"genomic changes in a rat model for intrinsic running capacity"
In humans, high aerobic exercise capacity is associated with decreased susceptibility to multiple diseases. The reason for this correlation is unclear. Understanding the genetics and epigenomics of aerobic exercise capacity may shed light on the molecular mechanisms of this relationship. In order to understand the epigenomics of aerobic exercise capacity, here we use a rat model for intrinsic (untrained) running capacity. This rat model is comprised of two lines that are divergent in their intrinsic running capacity, referred to as high capacity runners (HCRs) and low capacity runners (LCRs).
We hypothesize that selective pressure on skeletal muscle regulatory elements in the rats has led to differences in promoter/enhancer usage between the lines, and that this is partially responsible for the disparate exercise capacity of the HCRs and LCRs. In order to determine which promoters and enhancers are differentially accessible between the lines, our lab generated ATAC-seq data from the HCRs and LCRs, both at rest (n = 4 HCRs, n = 5 LCRs) and after 10 minutes of running (n = 5 HCRs, n = 5 LCRs). We identifed several hundred regions in which the HCRs and LCRs display differential chromatin accessibility. We plan to use allelic bias in the ATAC-seq data to determine if transcription factor binding to regulatory elements is altered by cross-line genetic differences.