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Archive - Jul 22, 2017


Elephant Seals Recognize Each Other by Rhythm of Their Calls; Finding Is First for Non-Human Mammals

Every day, humans pick up on idiosyncrasies such as slow drawls, high-pitched squeaks, or hints of accents to put names to voices from afar. This ability may not be as unique as once thought, researchers report on July 20, 2017 in Current Biology. The open-access article is titled "Northern Elephant Seals Memorize the Rhythm and Timbre of Their Rivals' Voices." The scientists find that, unlike all other non-human mammals that have been studied, northern elephant seal males consider the spacing and timing of vocal pulses in addition to vocal tones when identifying the calls of their rivals. "This is the first natural example where on a daily basis, an animal uses the memory and the perception of rhythm to recognize other members of the population," says first author Dr. Nicolas Mathevon, of the Université de Lyon/Saint-Etienne in France. "There have been experiments with other mammals showing that they can detect rhythm, but only with conditioning." Over several years studying an elephant seal colony in Año Nuevo State Park, California, the researchers were able to recognize many of the individual animals just by the rhythm of their voices, he says. To test whether the elephant seals themselves made those distinctions in the same way, the researchers designed an experiment based on the social behavior of the colony's "beta males," who shy away upon hearing the call of a more powerful "alpha male," but ignore or confront other beta males and still-weaker "peripheral males." Upon hearing computer-modified alpha male calls with a sped-up or slowed-down tempo or a shifted pitch range, the beta males fled the scene if the alteration was minute enough to be within the individual variation of a particular alpha male's roar, but stayed put when confronted with more extreme changes.

Patch-Clamp Technique Extended to Intracellular Vesicles

Ion channels in the membrane vesicles that mediate intracellular protein transport play a crucial role in cell physiology. A method developed by a team at Ludwig-Maximilians-Universitaet (LMU) in Munich now allows these vesicles to be studied with greater specificity than ever before. Tiny membrane-bound vesicles known as endosomes and lysosomes serve as vehicles for the transport of protein cargoes within animal cells. Embedded in the vesicle membranes are proteins called ion channels, which control the passage of ions into and out of these intracellular organelles. Defects in these proteins play a central role in the pathogenesis of many diseases, and dissection of their molecular functions is vital for the development of effective therapies for these disorders. PD Christian Grimm and Professor Christian Wahl-Schott of the Department of Pharmacy (Director: Professor Martin Biel) at LMU Munich are among Europe's leading specialists in the use of the so-called “patch-clamp” technique for the study of ion channels in cell membranes. In the July 20, 2017 issue of Nature Protocols, these scientists and colleagues describe how they have adapted the method for use with endolysosomal vesicles. The Nature Protocols article is titled “Patch-Clamp Technique to Characterize Ion Channels in Enlarged Individual Endolysosomes.” In a second study, published in the July 20, 2017 issue of Cell Chemical Biology, the scientists go on to demonstrate how patch clamping can be applied to specific functional classes of transport vesicles. This article is titled “Small Molecules for Early Endosome-Specific Patch Clamping.” The work described in the to articles opens up entirely new perspectives for the characterization of ion channels and the mechanisms that regulate them.

Animal Model for Coffin-Siris Disorder May Provide Insights into Genetic Bases of Some Neuropsychiatric Disorders

A study by scientists at the Children’s Medical Center Research Institute at University of Texas Southwestern (CRI) is providing insight into the genetic basis of neuropsychiatric disorders. In this research, the first mouse model of a mutation in the arid1b gene was created and then used to show that growth hormone treatments reverse some manifestations of the mutation. The ARID1B gene is one of the most commonly mutated genes in patients with intellectual disability and autism spectrum disorders, but scientists have not yet discerned if and how defects in the ARID1B gene contribute to these clinical manifestations. To understand how reduced levels of the protein product of the gene might cause these disorders, a team of researchers led by Hao Zhu, MD (photo) and including graduate student Cemre Celen genetically modified mice to carry a mutation in one of two copies of the arid1b gene. This mutation replicates the genetics of Coffin-Siris syndrome, a disorder that some patients with defects in the ARID1B gene have that is characterized by speech and social development problems, intellectual disability, and delayed physical growth. The hope is that by understanding the molecular basis of Coffin-Siris syndrome, scientists will gain a deeper understanding of more common diseases involving intellectual and social impairment. Scientists found mice with the mutated arid1b gene exhibited the same type of physical and social changes seen in children with Coffin-Siris syndrome, such as abnormal brain development, muscle weakness, and increased anxiety and fear. The mice also displayed features consistent with autism spectrum disorder, such as social interaction abnormalities, repetitive behaviors, and abnormal “squeaks” or vocalizations.