New mechanism of inheritance could advance study of evolution, disease treatment

UMD scientists have discovered a mechanism for transgenerational gene silencing in the roundworm Caenorhabditis elegans. Special fluorescent dyes help to visualize neurons (magenta) and germ cells (green) in the roundworm's body.

For more than a century, scientists have understood the basics of inheritance: if good genes help parents survive and reproduce, the parents pass those genes along to their offspring. And yet, recent research has shown that reality is much more complex: genes can be switched off, or silenced, in response to the environment or other factors, and sometimes these changes can be passed from one generation to the next.

The phenomenon has been called epigenetic inheritance, but it is not well understood. Now, UMD geneticist Antony Jose and two of his graduate students are the first to figure out a specific mechanism by which a parent can pass silenced genes to its offspring. Importantly, the team found that this silencing could persist for multiple generations--more than 25, in the case of this study.

The research, which was published in the Feb. 2, 2015 online early edition of the Proceedings of the National Academy of Sciences, could transform our understanding of animal evolution. Further, it might one day help in the design of treatments for a broad range of genetic diseases.

"For a long time, biologists have wanted to know how information from the environment sometimes gets transmitted to the next generation," said Jose, an assistant professor in the UMD Department of Cell Biology and Molecular Genetics. "This is the first mechanistic demonstration of how this could happen. It's a level of organization that we didn't know existed in animals before."

Jose and graduate students Sindhuja Devanapally and Snusha Ravikumar worked with the roundworm Caenorhabditis elegans, a species commonly used in lab experiments. They made the worms' nerve cells produce molecules of double-stranded RNA (dsRNA) that match a specific gene. (RNA is a close relative of DNA, and has many different varieties, including dsRNA.) Molecules of dsRNA are known to travel between body cells (any cell in the body except germ cells, which make egg or sperm cells) and can silence genes when their sequence matches up with the corresponding section of a cell's DNA.

The team's biggest finding was that dsRNA can travel from body cells into germ cells and silence genes within the germ cells. Even more surprising, the silencing can stick around for more than 25 generations. If this same mechanism exists in other animals--possibly including humans--it could mean that there is a completely different way for a species to evolve in response to its environment.

"This mechanism gives an animal a tool to evolve much faster," Jose said. "We still need to figure out whether this tool is actually used in this way, but it is at least possible. If animals use this RNA transport to adapt, it would mean a new understanding of how evolution happens."

The long-term stability of the silencing effect could prove critical in developing treatments for genetic diseases. The key is a process known as RNA interference, more commonly referred to as RNAi. This process is how dsRNA silences genes in a cell. The same process has been studied as a potential genetic therapy for more than a decade, because you can target any disease gene with matching dsRNA. But a main obstacle has been achieving stable silencing, so that the patient does not need to take repeated high doses of dsRNA.

"RNAi is very promising as a therapy, but the efficacy of the treatment declines over time with each new cell division," Jose said. "This particular dsRNA, from C. elegans nerve cells, might have some chemical modifications that allow stable silencing to persist for many generations. Further study of this molecule could help solve the efficacy problem in RNAi therapy."

Jose acknowledges the large gap between roundworms and humans. Unlike simpler animals, mammals have known mechanisms that reprogram silenced genes every generation. On the surface, it would seem as though this would prevent epigenetic inheritance from happening. And yet, previous evidence suggests that the environment may be able to cause some sort of transgenerational effect in mammals as well. Jose believes that his team's work provides a promising lead in the search for how this happens.

"This is a fertile research field that will keep us busy for 10 years or more into the future," Jose said. "The goal is to achieve a very clear understanding--in simple terms--of all the tools an animal can use to evolve."

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Biologists partner bacterium with nitrogen gas to produce more, cleaner bioethanol

Indiana University Bloomington biologists have discovered that the bioethanol-producing bacterium Zymomonas mobilis, when coupled with nitrogen gas, can produce fuel faster and more efficiently than current methods. Shown here is a whole field microscopy image of Z. mobilis, including some dividing cells.

Indiana University biologists believe they have found a faster, cheaper and cleaner way to increase bioethanol production by using nitrogen gas, the most abundant gas in Earth's atmosphere, in place of more costly industrial fertilizers. The discovery could save the industry millions of dollars and make cellulosic ethanol -- made from wood, grasses and inedible parts of plants -- more competitive with corn ethanol and gasoline.

The raw materials for cellulosic ethanol are low in nitrogen, a nutrient required for ethanol-producing microbes to grow, so cellulosic ethanol producers are estimated to spend millions of dollars annually on nitrogen fertilizers like corn steep liquor and diammonium phosphate. But an IU team led by biologist James B. McKinlay has found that the bioethanol-producing bacterium Zymomonas mobilis can use nitrogen gas (N2) as a nitrogen source, something that the more traditional ethanol-producer, baker's yeast, cannot do.

"When we discovered that Z. mobilis could use N2 we expected that it would make less ethanol. N2 utilization and ethanol production demand similar resources within the bacterial cell so we expected resources to be pulled away from ethanol production to allow the bacteria to grow with N2," McKinlay said. "To our surprise the ethanol yield was unchanged when the bacteria used N2. In fact, under certain conditions, the bacteria converted sugars to ethanol much faster when they were fed N2."

Knowing the bacterium could use N2 without hindering ethanol production, the team reasoned that N2 gas could serve as an inexpensive substitute for nitrogen fertilizers during cellulosic ethanol production.

"Until recently, ethanol has been produced almost entirely from food crops, but last year there was a surge in cellulosic ethanol production as several commercial facilities opened," McKinlay said. "Cellulosic ethanol offers more favorable land use and lower carbon emissions than conventional ethanol production. Even so, cellulosic ethanol is struggling to be cost-competitive against corn ethanol and gasoline."

The largest cost contributors to cellulosic ethanol production are the cellulosic plant material and the enzymes needed to degrade the plant material into sugars that are converted into ethanol, so they have received the most attention.

"But we recognized nitrogen fertilizers as a smaller, yet considerable, cost contributor that could potentially be more readily addressed," he said.

They estimated that using N2 gas, which can be produced on-site at production facilities, in place of costly nitrogen supplements could save an ethanol production facility over $1 million dollars a year. Using N­2 gas could also have environmental benefits such as avoiding carbon dioxide emissions associated with producing and transporting the industrial fertilizers.

"More work needs to be done to assess how this approach can be integrated and optimized on an industrial scale, but all of the data we've collected thus far are very encouraging," McKinlay said.

A provisional patent has also been filed in relation to the study with the United State Patent and Trademark Office, he added.
The research was published today in the journal Proceedings of the National Academy of Sciences by McKinlay and three past and present members of his laboratory: graduate student Timothy A. Kremer, postdoctoral fellow Breah LaSarre, and former research associate Amanda L. Posto. McKinlay is an assistant professor in the IU Bloomington College of Arts and Sciences' Department of Biology.

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Picking up on the smell of evolution: Researchers discover changes that let a species drastically change its lifestyle

This is a Scaptomyza flava female on a leaf of Arabidopsis thaliana, a popular model organism in plant biology.

For most of us, switching to a vegetarian diet might be a matter of a New Year's resolution and a fair amount of willpower, but for an entire species, it's a much more involved process -- one that evolutionary biologists have struggled to understand for a long time.

Researchers at the University of Arizona have taken a peek behind the curtain of evolution to find out what happens when an insect species dramatically changes its way of life. The processes they discovered involve never-seen-before remodeling of genes, behaviors and diet. The results, published in the Proceedings of the National Academy of Science, or PNAS, are likely to make you ponder evolutionary questions next time you find a fruit fly floating in your glass of wine.

Herbivorous insect species make up half of all known insect species, but the switch from a non-plant diet to herbivory evolved in only one-third of living insect orders. That discrepancy has puzzled biologists for a long time.

"It implies that the transition to herbivory happened rarely, but when it happened, it turned out to be a major push for speciation spawning the evolution of a disproportionate number of species in that group," said Benjamin Goldman-Huertas, a fifth-year doctoral candidate and National Science Foundation graduate research fellow in the UA's Department of Ecology and Evolutionary Biology, and the lead author of the paper.

One of the possible answers is that plants are very difficult to colonize, said Noah Whiteman, an assistant professor of ecology and evolutionary biology and senior author of the study. To ward off their predators, plants have evolved an arsenal of defenses, such as spines, tough outer "skin" or compounds that render their tissues indigestible, unpalatable or even fatally toxic to insects attempting to feed on them.

"Most plant-eating insects are parasites," Whiteman explained. "They're not like elephants roaming the savannah and ripping off leaves here and there. Insects have evolved ways to overcome those defenses but at the cost of becoming highly specialized. Many herbivorous insect species are extremely specialized, to the point where the animals have to spend their entire life cycle on their host plants.

"Switching from feeding on microbes, decaying meat or other insects to targeting plants requires ways to attract the insects to the plants, lay their eggs there and keep their larvae alive on the plant. We wanted to test the hypothesis that this transition required drastic changes in behavior, which in turn required remodeling of the genetic and neurological processes underlying those behaviors."

To find answers, the authors studied the fly species Scaptomyza flava, a close relative of the fruit fly Drosophila melanogaster. Unlike their cousins, which often are seen hovering around the produce aisle, feasting on fruit that's past its prime, Scaptomyza flies don't wait that long. The females seek out healthy plants in the mustard family, pierce tiny holes into their leaves, drink the plant juice seeping into the wounds and deposit their eggs in the leaves. Upon hatching, the larvae munch their way through the leaves, making tiny tunnels as they go, and sometimes even kill the plant.

To study the flies' responses in more detail, Goldman-Huertas collaborated with researchers in the group of John Hildebrand, a Regents' Professor in the UA's Department of Neuroscience, which allowed them to measure the electrical responses in the insects' antennae generated by olfactory receptors when presenting the animals with various scents.

"It's like recording from the population of receptor cells in your nose," Hildebrand said. "We look for electrical signals indicating that the antennal receptor cells have recognized and responded to a certain scent stimulus. If we don't see a signal, it means that the antenna doesn't respond to that compound."

Such neurological assays, combined with behavioral observations, revealed that the smell of yeast, which thrives on rotting fruit and acts a huge attractant to Drosophila, left Scaptomyza flies cold.

Conversely, "we found that Scaptomyza flava is very sensitive to the compound that is responsible for the scent of freshly cut grass, which is common in leafy plants," Whiteman said.

Goldman-Huertas hypothesized that the olfactory genes that are involved in sniffing out yeast should be lost in Scaptomyza, and indeed, "we could not find many of them in any of the populations we tested," he said.

According to Whiteman, the flies' preference for compounds associated with yeast and alcoholic fermentation is considered a more ancestral state than Scaptomyza's preference for fresh plants.

"The fruit fly species floating in your wine glass really represent 100 million years of evolution because the sensory mechanisms are conserved in species that are attracted to wine," he said.

To study the genetic basis of the flies' food preferences, the researchers took advantage of Scaptomyza's close kinship with D. melanogaster, whose olfactory system is the most extensively studied of any animal.

"Scaptomyza is a very useful model to study genetic underpinnings because on the one hand, it is closely related to D. melanogaster, but on the other hand, it is evolutionary diverged," Whiteman said. "In these flies, herbivory evolved in the last 20 million years at most. The changes are recent enough that we are able to detect them and compare them to non-herbivorous sister species like D. melanogaster.

"But loss of behaviors doesn't make you go on to new feeding grounds, so some gain of function must have happened as well."

Indeed, the team discovered a group of olfactory receptor genes that have undergone a disproportionately amount of sequence change.

"This suggests Darwinian evolution has changed the function of these genes," Whiteman said.

"Understanding how these ecological changes can come about can have huge economic and health implications," Goldman-Huertas said. "Scaptomyza flava is an emerging pest of canola in Europe and of mustard plants in New Zealand.

"Or take the Anopheles mosquitoes that spread malaria. How did they start feeding on humans? Or the Colorado potato beetle that originally fed on other related plants. How did that switch come about? How insects make decisions impacts the lives, health and wellbeing of people.

"We could only answer these questions because of UA's culture of collaboration," Goldman-Huertas added, "in particular the UA Center for Insect Science, which facilitated the collaboration between the departments of neuroscience and ecology and evolutionary biology through a seed grant."

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Latent HIV may lurk in 'quiet' immune cells, research suggests

Drugs for HIV have become adept at suppressing infection, but they still can't eliminate it. That's because the medication in these pills doesn't touch the virus' hidden reserves, which lie dormant within infected white blood cells. Unlock the secrets of this pool of latent virus, scientists believe, and it may become possible to cure -- not just control -- HIV.

In a study published in Cell, researchers lead by Zanvil A. Cohn and Ralph M. Steinman Professor Michel C. Nussenzweig at Rockefeller University and their collaborators describe new insights on which cells likely do, and do not, harbor this lurking threat.

"It has recently been shown that infected white blood cells can proliferate over time, producing many clones, all containing HIV's genetic code. However, we found that these clones do not appear to harbor the latent reservoir of virus," says study author Lillian Cohn a graduate student in Nussenzweig's Laboratory of Molecular Immunology. "Instead our analysis points to cells that have never divided as the source of the latent reservoir."

HIV belongs to a family of viruses that insert themselves directly into the host cell's genome where they can hide out quietly after the initial infection. HIV mostly targets CD4 T lymphocytes, a type of T cell involved in initiating an immune response.
When HIV integrates itself into the genetic code of a CD4 T cell, it may produce an active infection, hijacking the cell to produce more copies of itself in order infect other cells, and killing it in the process. Antiretroviral drugs that suppress HIV infection work by disrupting this hijacking. But the virus may also fail to produce an active infection, remaining a quiet, tiny fragment of DNA tucked within the host cell's genome. If so, the drugs have nothing to disrupt, and the infection remains latent.

Most often, however, what happens is actually something in between. While the virus does manage to get at least some of itself into the T cell's genome, problems with the process leave it incapable of hijacking the cell to replicate itself. But those few successful integrations still do damage, and the resulting depletion in the victim's immune system leaves him or her vulnerable to potentially fatal opportunistic infections years, or even decades, after the initial infection.

"If a patient stops taking antiretrovirals, the infection rebounds. It is truly amazing that the virus can give rise to AIDS 20 years after the initial infection," Cohn says.

Researchers think the reservoir of latent virus may be hiding out in a type of CD4 T cell: long-lived memory cells that help the immune system remember particular pathogens. When these cells encounter a pathogen they have previously seen, they spur the proliferation of T cells tuned to recognize it, in a process called clonal expansion. Prior research has suggested clonal expansion is crucial to maintaining HIV's latent reservoir.

Following up on work initiated by Mila Jankovic, a senior research associate in the lab, Cohn and her colleagues examined cloned and unique CD4 T cells in blood samples from 13 people infected with HIV. An analytical computational technique developed by Israel Tojal da Silva, a research associate in the lab, made it possible to identify integration sites into which HIV had inserted itself within individual cells.

"Given the size of the human genome, it is highly unlikely the virus would insert itself in exactly the same place more than once. So, if multiple cells contained virus with identical integration sites, we classified them as clones. Meanwhile if a cell had a unique integration site, one not shared with any other cell, then we assumed that cell was unique" Cohn says.

The researchers tested 75 viral sequences taken from the expanded clones of cells to see if they had the potential to produce more of the virus. None could.

"While we cannot rule out the possibility that a rare clone of cells may contain an active virus, it appears most likely that latent reservoir -- and the potential target for therapies meant to cure HIV -- resides in the more rare single cells containing unique integrations," Cohn says.

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Stress shared by same-sex couples can have unique health impacts

Studies of stress and its effects on health have typically focused on the worries of an individual: money, love, health, work. But what about stress shared by two people in a romantic relationship?

New research by Allen LeBlanc, Health Equity Institute Professor of Sociology at San Francisco State University, studies how minority stress -- which results from being stigmatized and disadvantaged in society -- affects same-sex couples' stress levels and overall health. LeBlanc asserts that the health effects of minority stress shared by a couple can be understood as distinct from individual stress, a new framework in the field.

"Stress research has traditionally focused more on the individual experience of stress, which is very important, but social contexts get overlooked," LeBlanc said. "We are developing new ways of measuring stress at the couple level."

A gay man, for example, might feel individual stress if he conceals his sexual orientation from others, fearing discrimination in his workplace or rejection by his family. This situation can lead to couple-level stress if he asks that his partner hide their relationship, leading to new challenges affecting both men -- and the quality of their relationship.

In an article to be published in the February issue of the Journal of Marriage and Family, LeBlanc suggests that future research must strive to better understand stressors that originate within the context of intimate relationships, and that such studies will advance the entire field of stress research.

"Relationships aren't inherently seen as problematic or challenging," LeBlanc said. "A lot of important work has been focused on what is helpful or positive about being in a relationship. There is longstanding literature, for example, demonstrating that people who are married tend to have better health than those who are not. But relationships are also a source of stress, and we can learn from that."

Using their new framework of understanding shared stress, LeBlanc and his team are currently undertaking the first study of couple-level minority stress. Hundreds of couples across the country will participate in a study designed to measure their individual and couple-level stress as distinct entities. A year later, the couples will complete a second survey, with the goal of learning how stress experiences and health change over time -- and the effects they have on a relationship. The data from this survey will allow the researchers to test their new theory of stress and health and help identify the kinds of stress that are most challenging for same-sex couples.

While LeBlanc's work focuses on minority stress among same-sex couples, he said the insights can be applied to other couples that experience minority stress, such as interracial couples, interfaith couples and couples in which one partner is significantly older than the other.

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How pancreatic cancer cells sidestep chemotherapy

Pancreatic cancer is one of the deadliest forms of the disease. The American Cancer Society's most recent estimates for 2014 show that over 46,000 people will be diagnosed with pancreatic cancer and more than 39,000 will die from it. Now, research led by Timothy J. Yen, PhD, Professor at Fox Chase Cancer Center, reveals that one reason this deadly form of cancer can be so challenging to treat is because its cells have found a way to sidestep chemotherapy. They hijack the vitamin D receptor, normally associated with bone health, and re-purposed it to repair the damage caused by chemotherapy. The findings, which will be published in the January 3 issue of the journal Cell Cycle, raise hopes that doctors will one day find a way to turn this process against the tumor and help chemotherapy do its job.

Most patients diagnosed with pancreatic cancer receive a drug called gemcitabine, which works by preventing cells from replicating their DNA -- thus stopping tumor cells from dividing and causing them to die off. Sadly, many patients die within a few months, often because their cancer finds a way to work around treatment. But how does that happen? "Maybe there is something we don't understand about how gemcitabine works," says Dr. Yen. "More likely, cancer cells have found a way to avoid DNA-damaging drugs."

To determine how pancreatic cancers sidestep chemotherapy and the effects of gemcitabine, Dr. Yen and his colleagues removed every one of the ~24,000 genes, one by one, in pancreatic cancer cells, exposed the cells to gemcitabine, and noted which gene "knockout" caused cells to be more sensitive to the drug.

One of those "knocked-out" genes was particularly important, namely, the gene for a protein which normally binds to vitamin D. "When we inactivated this vitamin D receptor in cancer cells and added gemcitabine, almost all of them died," says Dr. Yen.

That's when the researchers realized they had identified a key mechanism driving chemotherapeutic effectiveness against pancreatic cancer. "If we find a drug that inactivates the vitamin D receptor, it may allow gemcitabine to selectively kill pancreatic cancer cells while leaving healthy cells unharmed," says Dr. Yen. "Patients would just need to drink lots of milk or take calcium supplements to make sure their bones stay healthy."

Although the precise role of the vitamin D receptor in pancreatic cancer remains uncertain, it's clear that pancreatic cancer cells need it, says Dr. Yen. "Cancer cells are good at finding ways to survive," he explains. "We suspect that cancer cells hijacked the vitamin D receptor and reassigned it to perform other cellular functions, such as by repairing DNA damage caused by gemcitabine so the cancer can continue to divide and spread."

Although pancreatic cancer cells need the vitamin D receptor to survive, other normal cells don't, which Yen says is good news for patients because future cancer treatments can knock out the receptor without causing too much collateral damage or side effects, as long as patients take calcium supplements to keep their bones healthy.

"By knocking out the vitamin D receptor, we could inactivate that DNA repair process that is allowing drug-treated tumor cells to live. As a result, we could eliminate more cancer cells at the outset," says Dr. Yen. "The Pancreatic Cancer Action Network has launched an initiative to double patients' survival by 2020; with this new finding, we believe it's a step in the right direction."

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Blue mussels not yet the bellwether of NE coastal environment

Marcy Cockrell installs cages to protect mussels from predators. In Maine, mussels inside cages faired as well as mussels in the wild. In Long Island Sound and Narragansett Bay it was a different story.

Ecologists sometimes look to mussel species, a well-studied and foundational genus in estuaries, as model organisms for assessing the condition of coastal habitats, which are crucial for people and well as the broader environment.

But a new study in the journal Ecosphere suggests that the seemingly simple blue mussel, when studied on regional scale from Maine to Connecticut, harbors at least three specific mysteries that must be solved if the mollusks are to serve as the "canaries in the coal mine" of the Northeast coast.

"Mussels could indeed be a good sentinel species for rocky shores, but what our work suggests is that we need to know a lot more about how they behave in these different estuarine settings to use them as an indicator of ecosystem health," said conservation scientist and study senior author Heather Leslie, the Peggy and Henry D. Sharpe Assistant Professor of Environmental Studies.

For the study, Leslie and former students Marcy Cockrell and Joanna Bernhardt monitored and experimented with mussels at 18 sites in the Casco Bay of Maine, the Narragansett Bay of Rhode Island, and the Long Island Sound of Connecticut and New York in 2010 and 2011 (a region spanning about 600 kilometers of coastline). They measured the abundance of mussels both at adult and larval stages, studied the populations of neighboring rocky shore animals and marine algae, and tracked data on ecosystem factors such as water salinity, temperature, nutrients, oxygen, and local human population density. In the experiments, the team protected some mussels with cages to expose the effect that birds, crabs and other predators have on their numbers.

In the end, the research uncovered three intriguing mysteries of mussel life across the region, particularly in Casco Bay:

Generation gaps: Adults were populous but "recruitment" of young mussels from surrounding waters was low in Long Island Sound and Narragansett Bay. The opposite was true in Casco Bay. There, juvenile recruitment was high but adult populations were low. Few Maine predators: The cage experiments showed a significant role for mussel predators in Long Island Sound and Narragansett Bay, but not in Casco Bay. There, unprotected mussels fared about as well as the protected ones. Inner vs. outer: In each estuary, Leslie's team made measurements at sites nestled well within the bay, as well as at sites closer to the open ocean. Prior research suggested that higher levels of food within the bay would promote growth and abundance for the filter-feeding mussels (due to higher levels of nutrients and phytoplankton at the inner estuary sites). The study results were notably mixed across the whole region, however, providing little support for that hypothesis.

Explanations await further research. Genetic studies could determine, for example, whether the young mussels that are so abundant in Casco Bay may be floating up from the more southerly shores. If so, that suggests that mussel population dynamics can only be understood on regional (or multi-estuary) geographic scale.

Meanwhile, understanding why predator activity seems low in Casco Bay might require learning more about the local predator populations there. The findings could shed light on whether the ecosystem is in balance or other factors are at play.

"We did this because we want to understand how these systems work," Leslie said. "Given their accessibility and how well-studied they have been in other locations, rocky shores are logical sentinel ecosystems. They provide an opportunity to investigate how climate change and other more local-scale human activities are affecting New England's coast."

It may take more work to crack open the mussels' mysteries, but the stakes are high enough to make it worthwhile, Leslie said.

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DNA clock helps to get measure of people's lifespans

Researchers studied chemical changes to DNA that take place over a lifetime, and can help them predict an individual's age. By comparing individuals' actual ages with their predicted biological clock age, scientists saw a pattern emerging.

Scientists have identified a biological clock that provides vital clues about how long a person is likely to live.

Researchers studied chemical changes to DNA that take place over a lifetime, and can help them predict an individual's age. By comparing individuals' actual ages with their predicted biological clock age, scientists saw a pattern emerging.

People whose biological age was greater than their true age were more likely to die sooner than those whose biological and actual ages were the same.

Four independent studies tracked the lives of almost 5,000 older people for up to 14 years. Each person's biological age was measured from a blood sample at the outset, and participants were followed up throughout the study.

Researchers found that the link between having a faster-running biological clock and early death held true even after accounting for other factors such as smoking, diabetes and cardiovascular disease.

Scientists from the University of Edinburgh, in collaboration with researchers in Australia and the US, measured each person's biological age by studying a chemical modification to DNA, known as methylation.

The modification does not alter the DNA sequence, but plays an important role in biological processes and can influence how genes are turned off and on. Methylation changes can affect many genes and occur throughout a person's life.

Dr Riccardo Marioni, of the University of Edinburgh's Centre for Cognitive Ageing and Cognitive Epidemiology, said: "The same results in four studies indicated a link between the biological clock and deaths from all causes. At present, it is not clear what lifestyle or genetic factors influence a person's biological age. We have several follow-up projects planned to investigate this in detail."

The study's principal investigator, Professor Ian Deary, also from the University of Edinburgh's Centre for Cognitive Ageing and Cognitive Epidemiology, said: "This new research increases our understanding of longevity and healthy aging. It is exciting as it has identified a novel indicator of aging, which improves the prediction of lifespan over and above the contribution of factors such as smoking, diabetes, and cardiovascular disease."

The study is published in the journal Genome Biology.

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Population genomics unveil seahorse domain

This is a lined seahorse (Hippocampus erectus).

In a finding vital to effective species management, a team including City College of New York biologists has determined that the lined seahorse (Hippocampus erectus) is more a permanent resident of the western mid-Atlantic Ocean than a vagrant.

The fish is commonly found in three western Atlantic zoogeographic provinces, although inhabitants of the temperate northern Virginia Province are often considered tropical vagrants that arrive during warm seasons from the southern provinces and perish as temperatures decline.

Researchers including PhD student J.T. Boehm and Dr. Michael Hickerson of City College decided to test the alternative hypotheses of historical persistence versus the ephemerality of a northern Virginia Province population. They used a dataset consisting of 11,708 randomly sampled spots from the genomes of individuals collected from the eastern Gulf of Mexico to Long Island, N.Y.

"Concordant results from genomic analyses all infer three genetically divergent subpopulations, and strongly support Virginia Province inhabitants as a genetically diverged and a historically persistent ancestral gene pool," said Boehm.

The results suggested that individuals that emerge in coastal areas during the warm season can be considered "local" and support offshore migration during the colder months.

"This research demonstrates how a large number of genes sampled across a geographical range can capture the diversity of coalescent histories (across loci) while inferring population history," said Hickerson. "Moreover, these results clearly demonstrate the utility of population genomic data to infer peripheral subpopulation persistence in difficult-to-observe species."

The study appeared in the journal PLOS ONE on January 28, 2015.

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Scientists investigate link between skyrocketing sea slug populations, warming seas

The warm ocean temperatures that brought an endangered green sea turtle to San Francisco in early fall have triggered a population explosion of bright pink, inch-long sea slugs in tide pools along California's central and northern coastline.

The warm ocean temperatures that brought an endangered green sea turtle to San Francisco in September have triggered a population explosion of bright pink, inch-long sea slugs in tide pools along California's central and northern coastline. The Hopkins' Rose nudibranch, while no strange sight in Southern California, is rarely spotted farther north. A team of scientists, including experts from the California Academy of Sciences, believes this far-flung Okenia rosacea bloom--along with a slew of other marine species spotted north of their typical ranges--may signal a much larger shift in ocean climate and a strong forthcoming El Niño.

Researchers from the California Academy of Sciences, UCSB, UCSC, and Bodega Marine Laboratory are carefully tracking the atypical sea slug distribution, reporting densities in the dozens per square meter in tide pools from San Luis Obispo to Humboldt Counties. The pink nudibranchs have not appeared so far north or in such high numbers since the strong El Niño events--periods of warmer-than-usual ocean water and heavy rains--of 1998 and 1983.

Without an official El Niño on record for 2015, scientists note that the recent sea slug bloom may mirror a much larger climate shift that occurred in the eastern Pacific Ocean nearly four decades ago. In 1977, rose-like Okenia rosacea appeared in record numbers along the California coast under weak El Niño conditions, coinciding with a major, decades-long period of elavated ocean temperatures. Warmer coastal waters altered the ranges of many ocean-dwellers, including several species of gastropods, fishes, and dolphins.

"While we are thrilled to see this beautiful bloom of normally-rare nudibranchs, we are concerned about the long term consequences of our changing coastal environment," says Dr. Terry Gosliner, Academy Curator of Invertebrate Zoology and Geology. "Our current climate conditions are great for some of my favorite slugs, but we can't ignore that warming seas mean less food for sea birds, and adverse impacts for all marine ecosystems. California's unique marine life can't always adapt to so much instability." Gosliner adds that frequent habitat disruptions could point to mass extinctions in coming decades.

In a 2011 report in Limnology and Oceanography, Gosliner and a team of marine experts linked widespread nudibranch blooms with periods of warming ocean temperatures. The report predicts a range-shift in sea slug populations when warm temperatures, northward ocean currents, and weak upwelling (a phenomenon that pushes cold, nutrient-rich water to the ocean's surface) overlap. "We're seeing this exact cocktail of climate conditions in California right now," says Gosliner. "We are tracking the trends to find out exactly what the shift means and how it might impact marine life."

Hopkin's Rose nudibranchs are ideal for tracking relatively rapid changes in ocean conditions. The showstopping slugs are fast-growing, live for about one year, and tend to spend their adult lives in a small patch of the ocean floor. Like previous population explosions of Okenia rosacea, the current nudibranch bloom includes species typically found farther south, including the bright purple and orange Spanish Shawl, Flabellina iodinea, and the California Sea Hare, Aplysia californica.

Though researchers believe the recent nudibranch population explosion might signal another major climate shift from cold to warm, it is simply too early to call. If a major ocean climate shift is in fact underway, Academy Research Associate Dr. Jeff Goddard believes there is a good chance the next El Niño will pack a punch on par with the 1983 and 1998 California events. As with any strong El Niño event, Californians should expect to see many species from Southern California appear farther north.

It doesn't take a scientist to spot a bright pink Hopkins' Rose nudibranch. Californians can snag a prime view of the current sea slug bloom in rocky shore tide pools along the Central Coast at Montaña de Oro and Asilomar State Parks, Scott Creek Beach, Pigeon and Pillar Points, and Fitzgerald Marine Reserve just north of Half Moon Bay. North Coast slug-finders can visit Duxbury Reef at Bolinas in Marin County. Check your local tide predictions, and aim for a "minus tide" when both the swell and wind are low. Tread lightly when exploring tide pools, and be sure to wear shoes you won't mind getting wet.

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Why do zebras have stripes? Temperature counts

A mother zebra with a foal in Tanzania's Tarangire National Park.

One of nature's fascinating questions is how zebras got their stripes.

A team of life scientists led by UCLA's Brenda Larison has found at least part of the answer: The amount and intensity of striping can be best predicted by the temperature of the environment in which zebras live.

In the January cover story of the Royal Society's online journal, Open Science, the researchers make the case that the association between striping and temperature likely points to multiple benefits -- including controlling zebras' body temperature and protecting them from diseases carried by biting flies.

"While past studies have typically focused their search for single mechanisms, we illustrate in this study how the cause of this extraordinary phenomenon is actually likely much more complex than previously appreciated, with temperature playing an important role," said Thomas B. Smith, professor of ecology and evolutionary biology in the UCLA College and senior author of the research.

Larison, a researcher in UCLA's department of ecology and evolutionary biology and the study's lead author, and her colleagues examined the plains zebra, which is the most common of three zebra species and has a wide variety of stripe patterns. On zebras in warmer climes, the stripes are bold and cover the entire body. On others -- particularly those in regions with colder winters such as South Africa and Namibia -- the stripes are fewer in number and are lighter and narrower. In some cases, the legs or other body parts have virtually no striping.

Zebras evolved from horses more than 2 million years ago, biologists have found. Scientists have previously hypothesized that zebras' stripes evolved for one, or a combination of, four main reasons: confusing predators, protecting against disease-carrying insects, controlling body temperature and social cohesion. And while numerous previous studies of the phenomenon focused on a single hypothesis, the Larison-led study was the first to fully test a large set of hypotheses against one another.

Analyzing zebras at 16 locations in Africa and considering more two dozen environmental factors, the researchers found that temperature was the strongest predictor of zebras' striping. The finding provides the first evidence that controlling body temperature, or thermoregulation, is the main reason for the stripes and the patterns they form.

Separate research by Daniel Rubenstein, a Princeton University professor of ecology and evolutionary biology and a co-author of the Open Science paper, and Princeton undergraduate Damaris Iriondo strongly suggests that boldly striped zebras have external body temperatures about five degrees Fahrenheit cooler than other animals of the same size -- like antelopes -- that do not have stripes but live in the same areas. The Rubenstein study is not yet published, but it is cited in the Open Science paper.

Larison has studied many zebras during her field work throughout Africa -- including in Kenya, South Africa, Tanzania, Uganda and Zimbabwe. Using the fact that their stripes are unique like fingerprints, she is able to distinguish one zebra from another.

In addition to Rubenstein, arguably the world's leading expert on zebras, the study's co-authors were Alec Chan-Golston and Elizabeth Li, former UCLA undergraduates in mathematics; Ryan Harrigan, an assistant adjunct professor in UCLA's Center for Tropical Research; and Henri Thomassen, a former UCLA postdoctoral scholar and current research associate at the Institute for Evolution and Ecology at Germany's University of Tübingen.

The research was supported by the National Geographic Society Committee for Research and Exploration.

Larison and her research team have also collected zebra tissue samples and have used cutting-edge technology to sequence zebra DNA to try to identify which genes code for striping. The team is continuing to study the benefits stripes provide.

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