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Archive - Jun 5, 2009

Genome of Honey Bee-Killing Parasite Is Sequenced

Researchers at the USDA’s Agricultural Research Service, and colleagues, have reported the draft sequencing of the genome of a parasite that can kill honey bees. The parasite, Nosema ceranae, is one of many pathogens suspected of being responsible for the current decline in honey bee populations. This decline has been attributed to what is called colony collapse disorder (CCD). In 2006, CCD began devastating commercial beekeeping operations, with some beekeepers reporting losses of up to 90 percent, according to the USDA. Researchers believe CCD may be the result of a combination of pathogens, parasites, and stress factors, but the cause remains elusive. At stake are honey bees that play a valuable part in a $15 billion industry of crop farming in the United States. The microsporidian Nosema is a fungus-related microbe that produces spores that bees consume when they forage. Infection spreads from the bee’s digestive tract to other tissues. Within weeks, colonies are either wiped out or lose much of their strength. One Nosema species, Nosema apis, was the leading cause of microsporidia infections among domestic bee colonies until recently, when N. ceranae jumped from Asian honey bees to the European honey bees used commercially in the United States. Sequencing the N. ceranae genome should help scientists trace the parasite's migration patterns, determine how it became dominant, and help resolve the spread of infection by enabling the development of diagnostic tests and treatments. This work was published June 5 in PLoS Pathogens. [Press release] [PLoS Pathogens article]

Novel Brain Protein May Be Key to Huntington Disease Mystery

Scientists at Johns Hopkins have shown evidence that a novel protein (Rhes) located chiefly in a key area of the brain (the corpus striatum), may be a clue to the mystery of why abnormal huntintin protein, although present in cells throughout the body, exerts its cell-killing and disease-causing effects primarily in the corpus striatum. The findings, according to the Hopkins scientists, explain the unique pattern of brain damage in Huntingtin disease (HD) and its symptoms, as well as offer a strategy for new therapy. “It's always been a mystery why, if the protein made by the HD gene is seen in all cells of the body, only the brain, and only a particular part of the brain, the corpus striatum, deteriorates," said Dr. Solomon H. Snyder, senior author of the report. "By finding the basic culprit (Rhes), the potential is there to develop drugs that target it and either prevent symptoms or slow them down." In their work, the researchers showed that the Rhes protein interacts with the huntingtin protein, but much more strongly with the mutant, disease-causing version than with the normal version. They further showed that presence of both the Rhes protein and the huntingtin protein in cells led to speedy cell death, while the presence of either protein alone did not. They also observed that the presence of the Rhes protein resulted in less clumping of the huntingtin protein in cells, than did the absence of Rhes protein. This could be an explanation for why, in HD, less clumping of huntingtin is observed in the corpus striatum than in the unaffected cells in the body, even though clumping has been proposed, by some, as a cause of the disease. "Here's the Rhes protein, we've known about it for years, nobody ever really knew what it did in the brain or anywhere else," said Dr. Snyder.