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Archive - 2018

January 2nd

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 (https://www.youtube.com/watch?v=vSmEsuhEDK0) 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.”