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Archive - Apr 8, 2017

New Studies Reveal How Some Chickens Developed Striped Feathers

Birds show an amazing diversity in plumage color and patterning. But what are the genetic mechanisms creating such patterns? In a new study published on April 7, 2017 in PLOS Genetics, Swedish and French researchers report that two independent mutations are required to explain the development of the sex-linked barring pattern in chickens. Both mutations affect the function of CDKN2A, a tumor suppressor gene associated with melanoma in humans. Research in pigmentation biology has made major advances the last 20 years in identifying genes controlling variation in pigmentation in mammals and birds. However, the most challenging question is still how color patterns are genetically controlled. Birds are outstanding as regards the diversity and complexity in color patterning. The study published in the open-access PLOS Genetics has revealed the genetic basis for the striped feather characteristic of sex-linked barring. One example of this fascinating plumage color is the French breed Coucou de Rennes. The name refers to the fact that this plumage color resembles the barring patterns present in the common cuckoo (Cuculus canorus). The sex-linked barring locus is on the Z chromosome. (In chickens, as well as in other birds, the male has chromosomes ZZ, while females have ZW). The PLOS Genetics article is titled The evolution of Sex-linked barring alleles in chickens involves both regulatory and coding changes in CDKN2A.” "Our data show that sex-linked barring is caused by two independent mutations that act together. One is a regulatory mutation that increases the expression of CDKN2A. The other changes the protein sequence and makes the protein less functionally active.

Salk Institute & Peking University Scientists Develop Stable Stem Cell Line with Totipotent-Like Features; Single Derived “Extended” Stem Cell Could Give Rise to Whole Mouse; Advance “Will Have Broad and Resounding Impact on Stem Cell Field”

When scientists talk about laboratory stem cells being totipotent or pluripotent, they mean that the cells have the potential, like an embryo, to develop into any type of tissue in the body. What totipotent stem cells can do that pluripotent ones can't do, however, is develop into tissues that support the embryo, like the placenta. These are called extra-embryonic tissues, and are vital in development and healthy growth. Now, scientists at the Salk Institute, in collaboration with researchers from Peking University, in China, are reporting their discovery of a chemical cocktail that enables cultured mouse and human stem cells to do just that: generate both embryonic and extra-embryonic tissues. Their technique, described in the April 6, 2017 issue of Cell, could yield new insights into mammalian development that lead to better disease modeling, drug discovery and even tissue regeneration. This new technique is expected to be particularly useful for modeling early developmental processes and diseases affecting embryo implantation and placental function, possibly paving the way for improved in vitro fertilization techniques. The Cell article is titled” Derivation of Pluripotent Stem Cells with In Vivo Embryonic and Extraembryonic Potency.” "During embryonic development, both the fertilized egg and its initial cells are considered totipotent, as they can give rise to all embryonic and extra-embryonic lineages. However, the capture of stem cells with such developmental potential in vitro has been a major challenge in stem cell biology," says Salk Professor Juan Carlos Izpisua Bemonte, Ph.D., co-senior author of the paper and holder of Salk's Roger Guillemin Chair.

Neighboring Biofilms Practice Time-Sharing When Nutrients Are Scarce

While the idea of splitting getaway condos in exotic destinations among various owners has been popular in real estate for decades, biologists at the University of California San Diego have discovered that communities of bacteria have been employing a similar strategy for millions of years. Researchers in molecular biologist Dr. Gürol Süel's laboratory in UC San Diego's Division of Biological Sciences, along with colleagues at the Universitat Pompeu Fabra in Spain, asked what competing communities of bacteria might do when food becomes scarce. The team found that bacteria faced with limited nutrients will enter an elegant time-sharing strategy in which communities alternate feeding periods to maximize efficiency in consumption. The study was published online on April 6, 2017 in Science. The article is titled “Coupling Between Distant Biofilms and Emergence of Nutrient Time-Sharing.” "What's interesting here is that you have these simple, single-celled bacteria that are tiny and seem to be lonely creatures, but in a community, they start to exhibit very dynamic and complex behaviors you would attribute to more sophisticated organisms or a social network," said Dr. Süel, Associate Director of the San Diego Center for Systems Biology and a Howard Hughes Medical Institute - Simons Faculty Scholar at UC San Diego. "It's the same time-sharing concept used in computer science, vacation homes, and a lot of social applications. "In January, Dr. Süel and his colleagues discovered that structured communities of bacteria, or "biofilms," use electrical signals to communicate with, and recruit, neighboring bacterial species. The new study investigates how two biofilm communities interact.

ESCRT-III Acts Downstream of MLKL to Regulate Necroptotic Cell Death

A research team led by St. Jude Children's Research Hospital immunologists has discovered how a set of proteins delays the "executioner" machinery that kills damaged or infected cells in a process called necroptosis. The scientists believe the finding may have wide clinical implications if researchers can develop drugs to control the cellular rescue machinery. Rescue treatments that prevent necroptosis in transplanted organs could reduce injury to the transplant caused by lack of oxygen, researchers said. Drugs to rescue cells from necroptosis could also help prevent injuries to tissue deprived of blood by heart attack and stroke. In such cases, restoring blood flow and oxygenation triggers inflammation that kills tissue. The researchers said cell-rescuing drugs could also thwart cancer spread by protecting blood vessel cells from being killed by tumor cells. Tumor cells escape the bloodstream to spread in the body by killing blood vessels. Blocking the rescue machinery might also prove useful in treating cancers, by enhancing death of cancer cells by necroptosis. In treating neurodegenerative disorders such as ALS--also known as Lou Gehrig's Disease--activating the rescue machinery could help prevent death of brain cells. And in treating viral infections such as influenza, rescue treatment could extend the life of cells infected by the virus, so that the body's immune system would be more strongly alerted to fight the infection. The researchers were led by Douglas Green, Ph.D., Chair of the St. Jude Department of Immunology. The first author was Yi-Nan Gong, Ph.D., a scientist in Dr. Green's laboratory. The research appears in the the April 6, 2017 issue of the prestigious journal Cell.

Involuntary Movement (Tardive Dyskinesia) Side-Effects of Anti-Psychotic Drugs Are Reduced by Treatment with Valbenzanine, an Anti-VMAT2 Inhibitor

Involuntary Movement (Tardive Dyskinesia) Side-Effects of Anti-Psychotic Drugs Are Reduced by Treatment with Valbenzanine,an Anti-VMAT2 Inhibitor. Anti-psychotic medications can cause involuntary movements such as lip smacking, tongue protrusions and excessive eye blinking. These movements typically occur after more than three months of treatment and are called tardive dyskinesia. Robert A. Hauser, M.D., M.B.A., Professor of Neurology at the University of South Florida (USF) in Tampa, is the lead author of a study published recently in the American Journal of Psychiatry that concludes that valbenazine administered once daily can significantly reduce tardive dyskinesia in patients with schizophrenia, schizoaffective disorder, and mood disorder. The article is titled “KINECT 3: A Phase 3 Randomized, Double-Blind, Placebo-Controlled Trial of Valbenazine for Tardive Dyskinesia.”"One approach to managing tardive dyskinesia is to discontinue anti-psychotic treatment or reduce the dosage, but these options are not always feasible, because withdrawal can exacerbate tardive dyskinesia symptoms or have a negative impact on psychiatric status. Moreover, tardive dyskinesia symptoms often persist even after discontinuation or dosage reduction," wrote Dr. Hauser, who directs the Parkinson's Disease and Movement Disorders Center at USF. Valbenazine is a selective vesicular monoamine transporter 2 (VMAT2) inhibitor. VMAT2 is an integral membrane protein that transports monoamines—particularly neurotransmitters such as dopamine, norepinephrine, serotonin, and histamine—from the cellular cytosol into synaptic vesicles. In nigrostriatal pathway and mesolimbic pathway dopamine-releasing neurons, VMAT2 function is also necessary for the vesicular release of the neurotransmitter GABA.