Virtually all organisms interact with pathogens, and C. elegans is no exception. In the wild, C. elegans have been shown to be infected by a variety of harmful bacteria, viruses, and fungi. These infections can cause dramatic fitness decreases, and are likely to be a strong selective pressure in natural populations. Bacillus thuringiensis (Bt) is a soil dwelling bacterium that produces crystal proteins which are toxic to many insects and other invertebrates, including C. elegans. Bt GMO crops are commercially important, and protect over 25 million ha of crop plants against insect pests. A subset of Bt crystals are nematode specific, and there is interest in using these Bt crystals to control parasitic crop nematodes. Two Bt crystals with nematicidal activity have been well characterized in C. elegans: Cry5Ba and Cry6Aa. The 3D structures of these crystals are very different, as is their mode of action. The receptors for Cry5Ba are invertebrate-specific glycolipids, while Cry6Aa toxicity is mediated through the ASP-1 pathway. One of the genes in the ASP-1 pathway,
tra-3 was previously found to have a single nucleotide difference between the N2 (Bristol) and CB4856 (Hawaiian) strains of C. elegans, and this polymorphism is known to affect TRA-3 protein structure and activity. Using the Caenorhabditis elegans Natural Diversity Resource (CeNDR) database, we found that this polymorphism is widespread, and present in about half of all wild C. elegans isolates. We show that this SNP has undergone a strong selective sweep in C. elegans, and we isolate other regions of the genome that have potentially also undergone selective sweeps. We are currently determining whether the
tra-3 SNP confers resistance to Cry6Aa crystals in lab populations of C. elegans, and we are re-analyzing the protein structure of the two TRA-3 variants to better determine how this SNP affects its 3D structure and function.