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 hhl^mau.

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.