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Abstract

Despite the wealth of knowledge of C. elegans dauer formation, regulation of dauer formation in other nematode species is relatively poorly understood. To address how environmental regulation of dauer formation evolved, we are studying dauer formation in the satellite model nematode Pristionchus pacificus. P. pacificus shares with C. elegans most of the advantageous features of experimental organisms and has genetic tools such as forward and reverse genetics, a complete genome, and transgenic techniques. In the wild P. pacificus associates with scarab beetles as dauer larvae and occupies a distinct ecological niche from C. elegans. Since dauer formation play critical roles in the adaptive strategy of P. pacificus, one can expect many evolutionary novelties in P. pacificus dauer formation. Also genetic analysis of dauer formation in P. pacificus may lead to identification of conserved genetic components of dauer formation that are missed in C. elegans studies. This is because multiple genes may be involved in the same step of the regulatory cascade (redundancy) or there may be genes that are involved in both dauer formation and earlier development (pleiotropy). Such genes are hard to identify in conventional genetic and RNAi screens and studies in P. pacificus that may have different patterns of redundancy and pleiotropy might help identify such genes. So far we have shown that i) P. pacificus uses a distinct pheromone(s) from C. elegans to sense the population density ii) An endocrine module involving dafachronic acids (DAs) and DAF-12 controls dauer formation in P. pacificus. The latter finding was further extended to infective larva formation of the parasitic nematode Strongyloides papillosus. Exogenous administration of ∆7-DA completely suppresses the formation of infective larva in S. papillosus suggesting infective and dauer larvae share a common evolutionary origin. To elucidate the genes that control P. pacificus dauer formation we screened daf-c and daf-d mutants, and obtained more than 10 strains of each class. In a small-scale screen for daf-c mutants, we obtained several fully penetrant daf-c strains that are relatively rare in C. elegans, as well as partially penetrant strains. All the daf-c strains tested could be at least partially rescued by exogenous administration of ∆7-dafachronic acid, suggesting they have a mutation in a gene upstream of DA/DAF-12. Interestingly the fully penetrant daf-c strains we obtained did not respond to up to 250 nM of ∆4-dafachronic acid. Positional mapping of the gene responsible for one of the daf-c strains is ongoing.