View Program - 2022 Population, Evolutionary, and Quantitative Genetics Conference

Identifying the alleles that reduce hybrid fitness is a major goal in the study of speciation genetics. It is rare to identify systems in which hybrid incompatibilities with minor phenotypic effects are segregating in genetically diverse populations of the same biological species. Such traits do not themselves cause reproductive isolation, but they might initiate the process. In the nematode Caenorhabditis briggsae, a small percent of F2 generation hybrids between two wild isolates suffer from developmental delay, in which adulthood is reached after 33% more time than their wild-type siblings. Prior efforts to identify the genetic basis for this hybrid incompatibility found association with one autosome. Here, we have used F2 hybrids and near-isogenic lines to map one locus to a roughly 1 Mbp region of chromosome III. This architecture agrees with the suggestion that developmental delay is caused by a maternal-effect toxin-antidote element. In order to more specifically define the developmental delay phenotype, we monitored the development rate of F2 hybrids and discovered that delay is not restricted to a particular larval developmental stage, unlike many known developmental pathway mutations. Additional analyses with cytoplasmic-nuclear hybrids suggests that a mitochondrial-nuclear epistatic interaction might also contribute to hybrid developmental delay. Our mapping and refinement of the delay phenotype motivates future efforts to study the genetic architecture of hybrid dysfunction between populations of C. briggsae.

Genetic Architecture and Temporal Analysis of Developmental Delay in Intra-species Caenorhabditis briggsae Hybrids

**Genetic Architecture and Temporal Analysis of Developmental Delay in Intra-species Caenorhabditis briggsae Hybrids**