Essential roles for RNAi/hpRNAs to resolve intragenomic conflicts in the male germline

PROJECT ABSTRACT Intragenomic conflicts are fueled by rapidly evolving selfish genetic elements, which emerge intrinsically within genomes. If left unchecked, these can be disastrous to the individual and/or the population. Thus, such conflicts induce strong pressures to innovate opposing mechanisms of repression. This is patently manifest in paradoxical meiotic drive systems, in which the wildtype activities of selfish genes can have deleterious consequences to bias the sex ratio of progeny (typically eliminating males), or to induce frank sterility. However, relatively little is known about the molecular mechanisms of meiotic drive genes and their control. Our recent work provides first evidence that related, recently-evolved, sex-biasing and sterility-inducing systems in the non-model fruitfly D. simulans are suppressed by endogenous siRNA loci. This provides a unique foundation to study how meiotic drive loci are tamed at the post-transcriptional level. Although little is generally known about the biochemical function of selfish meiotic drive loci, our data support testable models in which these D. simulans distorter gene products may interfere with chromatin packing in sperm. Finally, we will examine the broader evolutionary implications for how endogenous siRNAs may unlock maps of intragenomic conflicts in multiple Drosophila species, and examine a rationale for analogous molecular battles during mammalian meiosis. Our multidisciplinary investigations will elucidate mechanisms that link tissue-specific de novo gene activity and small RNAs with rapid genome dynamics that may impose the reproductive isolation of individuals, potentially early steps on the path towards speciation.