mutation in sodh-1 in AL2B, which would result in a Glycine 158 to Glutamate missense mutation (for consistency of nomenclature, AL2B is hereafter referred to as sodh-1(bet20)). Additionally, RNA inactivation of H24K24.3 conferred resistance to allyl-alcohol, however, knock-down of function with RNAi of neither sodh-2 nor D2063.1 was able to confer strong resistance to allyl-alcohol (Table 1). It is important to note that these RNAi experiments do not unambiguously rule out a role for sodh-2 or D2063.1 in the metabolism of ethanol. This RNAi treatment does not completely eliminate the mRNA for either candidate ADH (Table 2), and the residual mRNA may be sufficient to confer function of the candidate. In addition, C. elegans tissues are differentially susceptible to RNAi. Worm neurons are quite refractive to RNAi using this method, and it is possible that expression of the candidate gene is preserved in neurons. In this case, expression of the gene in neurons may be sufficient to provide function. Because inactivation of both sodh-1 and H24K24.3 altered allyl-alcohol sensitivity, we therefore used strains inactivated for sodh-1 and H24K24.3 in our subsequent studies.
