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.