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Archive - Jan 2018


January 3rd

New Work Demonstrates Breakdown of Simplest, But Most Widely Used Version of “Kill the Winner” Model to Explain High Levels of Biodiversity, Presents Way to Restore Model’s Explanatory Power

There is remarkable biodiversity in all but the most extreme ecosystems on Earth. When many species are competing for the same finite resource, a theory called “competitive exclusion” suggests one species will outperform the others and drive them to extinction, limiting biodiversity. But this isn't what is actually observed in nature. Theoretical models of population dynamics have not presented a fully satisfactory explanation for what has come to be known as the “diversity paradox.” Now, researchers at the Carl R. Woese Institute for Genomic Biology at the University of Illinois at Urbana-Champaign have shed new light on this fundamental question in ecology, by improving a popular proposed scenario for diversity known as "Kill the Winner." Dr. Chi Xue and Dr. Nigel Goldenfeld (pictured together here), supported by the NASA Astrobiology Institute for Universal Biology, which Dr. Goldenfeld directs, approached the diversity paradox from the perspective of non-equilibrium statistical mechanics. Dr. Goldenfeld and Dr. Xue developed a stochastic model that accounts for multiple factors observed in ecosystems, including competition among species and simultaneous predation on the competing species. Using bacteria and their host-specific viruses as an example, the researchers showed that as the bacteria evolve defenses against the virus, the virus population also evolves to combat the bacteria. This "arms race" leads to diverse populations of both and to boom-bust cycles when a particular species dominates the ecosystem then collapses--the so-called "Kill the Winner" phenomenon. This coevolutionary arms race is sufficient to yield a possible solution to the diversity paradox.

January 2nd

Epigenetic Changes to CRH Gene Linked to Severity of Suicide Attempts

Researchers have linked genetic changes in the corticotropin-releasing hormone (CRH) gene, which affects the regulation of the body's stress system, to suicide risk and psychiatric illness. The study of epigenetic changes in the body's hormone-based stress system has shown that stress-related changes in the CRH gene are linked to both serious suicide attempts in adults and psychiatric illness in adolescents. The research study, which is a collaboration among researchers at Umeå University, Karolinska Institutet, and Uppsala University in Sweden, was published online on December 18, 2017 in EBioMedicine. The open-access article is titled “Epigenetic Changes in the CRH Gene Are Related to Severity of Suicide Attempt and a General Psychiatric Risk Score in Adolescents.” Previous studies have indicated an overactive stress system in individuals with increased suicide risk. In the current study, researchers report that epigenetic changes in the CRH gene, which are linked to serious suicide attempts in adults, could also be found in adolescents with high risk of psychiatric illness. Recently published research output shows that serious suicide attempts lead to a heavily reduced lifespan with an increased suicide risk and risk of mortality from natural causes, particularly in adolescents. In the last ten years, it has become twice as common for Swedish adolescents between the ages of 10 and 17 to suffer from psychiatric illness. An alarming increase also in young adults can be seen. This is according to a recently published report from the Swedish National Board of Health and Welfare. In the current study described in EBioMedicine, researchers examined 88 individuals who had attempted suicide. The participants were divided into high- and low-risk groups based upon the severity of their suicidal behavior.

Nature’s Smallest Rainbows Created by Specialized Abdominal Scales of Peacock Spider; Finding May Have Application to Wide Array of Fields, from Life Sciences & Biotechnologies to Material Sciences & Engineering

Brightly colored Australian peacock spiders (Maratus spp.) captivate even the most arachnophobic viewers with their flamboyant courtship displays featuring diverse and intricate body colorations, patterns, and movements - all packed into miniature bodies measuring less than 5 mm (~0.2 inches) in size for many species. However, these displays aren't just pretty to look at, they also inspire new ways for humans to produce color in technology. One species of peacock spider - the rainbow peacock spider (Maratus robinsoni) - is particularly impressive, because it showcases an intense rainbow iridescent signal in males' courtship displays to the females. This is the first known instance in nature of males using an entire rainbow of colors to entice females to mate. But how do males make their rainbows? Figuring out the answer was inherently interdisciplinary so Dr. Bor-Kai Hsiung - now a postdoctoral scholar at Scripps Institution of Oceanography at the University of California San Diego - assembled a team that included biologists, physicists, and engineers while he was a PhD student at The University of Akron's (UA) Integrated Bioscience PhD program under the mentorship of Dr. Todd Blackledge and Dr. Matthew Shawkey (now at University of Ghent), and supported by UA's Biomimicry Research and Innovation Center. The team included researchers from the United States - UA, Scripps Institution of Oceanography, California Institute of Technology (Caltech), and University of Nebraska-Lincoln (UNL) - Belgium (University of Gent), Netherlands (University of Groningen), and Australia to discover how rainbow peacock spiders produce this unique iridescent signal.

Lethal Fungus That Causes White-Nose Syndrome in Bats May Have Achilles' Heel; Fungus Lacks DNA Repair Enzyme and Is Vulnerable to UV Light

The fungus that causes white-nose syndrome (WNS), a disease that has ravaged bat populations in North America, may have an Achilles' heel: UV light. WNS has spread steadily for the past decade and is caused by the fungus Pseudogymnoascus destructans, known as P. destructans or Pd. In the course of genomic analyses of P. destructans, a team of scientists from the U.S. Forest Service, U.S. Department of Agriculture, and the University of New Hampshire found that the fungus is highly sensitive to UV light. P. destructans can only infect bats during hibernation because it has a strict temperature growth range of about 39-68 degrees Fahrenheit. However, treating bats for the disease during hibernation is challenging, so any weakness of the fungus may be good news to managers trying to develop treatment strategies. In an open-access article published online on January 2, 2018 in Nature Communications titled "Extreme Sensitivity to Ultra-Violet Light in the Fungal Pathogen Causing White-Nose Syndrome of Bats," the research team suggests that P. destructans is likely a true fungal pathogen of bats that evolved alongside bat species in Europe and Asia for millions of years, allowing Eurasian bats to develop defenses against it. In the course of comparing P. destructans to six closely related non-pathogenic fungi, researchers discovered that P. destructans is unable to repair DNA damage caused by UV light, which could lead to novel treatments for the disease. The study, which was funded by the U.S. Fish and Wildlife Service, is available at: "This research has tremendous implications for bats and people," said Dr. Tony Ferguson, Director of the Forest Service's Northern Research Station and the Forest Products Laboratory.

Mystery of How Midshipman Fish Can Sustain Continuous Mating Hum for Up to an Hour Solved; Midshipman Swimbladder Muscles Can Contract Over 360,000 Times in Hour-- Fast Calcium Pumping and Small Calcium Release Are Key

Researchers at the University of Pennsylvania have discovered how the Pacific midshipman fish can hum continuously for up to an hour in order to attract potential mates. The study, which is featured on the cover of the January 2018 issue of the Journal of General Physiology, explains how the muscle fibers surrounding the fish's swimbladder can sustain the high rates of contraction--up to 100 times per second--that are needed to produce the animal's distinctive call. The article is titled “Small Ca2+ Releases Enable Hour-Long High-Frequency Contractions in Midshipman Swimbladder Muscle.” It can be difficult to find a mate within the dark and cloudy waters of the ocean, so the males of several fish species have evolved the ability to emit loud calls that can attract potential female partners to their nest. These mating calls are generated by superfast muscle fibers that surround the fishes' swimbladders and undergo rapid cycles of contraction and relaxation in order to make these gas-filled organs vibrate. Male Atlantic toadfish, for example, contract and relax their swimbladder muscles up to 100-200 times per second to produce short, repetitive "boatwhistle" calls interspersed with relatively long periods of silence. Type I males of the Pacific midshipman fish (Porichthys notatus) are even more remarkable, producing a continuous mating hum for as long as an hour (you can hear a brief snippet in this YouTube video ( a rate of 100 contractions and relaxations per second, the midshipman swimbladder muscle can therefore contract as many as 360,000 times over the course of an hour-long call. "The midshipman swimbladder muscle generates more contractions per hour than any other known vertebrate muscle, explains Lawrence C.

Scheduled Feeding Improves Neurodegenerative Symptoms in Mouse Model of Huntington’s Disease; Results Suggest Eating on Strict Schedule Could Improve Quality Of Life for Those with Neurodegerative Disease

Restricting meals to the same time each day improves motor activity and sleep quality in a mouse model of Huntington's disease, according to new research published online on xxxx in eNeuro, the open-access journal of the Society for Neuroscience. The findings suggest that eating on a strict schedule could improve quality of life for patients with neurodegenerative diseases for which there are no known cures. The eNeuro article is titled “Time Restricted Feeding Improves Circadian Dysfunction As Well As Motor Symptoms in the Q175 Mouse Model of Huntington's Disease.” Dr. Christopher Colwell and colleagues used a well-studied mouse line (Q175) that models the genetic cause and symptoms of Huntington's disease, including sleep disruptions that appear to be a general feature of neurodegenerative disorders. By restricting food availability to a 6-hour period in the middle of the period when the mice are active, the researchers demonstrate in these mice improved performance on two different motor tasks and a more typical rhythm of daily activity. In addition, these mice showed improved heart rate variability, a marker of cardiovascular health, and more typical gene expression in the striatum, a brain region involved in motor control that is susceptible to degeneration in Huntington's disease. This study, which manipulated the availability but not the quantity of food, point to time of feeding as an additional environmental signal that might work in conjunction with light to regulate the body clock. The image illlustrates that, after three months of treatment (when mice reached the early disease stage), the time-restricted feeding-treated Q175 mouse model of Huntington's disease showed improvements in locomotor activity rhythm and sleep awakening time. (Image credit: Wang et al., eNeuro (2018).

January 1st

Scientists Study Relationship Between Epigenetics and Human Egg Cell Stasis

Keeping egg cells in stasis during childhood is a key part of female fertility in humans. New research published online on January 1, 2018 in Nature Structural and Molecular Biology sheds some light on the role of epigenetics in placing egg cells into stasis. A team led by Dr. Gavin Kelsey at the Babraham Institute in the UK and colleagues in Dresden and Munich studied a protein called MLL2 and discovered how it produces a distinctive pattern of epigenetic marks that are needed for egg cell stasis. The article is titled “MLL2 Conveys Transcription-Independent H3K4 Trimethylation in Oocytes.” A fertilized egg cell is the start of every human life. Yet, egg cells are created inside a woman's body before she is born. The eggs are then kept in stasis throughout childhood until they're needed as an adult. If egg cells don't go into stasis they can't become mature eggs and they will never have the chance to form a new life. Putting an egg cell into stasis involves adding many epigenetic marks throughout its DNA. Epigenetic marks attached to DNA act as footnotes, indicating which genes are turned “on” or “off.” The scientists wanted to understand where these marks come from in egg cells and how mistakes can cause disease. It is particularly challenging to study epigenetics in egg cells as there are so few of them. The team had to create new, highly sensitive ways to detect epigenetic marks in such small numbers of cells. Using this approach, they found that, as eggs develop, a mark called H3K4me3 spreads throughout the genome. Scientists have already seen the same mark close to the start of active genes in many cells, but the team discovered that its role in egg cells is different.

Inhibition of Host Factor Enzyme Inhibits Ebola Virus in Cell Culture; Host Phosphatase Is Potential Target for Therapeutic Intervention

A single enzyme. That is all the researchers behind a new study need to manipulate to prevent the feared Ebola virus from spreading. Because with the enzyme they also take away the virus' ability to copy itself and thus produce more virus particles and more infection. The study was published online on December 28, 2017 in Molecular Cell and was conducted by researchers from the University of Copenhagen and Phillips Universität Marburg in Germany. The article is titled “The Ebola Virus Nucleoprotein Recruits the Host PP2A-B56 Phosphatase to Activate Transcriptional Support Activity of VP30.” “When the Ebola virus enters the human cell, its only purpose is to copy itself, fast. First, it must copy all its proteins, then its genetic material. But by inhibiting a specific enzyme we rob the Ebola virus of its ability to copy itself. And that may potentially prevent an Ebola infection from spreading,” says Professor Jakob Nilsson from the Novo Nordisk Foundation Center for Protein Research. A few years ago, the Ebola virus ravaged West Africa, where thousands of people died from the extremely infectious Ebola infection. Once you are infected, all you can do is hope that your own immune system is able to kill the infection because there is currently no available treatment. However, the researchers behind the new study have found what is called a new host factor for Ebola virus. It can be described as a small part of the host's - for example the human body's - own cells, which the Ebola virus uses to copy itself and produce more infection. The virus uses the host factor enzyme PP2A-B56 to start producing proteins. So, if the researchers switch off PP2A-B56, the virus' ability to copy itself and produce more infection is never “switched on.”