Molecular studies in yeast have yielded surprising evidence that the contorted proteins known as prions, often deadly to cattle and humans, may serve a beneficial role in some organisms, and possibly in humans. By analyzing the gene sequences of yeast and more complex organisms, researchers at UC San Francisco have also found evidence that prions might be far more common than had been previously suspected.
The scientists also searched for and discovered a yeast species containing more than one kind of prion-forming protein, the first time a search has netted multiple prions in the same organism. The discoveries and analysis are published in the January 21 issue of the journal Cell.
Prions' capacity to replicate in the brains of cattle and humans is thought to cause deadly or debilitating disease. But the researchers have detected the prion-forming trait intact in distantly related yeast species spanning 300 million years of evolution, suggesting prions perform a function important to yeast survival, since traits conserved over evolutionary time tend aid survival. Other researchers have found that yeast with prions known as PSI+ are more resistant to certain environmental insults than those lacking prions, hinting at a possible prion role in yeast survival.
The research also sheds light on the mechanism underlying the "species barrier" that usually prevents prions in one species from infecting other species. The barrier has been thought to prevent the transmission of scrapie and mad cow disease from livestock to humans, but recently researchers found alarming evidence that in some cases prions from cattle may infect other species, including humans.
The research in Cell shows that at least in yeast, the species barrier is an inherent property of prions and does not require assistance from a helper protein, or chaperone. The specificity, the researchers found, results form a small, well defined region on the prion
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Contact: Wallace Ravven
wravven@pubaff.ucsf.edu
415-476-2557
University of California - San Francisco
19-Jan-2000