The fundamental asymmetry of female meiosis (only one of the four products becomes and egg) creates an arena for chromosomes to compete, promoting the selfish evolution of centromere variants that maximize their transmission to the future egg. Such 'female meiotic drive' has been hypothesized to explain the paradoxically complex and rapidly evolving nature of centromere proteins and DNA in nearly all eukaryotes, to influence karyotypic evolution, and to drive the evolution of hybrid incompatibilities. Chromosomal competition may directly decrease fertility or transmit linked deleterious variation. Understanding female meiotic drive, therefore, also illuminates the causes of variation in reproductive fitness--a central issue in evolutionary biology, agriculture, and human health.
In Mimulus, populations vary for the presence of a centromere that evolves selfishly through female meiotic drive. This creates a natural laboratory to investigate the causes and consequences of female meiotic drive. In the Finseth lab, we combine bioinformatics, genetic , and molecular ecology approaches to understand how female meiotic drive shapes genomic and phenotypic variation.
A selfishly evolving centromere (red bars) dramatically affects molecular variation across chromosome 11 in Mimulus guttatus. The centromere spans a large, re-arranged region with elevated linkage disequilibrium (boxed) and exhibits a striking reduction in nucleotide diversity (horizontal bar, purple) for individuals with the selfish centromere.