Melissa Wilson Sayres is an evolutionary and computational biologist broadly interested in questions of genome evolution, mutation rate variation, and the consequences on species biology. She analyzes large-scale datasets to study questions relating to sex-specific mutational processes, including, how sex chromosomes arise and evolve, and how and why mutation rates differ between the sexes. She also develops models and analyzes experimental data to understand the genomic effects of natural selection, background selection, and convergent evolution.
Wilson Sayres received her B.S. in Medical Mathematics from Creighton University in Omaha, Nebraska, her Ph.D. in Integrative Biology: Bioinformatics & Genomics from The Pennsylvania State University, and currently works as a Miller postdoctoral fellow at the University of California, Berkeley.
Title: Sex-biased evolution and disease
Sex-biased processes occur on a variety of levels, from the differentiation of our sex chromosomes, to population dynamics, to the way that diseases affect each sex. The inundation of genomic and transcriptomic sequences provide the opportunity to apply computational and statistical approaches to understand sex-biased processes. The human sex chromosomes, X and Y, were once an indistinguishable pair of autosomes, but over the past 180 million years have become quite different. The Y has lost 90% of the ancestral gene content, but still retains relics of its ancestral partnership with the X. The Y chromosome, inherited through the genetic paternal line, and being nearly devoid of homologous recombination, also experiences evolutionary processes differently that regions that recombine. As such, studying patterns of genome-wide diversity can provide a unique insight into the history of sex-biased demography and selection acting on the Y chromosome. In addition to sex-biased genomics, many diseases, such as the autoimmune disease, Rheumatoid Arthritis (RA), act in a sex-biased manner. RA affects three times as many women as men, and its onset and severity are affected by a complex interaction between genotype and environment. Particularly, pregnancy often has an ameliorating effect on RA disease activity. I will discuss our computational approaches to: 1) understand the degradation of the Y, and how this process has affected the X chromosome; 2) illuminate the history of sex-biased demography and selection acting on the Y chromosome; and, 3) evaluate gene expression variation across clinical RA patients in the natural human model system of pregnancy.
Wednesday April 2nd, 2014
1:00 PM Lunch (sign up below)
1:15 PM Seminar
Location: Clark Center S360
If you would like to speak with Melissa, contact Pleuni Pennings (email@example.com)