Genetic Analysis of Postzygotic Isolation and Recombination Rate Differences in Drosophila

My dissertation research explores the genetics of hybrid incompatibilities and, separately, the evolution of recombination rates in D. melanogaster and its sibling species. In Chapter 1, I show that a hybrid lethality factor(s) in the pericentric heterochromatin of the D. mauritiana X chromosome, hybrid lethal on the X (hlx), is incompatible with a factor(s) in the same ∼26-kb autosomal region from both D. sechellia and D. simulans, Suppressor of hlx (Su[hlx] ). By combining genetic and phylogenetic information, I infer that hlx-Su(hlx) hybrid lethality is most likely caused by a derived-ancestral incompatibility. In Chapter 2, I map a recessive factor to the pericentromeric heterochromatin of the X chromosome in D. simulans and D. mauritiana, heterochromatin hybrid lethal (hhl), that causes lethality in F1 hybrid females with D. melanogaster. Using small segments of the D. melanogaster X chromosome duplicated onto the Y chromosome, I then map a dominant factor that causes hybrid lethality to a small 24-gene region of the D. melanogaster X and provide evidence suggesting that it interacts with hhlmau. In Chapter 3, I estimate crossover frequencies for seven segments that tile across the euchromatic length of the D. mauritiana X chromosome when introgressed into the genetic backgrounds of D. simulans and D. sechellia. My analyses suggest that both cis- and trans-acting factors contribute to differences in the genetic control of crossover frequencies on the X among the D. simulans clade species. In Chapter 4, I perform an evolutionary screen of meiotic genes to identify potential candidate genes that might contribute to species differences in the rate of crossing over. I then use a transgenic approach to introduce the D. mauritiana allele of mei-218 into D. melanogaster flies homozygous for a loss-of-function mutation at mei-218 and ask if the D. mauritiana mei-218 allele produces a D. mauritiana-like map in otherwise D. melanogaster flies. I show that the highly divergent meiosis gene, mei-218, is responsible for most of the 1.55-fold phenotypic difference in genetic map length of chromosome 2 between D. melanogaster and D. mauritiana