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DMNS FAIR Queens College, City University of New York Division of Mathematics and Natural Sciences Faculty Achievement In Research MY NAME: Stephane Boissinot MY DEPARTMENT: Biology SOMETHING INTERESTING ABOUT ME (OPTIONAL, MAY BE LEFT BLANK): I am homozygous for an allele at the SNAP-25 gene associated with lower non-verbal I.Q. performances. MY RESEARCH (IN SIMPLE WORDS THAT CAN BE UNDERSTOOD BY ANYONE ON THE Q64 BUS): My laboratory is interested in the process of evolution at the molecular level. More specifically we are investigating two fundamental evolutionary questions: 1- Why does the size of genomes vary so much among vertebrates? The amount of genetic material in a cell is not correlated to the complexity of organisms. In fact, differences in genome size are caused by the differential accumulation of mobile genetic elements called transposable elements or “jumping genes”. Although most transposable elements impose a genetic load on their host they can also be a rich source of evolutionary novelties. However, it is unknown why some species like human have more than 3 millions of these elements whereas most fish carry less than a few 1,000 copies. To address this question we are using a combination of computational and population genetics approaches in several species that differ in their profile of transposable element abundance and diversity. 2- Why do organisms respond differently to viral infection? Why do some individuals get sick, while others remain healthy or mildly affected by viral infection? Among other factors, the genetic background of individuals influences significantly the outcome of viral infection. One of the major players in the defense against viral infection is the oligo-adenylate synthetase (OAS) pathway. Studies in human and mouse strongly suggest that genetic variation at the OAS genes could be influencing host susceptibility to viral infection. However, little is known about the polymorphism of OAS genes and, more importantly, about the selective forces that have shaped their evolution. This is an important issue since patterns of molecular evolution can in turn provide valuable information about the mechanism of resistance to viral infection. We are addressing this issue using a combination of evolutionary, molecular and cellular approaches. MY RESEARCH IN 140 CHARACTERS (OPTIONAL, MAY BE LEFT BLANK):