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 might initiate the process. In the nematode Caenorhabditis briggsae, a small percent of F2 generation hybrids between two natural populations suffer from developmental delay, in which adulthood is reached after approximately 33% more time than their wild-type siblings. Prior efforts to identify the genetic basis for this hybrid incompatibility assessed linkage using one or two genetic markers on chromosome III and suggested that delay is caused by a toxin-antidote element. Here, we have genotyped F2 hybrids using multiple chromosome III markers to refine the developmental delay locus. Also, to better define the developmental delay phenotype, we measured the development rate of 66 F2 hybrids and found that delay is not restricted to a particular larval developmental stage. Deviation of the developmental delay frequency from hypothetical expectations for a toxin-antidote element adds support to the assertion that the epistatic interaction is not fully penetrant. Our mapping and refinement of the delay phenotype motivates future efforts to study the genetic architecture of hybrid dysfunction between genetically distinct populations of one species by identifying the underlying loci.