represent a direct result of the drugs or if other factors, such as a genetic propensity for those outcomes or growing up with a parent with a mood disorder, may also play a part. © 1986 - 2018 The Scientist

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: 25781 - Posted: 12.12.2018

By Benedict Carey In mid-October, researchers in California published a study of Civil War prisoners that came to a remarkable conclusion. Male children of abused war prisoners were about 10 percent more likely to die than their peers were in any given year after middle age, the study reported. The findings, the authors concluded, supported an “epigenetic explanation.” The idea is that trauma can leave a chemical mark on a person’s genes, which then is passed down to subsequent generations. The mark doesn’t directly damage the gene; there’s no mutation. Instead it alters the mechanism by which the gene is converted into functioning proteins, or expressed. The alteration isn’t genetic. It’s epigenetic. The field of epigenetics gained momentum about a decade ago, when scientists reported that children who were exposed in the womb to the Dutch Hunger Winter, a period of famine toward the end of World War II, carried a particular chemical mark, or epigenetic signature, on one of their genes. The researchers later linked that finding to differences in the children’s health later in life, including higher-than-average body mass. The excitement since then has only intensified, generating more studies — of the descendants of Holocaust survivors, of victims of poverty — that hint at the heritability of trauma. If these studies hold up, they would suggest that we genetically inherit some trace of our parents’ and even grandparents’ experience, particularly their suffering, which in turn modifies our own day-to-day health — and perhaps our children’s, too. But behind the scenes, the work has touched off a bitter dispute among researchers that could stunt the enterprise in its infancy. Critics contend that the biology implied by such studies simply is not plausible. Epigenetics researchers counter that their evidence is solid, even if the biology is not worked out. © 2018 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25768 - Posted: 12.10.2018

By Mitch Leslie Male mice that work out spawn healthier offspring than their lethargic counterparts, according to a new study. Whether the results hold true for humans remains uncertain, but they support the notion that some of the benefits of exercise are somehow passed on to the next generation. “The science is solid, and it’s pretty exciting,” says epigeneticist Sarah Kimmins of McGill University in Montreal, Canada, who wasn’t connected to the work. Scientists already know that a parent’s bad exercise or dietary habits can affect their offspring. Mothers who are obese during pregnancy, for example, give birth to children who are more likely to be obese as adults and develop metabolic illnesses such as cardiovascular disease. Another study found that male rats that snarfed high-fat chow fathered offspring that didn’t respond normally to glucose, a hallmark of type 2 diabetes. To determine whether the opposite is true, molecular exercise physiologist Kristin Stanford of The Ohio State University College of Medicine in Columbus and colleagues fed male mice a fat-rich diet for 3 weeks. One group of animals had access to running wheels, scampering nearly 6 kilometers per night on average, but the rest were couch potatoes. After dissecting some of the rodents to obtain samples of their sperm, the researchers allowed the remaining mice to mate. Stanford and her colleagues tracked the resulting offspring until they were a year old, about middle age for a mouse. Even though the offspring of exercising and nonexercising dads all ate a high-fat diet their entire lives and didn’t get any physical activity, the offspring of healthy fathers seemed to inherit their dads’ metabolism. The progeny of the runners showed a better response to increases in blood glucose and had lower insulin levels—both hallmarks of a sound metabolism—the researchers report today in Diabetes. “Exercise was completely negating the effect of a high-fat diet” on the offspring, Stanford says. © 2018 American Association for the Advancement of Scienc

Related chapters from BN: 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 4: Development of the Brain
Link ID: 25607 - Posted: 10.23.2018

Kerry Grens Nicotine can wield its effects on offspring in more ways than from exposures in utero or secondhand smoke: the sperm of mice that ingested nicotine carry epigenetic signatures of that exposure, a study published in PLOS Biology today (October 16) reports. The result might explain why the experiments also found the male mice’s offspring—and grandoffspring—exhibited abnormal behavior and learning impairments. “Until now, much attention had been focused on the effects of maternal nicotine exposure on their children,” Florida State University’s Pradeep Bhide, who led the study, tells The Boston Globe in an email. “Not much had been known about the effects of paternal smoking on their children and grandchildren. Our study shows that paternal nicotine exposure can be deleterious for the offspring in multiple generations.” To investigate paternal exposure, Bhide’s team spiked male mice’s drinking water with nicotine for 12 weeks. The researchers then bred those animals with unexposed females, and mated the offspring to produce the third generation. The second- and third-generation mice underwent a battery of cognitive and behavioral tests to see if their father’s or grandfather’s nicotine exposure had any effect. On some examinations, the mice performed typically, but they didn’t do as well on certain learning tasks as mice whose parent or grandparent had not been given nicotine. The second generation also exhibited hyperactivity and had lower levels of certain neurotransmitters in the brain than the offspring of unexposed animals had. © 1986 - 2018 The Scientist

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25588 - Posted: 10.18.2018

By Katherine J. Wu Eat poorly, and your body will remember—and possibly pass the consequences onto your kids. In the past several years, mounting evidence has shown that sperm can take note of a father’s lifestyle decisions, and transfer this baggage to offspring. Today, in two complementary studies, scientists tell us how. As sperm traverse the male reproductive system, they jettison and acquire non-genetic cargo that fundamentally alters sperm before ejaculation. These modifications not only communicate the father’s current state of wellbeing, but can also have drastic consequences on the viability of future offspring. Each year, over 76,000 children are born as a result of assisted reproduction techniques, the majority of which involve some type of in vitro fertilization (IVF). These procedures unite egg and sperm outside the human body, then transfer the resulting fertilized egg—the embryo—into a woman’s uterus. Multiple variations on IVF exist, but in some cases that involve male infertility—for instance, sperm that struggle to swim—sperm must be surgically extracted from the testes or epididymis, a lengthy, convoluted duct that cradles each testis. After sperm are produced in the testes, they embark on a harrowing journey through the winding epididymis—which, in a human male, is about six meters long when unfurled—on their way to storage. Sperm wander the epididymis for about two weeks; only at the end of this path are they fully motile. Thus, while “mature” sperm can essentially be dumped on a waiting egg and be reasonably expected to achieve fertilization, sperm plucked from the testes and epididymis must be injected directly into the egg with a very fine needle. No matter the source of the sperm, these techniques have birthed healthy infants in four decades of successful procedures.

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: 25268 - Posted: 07.30.2018

By Robert Martone We normally think that every cell in our body contains the same genome, the complete set of genetic information that makes up the biological core of our individuality. However, there are exceptions where the body contains cells that are genetically different. This happens in cancers, of course, which arise when mutations create genetically distinct cells. What most people do not realize, however, is that the brain has remarkable genetic diversity, with some studies suggesting there may be hundreds of mutations in each nerve cell. In the developing brain, mutations and other genetic changes that occur while brain cells divide are passed down to a cluster of daughter cells. As a result, the adult brain is composed of a mosaic of genetically distinct cell clusters. We know that the activity and organization of the brain changes in response to experience. Memories and learning are reflected in the number and strength of connections between nerve cells. We also know that the brain is genetically mosaic, but a new study makes a remarkable connection between experience and the genetic diversity of the brain. It suggests that experience can change the DNA sequence of the genome contained in brain cells. This is a fundamentally new and unexplored way in which experience can alter the brain. It is of great scientific interest because it reveals the brain to be pliable, to its genetic core, in response to the world. © 2018 Scientific America

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: 25193 - Posted: 07.11.2018

By Carl Zimmer James Priest couldn’t make sense of it. He was examining the DNA of a desperately ill baby, searching for a genetic mutation that threatened to stop her heart. But the results looked as if they had come from two different infants. “I was just flabbergasted,” said Dr. Priest, a pediatric cardiologist at Stanford University. The baby, it turned out, carried a mixture of genetically distinct cells, a condition known as mosaicism. Some of her cells carried the deadly mutation, but others did not. They could have belonged to a healthy child. We’re accustomed to thinking of our cells sharing an identical set of genes, faithfully copied ever since we were mere fertilized eggs. When we talk about our genome — all the DNA in our cells — we speak in the singular. But over the course of decades, it has become clear that the genome doesn’t just vary from person to person. It also varies from cell to cell. The condition is not uncommon: We are all mosaics. For some people, that can mean developing a serious disorder like a heart condition. But mosaicism also means that even healthy people are more different from one another than scientists had imagined. In medieval Europe, travelers making their way through forests sometimes encountered a terrifying tree. A growth sprouting from the trunk looked as if it belonged to a different plant altogether. It formed a dense bundle of twigs, the sort that people might fashion into a broom. Germans call it Hexenbesen: witches’ broom. As legend had it, witches used magic spells to conjure the brooms to fly across the night sky. The witches used some as nests, too, leaving them for hobgoblins to sleep in. In the 19th century, plant breeders found that if they cut witches’ broom from one tree and grafted it to another, the broom would grow and produce seeds. Those seeds would sprout into witches’ broom as well. © 2018 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: 25006 - Posted: 05.22.2018

By Gretchen Reynolds Exercise changes the brains and sperm of male animals in ways that later affect the brains and thinking skills of their offspring, according to a fascinating new study involving mice. The findings indicate that some of the brain benefits of physical activity may be passed along to children, even if a father does not begin to exercise until adulthood. We already have plenty of scientific evidence showing that exercise is good for our brains, whether we are mice or people. Among other effects, physical activity can strengthen the connections between neurons in the hippocampus, a crucial part of the brain involved in memory and learning. Stronger neuronal connections there generally mean sharper thinking. Studies also indicate that exercise, like other aspects of lifestyle, can alter how genes work — whether and when they get turned on or off, for instance — and those changes can get passed on to children. This process is known as epigenetics. But it had not been clear whether structural changes in the brain caused by exercise might also have epigenetic effects that would result in meaningful changes in the brains of the next generation. In other words, would exercise by a parent help to produce smarter babies? And, in particular, would this process occur in males, who contribute sperm but not a womb and its multitude of hormones, cells and tissues to their children? To find out, researchers at the German Center for Neurodegenerative Diseases in Göttingen, Germany, and other institutions gathered a large group of genetically identical male mice. Because the animals were genetically the same at the start, any differences in their bodies and behavior that cropped up later should be a result of lifestyle. © 2018 The New York Times Company

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 24951 - Posted: 05.09.2018

By Abby Olena Some mouse mothers groom, lick, and nurse their babies more than others. In a study published in Science today (March 23), researchers demonstrate that this natural variation in maternal behavior is linked to the structure of pups’ genomes, specifically, the activation of one of the most common jumping genes in the genome, LINE-1. “What’s fascinating about the paper is the connection between experience, epigenetics, and restructuring of the genome,” says Moshe Szyf, a geneticist at McGill University in Montreal who did not participate in the work. “We usually think about epigenetics changes that don’t change the sequence, but here there was a connection of the maternal care, the change in methylation . . . and then restructuring.” Coauthor Tracy Bedrosian, who did the work as a postdoc at the Salk Institute and is now a scientist at Ohio-based Neurotechnology Innovations Translator, and her colleagues did not set out to study maternal behavior. Instead, they wanted to explore the effects of maternal stress and environmental enrichment on the retrotransposon LINE-1 (L1), which can copy and paste itself into new locations in the genome, in pups. To manipulate stress levels, they isolated and confined pregnant mice to a small area for a couple hours each day, and for enrichment, mice lived in groups in a large enclosure with toys and running wheels. Bedrosian says that they saw wild variations in L1 copy number between different litters of mice that didn’t seem to relate to their experimental manipulations. Perhaps, they reasoned, maternal behavior was involved. © 1986-2018 The Scientist

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 8: Hormones and Sex
Link ID: 24784 - Posted: 03.26.2018

Carl Zimmer In September 1944, trains in the Netherlands ground to a halt. Dutch railway workers were hoping that a strike could stop the transport of Nazi troops, helping the advancing Allied forces. But the Allied campaign failed, and the Nazis punished the Netherlands by blocking food supplies, plunging much of the country into famine. By the time the Netherlands was liberated in May 1945, more than 20,000 people had died of starvation. The Dutch Hunger Winter has proved unique in unexpected ways. Because it started and ended so abruptly, it has served as an unplanned experiment in human health. Pregnant women, it turns out, were uniquely vulnerable, and the children they gave birth to have been influenced by famine throughout their lives. When they became adults, they ended up a few pounds heavier than average. In middle age, they had higher levels of triglycerides and LDL cholesterol. They also experienced higher rates of such conditions as obesity, diabetes and schizophrenia. By the time they reached old age, those risks had taken a measurable toll, according to the research of L.H. Lumey, an epidemiologist at Columbia University. In 2013, he and his colleagues reviewed death records of hundreds of thousands of Dutch people born in the mid-1940s. They found that the people who had been in utero during the famine — known as the Dutch Winter Hunger cohort — died at a higher rate than people born before or afterward. “We found a 10 percent increase in mortality after 68 years,” said Dr. Lumey. The patterns that Dr. Lumey and his colleagues documented are not disputed, but scientists still are struggling to understand how they come about. “How on earth can your body remember the environment it was exposed to in the womb — and remember that decades later?” wondered Bas Heijmans, a geneticist at Leiden University Medical Center in the Netherlands. © 2018 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: 24599 - Posted: 02.01.2018

By Marissa Fessenden, A new technique classifies neurons by surveying chemical tags that turn genes on or off on the neurons’ DNA1. The approach represents a new way to chart the brain’s cellular diversity. It could reveal how patterns of chemical tags known as methyl groups are altered in autism. Methyl groups bind to the DNA base cytosine. Patterns of methylation can be inherited, but they can also change in response to environmental factors, such as exposure in the womb to stress hormones or to the mother’s diet. Studies have reported altered methylation patterns in postmortem brains of people with autism. Methylation patterns also vary by cell type. In a new study, published 11 August in Science, researchers classified neurons from mouse and human brain tissue by their methylation patterns. The researchers looked at cells from specific layers of the brain’s outer shell, the cerebral cortex. They used a chemical cocktail to isolate the cells’ nuclei, and placed a single nucleus in each well of a 384-well plate. They then treated the nuclei with a chemical that converts cytosines without methyl groups to the RNA base uracil. They sequenced the DNA to pinpoint the remaining cytosines, yielding a map of every methyl group. © 2017 Scientific American,

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: 24073 - Posted: 09.19.2017

By Becca Cudmore A mother rat’s care for her pup reaches all the way into her offspring’s DNA. A young rat that gets licked and groomed a lot early on in life exhibits diminished responses to stress thanks to epigenetic changes in the hippocampus, a brain region that helps transform emotional information into memory. Specifically, maternal solicitude reduces DNA methylation and changes the structure of DNA-packaging proteins, triggering an uptick in the recycling of the neurotransmitter serotonin and the upregulation of the glucocorticoid receptor. These changes make the nurtured rat’s brain quicker to sense and tamp down the production of stress hormones in response to jarring experiences such as unexpected sound and light. That pup will likely grow into a calm adult, and two studies have shown that female rats who exhibit a dampened stress response are more likely to generously lick, groom, and nurse their own young. Caring for pups is one example of what casual observers of behavior might call an animal’s instinct—generally considered to be an innate, genetically encoded phenomenon. But could such epigenetic changes, when encoded as ancestral learning, also be at the root of maternal care and other seemingly instinctual behaviors we see across the animal kingdom? “We don’t have a general theory for the mechanics of instinct as we do for learning, and this is something that has troubled me for a very long time,” says University of Illinois entomologist Gene Robinson. He studies social evolution in the Western honey bee and recently coauthored a perspective piece in Science together with neurobiologist Andrew Barron of Macquarie University in Sydney, Australia, suggesting methylation as a possible mechanism for the transgenerational transmission of instinctual behavior, rather than those behaviors being hardwired in the genome (356:26-27, 2017). Robinson and Barron suggest that instinctual traits, such as honey bees’ well-known waggle dance or a bird’s in-born ability to sing its species’ songs, are the result of traits first learned by their ancestors and inherited across generations by the process of methylation. This differs from classical thoughts on animal learning, which say that if a behavior is learned, it is not innate, and will not be inherited. © 1986-2017 The Scientist

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 23861 - Posted: 07.22.2017

Ian Sample Science editor Older men tend to have “geekier” sons who are more aloof, have higher IQs and a more intense focus on their interests than those born to younger fathers, researchers claim. The finding, which emerged from a study of nearly 8,000 British twins, suggests that having an older father may benefit children and boost their performance in technical subjects at secondary school. Researchers in the UK and the US analysed questionnaires from 7,781 British twins and scored them according to their non-verbal IQ at 12 years old, as well as parental reports on how focused and socially aloof they were. The scientists then combined these scores into an overall “geek index”. Magdalena Janecka at King’s College London said the project came about after she and her colleagues had brainstormed what traits and skills helped people to succeed in the modern age. “If you look at who does well in life right now, it’s geeks,” she said. Drawing on the twins’ records, the scientists found that children born to older fathers tended to score slightly higher on the geek index. For a father aged 25 or younger, the average score of the children was 39.6. That figure rose to 41 in children with fathers aged 35 to 44, and to 47 for those with fathers aged over 50. The effect was strongest in boys, where the geek index rose by about 1.5 points for every extra five years of paternal age. The age of the children’s mothers seemed to have almost no effect on the geek index. © 2017 Guardian News and Media Limited

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: 23757 - Posted: 06.21.2017