Our research is focused on understanding the genetic processes involved in species formation. Understanding how species persist in the face of ongoing hybridization has been a major question in evolutionary biology since Darwin, and is best answered by examining populations at the interface of speciation – closely related species known to hybridize. Recent genetic advances have highlighted the pervasiveness of hybridization in many taxa, increasing the number of relevant species for studying this question. Further, dense marker analysis has revealed that genetic exchange between these species is not uniformly distributed across the genome. This work suggests that species persist despite ongoing gene flow due to local genetic barriers that prevent incorporation of hybrid alleles within the genome. My work has examined how chromosomal inversions accomplish this task by reducing recombination rates specifically in hybrid individuals, thus limiting gene flow between species in these inverted segments of the genome. As a result, these regions have higher nucleotide divergence and less evidence of gene flow between species.
Variation in hybridization depends on the molecular processes that result in the merging of two disparate genetic backgrounds in the F1, specifically recombination. Therefore, a fundamental part of our research program involves understanding variation in recombination and how recombination rates change between species as well as across the genome. Although recombination rates have been shown to vary depending on environmental conditions for over a century now, recombination events were assumed to be uniformly distributed across the genome until about three decades ago. However, we now know that recombination rates are highly variable across taxa and along genomes, but rates are limited both mechanistically and evolutionarily in the degree to which they can change due to tight regulation. Mechanistically, recombination is necessary to stabilize chromosomes during meiosis, but excessive recombination or errors in this pathway can lead to birth defects/ disease (e.g. Bloom syndrome or some breast/ovarian cancers). Evolutionarily, recombination helps to shuffle beneficial alleles onto common genetic backgrounds, facilitating the efficacy of selection. However, too much recombination can break down these associations. My work aims to document the extent of variation in recombination rate across various taxa and understand the evolutionary consequences of this variation, specifically in the context of speciation.
The Stevison Lab uses model systems, such as primates and fruit flies, for understanding evolutionary genetics. We take a population genetics approach to understanding speciation by looking at both within and between species variation and how that contributes to speciation, facilitates selection, and contributes to recombination rate variation. The data that are generated from these types of questions can also be useful in examining patterns of diversity and selection within species.
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