Genomic conflict & germline developmental epigenetics
1 PhD project proposal in the IPP summer call 2019
Transposons are obligated genetic parasites that drive their own heritability by over-replicating in the germline of a host genome. They are extremely successful: the genome of every eukaryote is populated with transposons and they constitute nearly half the total sequence of a typical mammalian genome. They are a source of genome instability, threatening fertility and the genetic quality of the gametes. This strongly favors selection for host mechanisms that restrict their activity in the germline. In turn, if transposons are to evolutionarily survive, they must evade these mechanisms and become active specifically within the germ cell lineage. This self-propagating conflict effectively constitute an arms-race in which germ cells represent an ancient front of battle. As we know it today, mammalian gametogenesis involves waves of transposon expression that are timely matched by the presence of genome defense mechanisms. These provide an efficient molecular system that identifies –among many millions of transposon sequences– the potentially dangerous copies for targeted, life-long epigenetic suppression. This elegant choreography carved upon millions of years of positive selection conceals a grim perspective that is unearthed on mutants of genome defense genes: germ cell death and complete infertility due to massive transposon reactivation.
PhD project: Uncovering a regulatory arms-race during mammalian germ cell development