Abstract

C. elegans enters diapause in response to starvation, high temperatures and elevated concentrations of pheromones. Additionally, C. elegans forms the dauer larvae as defense mechanism against bacterial pathogens (Palominos et al., submitted). This phenomenon is transgenerational and is mediated by the RNAi machinery. Our unpublished results suggested that there is an interspecies communication, where a bacterial dsRNA triggers an RNAi dependent process, generating secondary endo-siRNAs that are in turn accumulated in the germline and transmitted to the progeny to promote dauer formation. But, which is the functional network that triggers this events in the worm, and which are the essential components of transgenerationality? To understand the underlying networks of diapause formation in the presence of pathogens, we performed transcriptomic analysis of small RNAs and mRNAs of worms and the bacteria residing in their intestines in the first (F1) and second (F2) generation of animals exposed to P. aeruginosa, S. Typhimurium and E. coli OP50. Simple analysis of differential gene expression revealed that mir-243, mir-51 and mir-52, are up regulated in pathogens but not E. coli in the F1 and F2. To determine which genes could be downregulated by these miRNAs, we used the IntaRNA tool (Busch et al., 2008). We are currently performing the in silico network interaction analysis of all the differentially expressed genes in response to pathogens, using the Cytoscape algorythm (Shannon et al., 2003). These sRNA-mRNA interactions are likely to underlie the transgenerational nature of dauer formation in response to pathogens.