In the nematode C. elegans, male mating is considered to be the most complex behavior, consisting of several stereotyped substeps. Additionally, males engage in mate searching, in which animals will leave a food source in order to find hermaphrodites. Many genes have been found to impact one or more of these routines. Despite noticeably disrupting these behaviors, mutations in these genes have never completely abolished sexual behaviors as a whole. The mutation
bx129 was recovered from a genetic screen for ray sensory axon guidance defects. Aside from this phenotype,
bx129 adult males, though morphologically near-normal, appear to lack all sexual behavior. These males fail to copulate, appear not to detect hermaphrodites, and do not go mate-searching. Both males and hermaphrodites exhibit reduced serotonin sensitivity and hermaphrodites are egg-laying defective. Additionally,
bx129 is temperature-sensitive sterile. This interesting spectrum of phenotypes prompted us to pursue the nature of the
bx129 mutation. Whole genome sequencing of
bx129 animals yielded a mutation in the 3' splice site of the first intron of the gene
pqn-80. The
pqn-80 gene is 25 kb in length and the protein has a glutamine/asparagine-rich domain in its C-terminus. We obtained a deficiency allele (
tm4167) of
pqn-80, which is a presumptive null, and observed very similar phenotypes to
bx129 for both sexes. However,
pqn-80(
tm4167) exhibits some more extreme phenotypes, such as severe gonad migration defects in both sexes and crumpled spicules in males.
tm4167 fails to complement
bx129 for these defects. Interestingly,
pqn-80(
tm4167) also exhibits temperature-sensitive sterility and a portion of males develop leptoderan tails. In view of this spectrum of phenotypes, we speculate that
pqn-80 is a member of the heterochronic gene pathway required for larval-to-adult developmental transitions, specifically for the gonad, male tail structures, and expression of adult sexual behavior.