The rat has provided several models of cardiovascular disease in which genetic susceptibility arises from natural genetic variation and in which such variants have been fixed in homozygosity by inbreeding. This removes the genetic complexity and environmental factors that have impeded the identification of the genetic basis of cardiovascular disease risk in humans. We have been enhancing rat genomic resources with state of the art de novo genome assembly to advance these studies and find that some genetic influences are the result of single nucleotide variation, while others arise from structurally complex regions of the genome that are only now yielding to new assembly methods.

Presented by: Dr. Peter Doris, The University of Texas

CE Eligible: Yes

If attend in-person at the Gluck Center Auditorium. Parking restrictions have been lifted after 3:30pm for the Gluck parking lot.