ena-STUDY-Centre for Trophoblast Research-11-06-2019-10:27:12:577-145
RNA-seq of C. elegans adults and embryos exposed to P. vranovensis, P. aeruginosa, P. luminescens or wdr-23 mutant embryos.
Parental exposure to environmental stress can program adaptive changes in offspring development and physiology in diverse organisms1–4. The mechanisms by which parental exposure to environmental stresses can program predictive adaptive responses in offspring remain almost completely unknown. Here we report that the soil bacteria Pseudomonas vranovensis is a natural pathogen of the nematode Caenorhabditis elegans and that parental exposure of C. elegans to P. vranovensis promotes offspring resistance to infection. This adaptation can be transmitted transgenerationally such that, under certain conditions, great-grandparental infection can enhance the immunity of their descendants three generations later. We find that parental infection by P. vranovensis results in increased expression of the cysteine synthases CYSL-1 and CYSL-2 and the regulator of hypoxia inducible factor RHY-1 in progeny and the expression of these three genes in offspring is required for adaptation to P. vranovensis. Furthermore, we demonstrate that these heritable changes in gene expression are regulated by signalling via the WD repeat protein WDR-23 and the Nrf2-like transcription factor SKN-1. We speculate that analogous heritable regulation of gene expression controls other observations of parental environment programming changes in offspring physiology, including observations of parental exposure to pathogens priming offspring immunity4.
Parental exposure to environmental stress can program adaptive changes in offspring development and physiology in diverse organisms1–4. The mechanisms by which parental exposure to environmental stresses can program predictive adaptive responses in offspring remain almost completely unknown. Here we report that the soil bacteria Pseudomonas vranovensis is a natural pathogen of the nematode Caenorhabditis elegans and that parental exposure of C. elegans to P. vranovensis promotes offspring resistance to infection. This adaptation can be transmitted transgenerationally such that, under certain conditions, great-grandparental infection can enhance the immunity of their descendants three generations later. We find that parental infection by P. vranovensis results in increased expression of the cysteine synthases CYSL-1 and CYSL-2 and the regulator of hypoxia inducible factor RHY-1 in progeny and the expression of these three genes in offspring is required for adaptation to P. vranovensis. Furthermore, we demonstrate that these heritable changes in gene expression are regulated by signalling via the WD repeat protein WDR-23 and the Nrf2-like transcription factor SKN-1. We speculate that analogous heritable regulation of gene expression controls other observations of parental environment programming changes in offspring physiology, including observations of parental exposure to pathogens priming offspring immunity4.