Intergenerational pathogen-induced diapause inC. elegansis modulated bymir-243

Abstract

15The interaction and communication between bacteria and their hosts modulate many 16 aspects of animal physiology and behavior. Dauer entry as a response to chronic exposure 17 to pathogenic bacteria in Caenorhabditis elegans is an example of a dramatic behavioral 18 decision to survive. This response depends on the RNAi machinery suggesting the 19 involvement of sRNAs as effectors. Interestingly, dauer formation occurs after two 20 87 we will first refer to mRNAs. Differential gene expression of animals feeding on 88 pathogenic bacteria was made in reference to non-pathogenic E. coli OP50 using DeSeq 89 and EdgeR (Dataset 1). We considered differentially expressed genes those found to be 90 statistically significant by either analysis (Table S1 and 2). Differentially expressed mRNA 91 genes included coding and non-coding transcripts. We found that transcriptional changes 92 in mRNAs (coding and non-coding) were larger in the first generation (F1) than in the 93 second (F2) of animals fed with either pathogen ( Fig. 1A and B). Fig. 1C to E illustrates 94 the distribution of non-coding RNA expression in numbers (C and D) and types (E). 95Among non-coding transcripts we found piRNAs, 7k ncRNA, pseudogenes, tRNAs, 96 lincRNAs, asRNAs, snoRNA, snRNA and rRNAs (Fig. 1E). The F1 generation was more 97 abundant and diverse in differential expression than the F2s when feeding on either 98 pathogen. This difference between generations could suggest that changes in the F1 are 99 most dramatic because they reflect changes in bacterial diet composition, as well as 100 exposure to a pathogen. In this context, the subsequent generation may respond more 101 specifically to each new bacterium. 102Most mRNA genes were overexpressed or repressed in a generation or pathogen 103 specific manner (Table S3). There were no shared upregulated mRNA genes in both 104 pathogens and generations ( Fig. 1F). However, a number of genes were commonly 105 expressed in the F1, independently of whether animals were feeding on P. aeruginosa or 106 S. Typhimurium. These genes grouped in Metabolic Processes by gene ontology (Fig. S1A) 107 suggesting there is a common expression pattern that likely responds early to the change in 108 diet from E. coli OP50 and it is not maintained after the F1 (see below). Interestingly, 109 downregulated genes shared many more coincidences between pathogenic conditions ( Fig. 110 1G). Three genes, acdh-1, hpdp-1 and F54D5.12 were downregulated in both bacteria and 111 generations. To distinguish the response to pathogens from changes in gene expression 112 caused by the switch from E. coli OP50 to other bacteria we compared the expression 113 changes in animals feeding P. aeruginosa PAO1 and S. Typhimurium in the F1 to those 114 reported for Comamonas. aquatica (15). There were no coincidences in the upregulated 115 genes ( Fig. S1B), but several genes were repressed in animals feeding on all three bacteria 116 ( Fig. S1C), showing the change itself from E. coli OP50 triggers a characteristic common 11...

A diet of oxidative stress–adapted bacteria improves stress resistance and lifespan in C. elegans via p38-MAPK

“…This implies that PMK-1–driven gene expression during exposure to OP50 PQE may be attributed to MET-2–mediated histone modification ( 51 ). The potential transgenerational impact of OP50 PQE on worms is further suggested by the enrichment of genes controlled by MIR-243, known for regulating intergenerational defense against pathogenic bacteria ( 52 ). A decrease in the levels of S -adenosylmethionine, a methylation donor, has been demonstrated to activate the pmk-1 pathway ( 53 ), possibly explaining that genes enriched by OP50 PQE are also regulated by genes controlling histone methylation ( met-2 , hpl-1 , and dpy-21 ).…”

Remembering your enemies: mechanisms of within‐generation and multigenerational immune priming in Caenorhabditis elegans

“…Signals to induce F2 diapause were maternally transmitted for both pathogens and required the expression of dsRNA transporters ( sid‐1 , sid‐2 and sid‐3 ), RNAi processing genes ( rde‐1 , rde‐4 , sago‐1 , sago‐2 ) and the germline RNAi mediator alg‐2 . Subsequent transcriptomics revealed upregulation of the microRNA mir‐243‐3p in F2 progeny exposed to MST1 or PAO1 [74]. Experiments using PAO1 showed that the transcription factors DAF‐16, PQM‐1 and CRH‐2 are required for mir‐243 expression, and this enables dauer formation.…”