Abstract
Mutations in lin-35, the worm ortholog of a mammalian tumor suppressor gene, and other synMuv B genes result in an increased sensitivity to RNAi and enhanced somatic transgene silencing.
Highlights
Genome-wide RNA interference (RNAi) screening is a very powerful tool for analyzing gene function in vivo in Caenorhabditis elegans
Loss of LIN-35 results in enhanced RNAi The loss of function phenotypes generated by RNAi, like those generated by classic genetics, are highly dependent on the genetic background - many genes have very different RNAi phenotypes in a wild-type worms from those seen in animals mutant for a specific gene
We have found that lin-35 and a subset of synthetic Multivulva (synMuv) B pathway genes negatively regulate RNAi in C. elegans, probably via a mechanism involving chromatin remodelling
Summary
Genome-wide RNA interference (RNAi) screening is a very powerful tool for analyzing gene function in vivo in Caenorhabditis elegans. Genes expressed in neurons appear largely refractory to RNAi, which has precluded the use of RNAi screens to identify genes with neuronal functions [4]. For this reason there has been great interest in identifying worm strains that display an enhanced sensitivity to RNAi. Previously, mutations in two genes have been shown to enhance RNAi sensitivity in C. elegans. We found that a straincarrying a null allele in lin-35 is more sensitive to RNAi than either rrf-3 or eri-1 mutant animals, making this strain an invaluable resource for future genome-wide RNAi screens
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