| Species are discrete groups of organisms that are reproductively isolated from other related groups of organisms. Variation in the strength of reproductive isolation between closely related taxa falls along a 'speciation continuum', from weakly isolated structured populations to fully isolated sister species. Efforts to understand the genetics of speciation have focused primarily on developmental defects in hybrids (intrinsic postzygotic isolation) leading to sterility or inviability. Once speciation is complete, species continue to diverge as a result of mutation, genetic drift, and selection, and new forms of reproductive isolation may continue to accumulate. Therefore, at later stages in the 'speciation continuum', it is unclear whether a given isolating barrier is a cause, or a consequence of speciation. In my dissertation, I focus on the genetics of intrinsic postzygotic isolation occurring early in the 'speciation continuum' at the onset of speciation. In chapter 1, I highlight where the assumptions of dominance theory are particularly problematic in marsupials, where X inactivation uniformly results in silencing the paternal X. I then present evidence of Haldane's rule for sterility but not for viability in marsupials, as well as the first violations of Haldane's rule for these traits among all mammals. Marsupials represent a large taxonomic group possessing heteromorphic sex chromosomes, where the dominance theory cannot explain Haldane's rule. In this light, I evaluate alternative explanations for the pre- ponderance of male sterility in interspecific hybrids, including faster male evolution, X-Y interactions, and genomic conflict hypotheses. In chapter 2, I revisit three mechanisms highlighted by Rose and Doolittle (1983) as a convenient conceptual scaffold for understanding the variety of ways TEs might directly, or indirectly, cause reproductive incompatibility. In chapter 3, I describe an example of hybrid incompatibility (called "still") segregating in F 1 hybrids between populations of T. castaneum, whereby affected offspring exhibit a suite of maladaptive traits upon eclosion from the pupal stage. To investigate the genetic cause of the still phenotype, I sequenced the genomes of still and normal siblings using pooled-DNA and employed a genome scan approach that compares allele frequencies between extremely discordant sib pairs (still vs normal) to identify discordant alleles. In total, I identified 97 genes with significantly discordant non-synonymous SNPs between still and normal siblings. An additional 355 genes possess nucleotide changes that are either synonymous, or non-coding (i.e. occur in introns or within 1000kb upstream or downstream). Interestingly, a set of 19 candidate loci were recently identified as candidate phosphine resistance genes. Phosphine is an insecticidal fumigant which acts as a metabolic toxin by targeting redox reactions, and is used worldwide in grain storage and processing facilities. The Chicago population was collected over 7 decades aco, predating the use of phosphine, while Tanzania populations were potentially subjected to 30 years, or roughly 330 generations of routine phosphine exposure before it was collected and kept in the laboratory. I discuss this observation in light of the role of genetic conflict in generating hybrid incompatibilities, especially where they are still segregating early in the 'speciation continuum'. |
