Conflict arises within genomes when genetic elements fail to play by the same rules. Selfish genetic elements (e.g. transposable elements, meiotic drivers, satellite DNAs) create conflict when they gain a transmission advantage to the next generation, often at a cost to the host. The Larracuente lab is interested in the mechanisms used by these selfish genetic elements to cheat and their impacts on the evolution of genomes and gametogenesis. Our focus is on the large blocks of rapidly evolving repeats that comprise most eukaryotic centromeres, telomeres, and sex chromosomes—satellite DNAs (satDNAs). SatDNAs play important roles in chromosome segregation and heterochromatin formation, but they also have the capacity to be selfish in the female germline, where there is an opportunity for centromeres to cheat their way into the egg. Misregulating satDNA is associated with genomic instability, mitotic defects, cancer, and aging phenotypes. We integrate methods in functional genomics, population genetics, and molecular genetics to study selfish repetitive sequences involved in intragenomic conflicts. Interests: Evolutionary genetics and genomics; Intragenomic conflict and the evolution of selfish DNA; Evolutionary and functional genomics of satellite DNA; Sex chromosome and dot chromosome evolution in Drosophila; Centromere organization and evolution Skills our lab is looking for: Genetics, molecular biology, computational biology