RNAi screen of XXXX /FOXO target genes in @entity2199 links pathogenesis and dauer formation.

@entity73043 @entity2199 @entity73040 @entity73042 @entity794 @entity73044 @entity5681 @entity7626 @entity73041
The @entity7626 /FOXO transcription factor is the major downstream output of the insulin/IGF1R signaling pathway controlling @entity2199 dauer larva development and aging. To identify novel downstream genes affecting dauer formation, we used RNAi to screen candidate genes previously identified to be regulated by @entity7626 . We used a sensitized genetic background [eri-1(mg366); @entity73040 (m708)], which enhances both RNAi efficiency and constitutive dauer formation (Daf-c). Among 513 RNAi clones screened, 21 displayed a synthetic Daf-c (SynDaf) phenotype with @entity73040 . One of these genes, @entity73041 , was previously identified to be SynDaf, but twenty have not previously been associated with dauer formation. Two of the latter genes, @entity73042 and @entity73043 , are known to participate in innate immunity and six more are predicted to do so, suggesting that the immune response may contribute to the dauer decision. Indeed, we show that two of these genes, @entity73042 and clc-1, are required for normal resistance to @entity794 . clc-1 is predicted to function in epithelial cohesion. Dauer formation exhibited by daf-8(m85), @entity73040 (m708), and the wild-type N2 (at 27  C) were all enhanced by exposure to pathogenic bacteria, while not enhanced in a @entity73044 (m130) background. We conclude that knockdown of the genes required for proper pathogen resistance increases pathogenic infection, leading to increased dauer formation in our screen. We propose that dauer larva formation is a behavioral response to pathogens mediated by increased dauer @entity5681 production.
