l infection in C. elegans and C. kamaaina to a deleterious intergenerational effect in C. briggsae. Lastly, we report that none of the effects of a number of different stresses on F1 gene expression that we detected here persisted transgenerationally into F3 progeny in C. elegans. Our findings demonstrate that intergenerational adaptive responses to pressure are evolutionarily conserved, tension -specific, and are predominantly not maintained transgenerationally. Furthermore, our findings suggest that the mechanisms that mediate intergenerational adaptive responses in some Caspase 9 site species may well be connected towards the mechanisms that mediate intergenerational deleterious effects in other species.Burton et al. eLife 2021;ten:e73425. DOI: doi.org/10.7554/eLife.2 ofResearch articleEvolutionary Biology | Genetics and GenomicsResultsIntergenerational adaptations to strain are evolutionarily conservedTo test if any with the intergenerational adaptations to tension which have been reported in C. elegans are evolutionarily conserved in other species we focused on four not too long ago described intergenerational adaptations to abiotic and biotic stresses osmotic strain (Burton et al., 2017), nutrient stress (Hibshman et al., 2016; Jordan et al., 2019), Pseudomonas vranonvensis infection (bacterial) (Burton et al., 2020), and Nematocida parisii infection (eukaryotic microsporidia) (Willis et al., 2021). All of these stresses are exclusively intergenerational and didn’t persist beyond two generations in any experimental setup previously analyzed (Burton et al., 2017; Burton et al., 2020; Willis et al., 2021). We tested if these four intergenerational adaptive responses have been conserved in four diverse species of Caenorhabditis (C. briggsae, C. elegans, C. kamaaina, and C. tropicalis) that shared a last common ancestor approximately 30 million years ago and have diverged for the point of having approximately 0.05 substitutions per website at the nucleotide level (Figure 1A; Cutter, 2008). These species have been selected simply because they represent various independent branches of your Elegans group (Figure 1A) and since we could probe the conservation of underlying mechanisms employing established genetics approaches. We exposed parents of all 4 species to P. vranovensis and subsequently studied their offspring’s survival rate in response to future P. vranovensis exposure. We identified that parental CCR3 supplier exposure towards the bacterial pathogen P. vranovensis protected offspring from future infection in each C. elegans and C. kamaaina (Figure 1B) and that this adaptive intergenerational impact in C. kamaaina expected precisely the same tension response genes (cysl-1 and rhy-1) as previously reported for C. elegans (Burton et al., 2020; Figure 1C), indicating that these animals intergenerationally adapt to infection through a comparable and potentially conserved mechanism. By contrast, we found that naive C. briggsae animals have been additional resistant to P. vranovensis than any from the other species tested, but exposure of C. briggsae parents to P. vranovensis triggered higher than 99 of offspring to die upon future exposure to P. vranovensis (Figure 1B). We confirmed that parental P. vranovensis exposure resulted in an adaptive intergenerational effect for C. elegans but a deleterious intergenerational effect for C. briggsae by testing many more wild isolates of both species (Figure 1–figure supplement 1A-C). Parental exposure to P. vranovensis had no observable effect on offspring response to infection in C. tropicalis