A genetic incompatibility in DNA mismatch repair: consequences for adaptive evolution
November 12, 2012
Academic Building A G008, 5:00 PM
This talk is cosponsored with the Department of Biological Sciences
Cells replicate their DNA once every cell cycle. Amazingly, this process occurs with extremely high fidelity, with errors occurring at rates as low as one in a billion per cell division. This low error rate results from both the fidelity of the replication machinery and the action of mismatch repair proteins that recognize rare errors made by the machinery. Over the years my lab has carefully analyzed the functions of the MLH1-PMS1 mismatch repair complex. Curiously we observed a defect in this complex when specific combinations of MLH1 and PMS1 were obtained from different baker’s yeast strains and then tested for function. We then showed that amino acid differences that could cause such an incompatibility are found in strains collected from across the globe. These observations provide a powerful model in which to understand the basis of disease penetrance and how segregation of defects in mismatch repair may allow for rapid yet reversible changes in genomic mutation rates that can help yeast adapt to changing or novel environments.
Alani received a B.S. degree from Massachusetts Institute of Technology in 1984 and a Ph.D. from Harvard University in 1990. He was a Life Sciences Research Foundation Merck fellow (1991-1994) at Harvard Medical School in Boston before joining the faculty at Cornell in 1995. Dr. Alani’s research has been supported by the National Institutes of Health and the United States Department of Agriculture. He works on functional aspects of DNA mismatch repair and genetic recombination, with occasional forays into molecular evolution.
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