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Abstract

Evolutionary ecology investigates how the developmental response to the environment and the ecological interactions of an organism shape the evolution of new phenotypes. Under harsh environmental conditions, Pristionchus pacificus can arrest its development and form dauer larvae. The association of P. pacificus with scarab beetles is exclusively in the dauer stage, indicating that the dauer stage is essential not only for enduring unfavorable conditions but also for dispersal. Dauer pheromone prepared from the supernatant of P. pacificus liquid cultures has dauer-inducing activity and contains two groups of small molecules, ascarosides and paratosides (Bose et al., 2012). We have investigated the ability of P. pacificus to enter the dauer stage by extracting dauer pheromone from 16 strains and testing for natural variation in dauer formation (DF) with cross-reactivity assays. Surprisingly, 13 of 16 strains produce pheromones that induce the highest DF in individuals of other strains, showing cross-preference rather than self-preference of pheromones (Mayer et al., 2011). The reference strain PS312 and the strain RS5134 show one-sided cross-preference since RS5134 forms more dauers in response to the PS312 pheromone than in response to its own pheromone. To identify the molecular basis of this difference in DF, we generated recombinant inbred lines and tested them with both pheromones. Using quantitative trait loci mapping, we identified a 5 kbp region with only one gene, Contig44-snap.18, which is a novel non-conserved “orphan” gene. Transgenic lines overexpressing the PS312 or RS5134 version of snap.18 show complete inhibition of DF in response to both pheromones, suggesting that the orphan gene represents a concentration-dependent inhibitor of DF. Indeed, snap.18 is located in a part of the genome for which the PS312 coverage is twice as high as for the adjacent regions, and this is not the case for RS5134. We hypothesize that the duplication of the orphan gene resulted in the low DF phenotype of PS312 and that overexpression of the orphan gene is sufficient to completely inhibit DF. (references: Bose et al. 2012 Angew. Chem. Int. Ed. 51:12438; Mayer et al. 2011 Proc. R. Soc. B 278:2784).