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Archive - Oct 21, 2015

New Bumblebee Study Contradicts Hypothesis That Single Group of Queen Pheromones Controls Reproduction Across Wide Group of Social Insects

Chemical signaling among social insects, such as bees, ants, and wasps, is more complex than previously thought, according to researchers at Penn State and Tel Aviv University. These scientists recently published data conteradicting earlier data that a single group of chemicals controls reproduction across numerous species. "While the hypothesis that many social insect lineages all use the same chemical signals -- known as pheromones -- was fascinating, we were skeptical that such complex behaviors could be regulated by a simple, common mechanism across such very different species," said Etya Amsalem, Ph.D., postdoctoral fellow in entomology at Penn State. "It seems more likely that pheromones evolved uniquely in different species, as these species experienced different environments and different social pressures." The new results were published in an open-access article in the October 22, 2015 issue of the Proceedings of the Royal Society B. The article is titled “A Conserved Class of Queen Pheromones? Re-Evaluating the Evidence in Bumblebees (Bombus impatiens).” According to Dr. Amsalem, in January 2014, a study was published suggesting that the chemical signals produced by queens from a variety of species, including bumblebees, ants, and wasps, are very similar. The paper posited that this common group of chemicals is responsible for inhibiting reproduction in workers across these different species. "One of the most fascinating behaviors in social insects is that most of the females in a colony (the workers) do not lay their own eggs, and instead help rear the eggs produced by their mother (the queen)," said Dr. Amsalem.

Sendai Virus C Protein Interferes with Domain Arrangement of STAT1 Dimer to Inhibit Signal Transduction Pathway of Interferon-Gamma & Avoid Innate Immune Response of Host; Possible New Clue to Combating Human Paramyxoviruses Such As Mumps and Measles

A research group at Hiroshima University in Japan has demonstrated the mechanism by which the rodent-infecting Sendai virus escapes attack by the rodent innate immune system. The researchers examined the crystal structure of the complex of Sendai virus C protein and rodent transcription factor STAT1, and found that the Sendai C protein inhibits STAT1 activation by the signal transduction pathway of interferon-gamma. This discovery will allow the design of drugs that can be used to overcome and recover from damage caused by inhibition of the interferon signal transduction pathway as the drugs can be designed to inhibit the binding between C protein and STAT1. The results were published online on September 2, 2015 in the Journal of Virology. The article is titled “Structural Basis of the Inhibition of STAT1 Activity by Sendai Virus C Protein.” Researchers are now trying to screen low-molecular-weight compounds to identify promising candidates for the development of new anti-viral drugs. Sendai virus, a prototype of the paramyxoviridae family, causes respiratory diseases in rodents. The paramyxoviridae family includes viruses that cause important diseases in humans and animals, such as measles virus, mumps virus, human parainfluenza virus, human respiratory syncytial virus, canine distemper virus, Newcastle disease virus, and Nipah virus. Sendai virus has unique C proteins. These C proteins are essential for efficient viral replication in cells and animals, as well as for causing diseases. Sendai virus C proteins were previously reported to obstruct STAT1 activation after interferon stimulation, but it remained unclear as to how C proteins bind and affect STAT1 and inhibit transcriptional activation.