l infection in C. elegans and C. kamaaina to a deleterious intergenerational effect in C. briggsae. Lastly, we report that none from the effects of many unique 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 anxiety are evolutionarily conserved, pressure -specific, and are predominantly not maintained transgenerationally. Additionally, our findings recommend that the mechanisms that mediate intergenerational adaptive responses in some species may be connected to 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 tension are evolutionarily conservedTo test if any of the intergenerational adaptations to anxiety that have been reported in C. elegans are evolutionarily conserved in other species we focused on 4 recently described intergenerational adaptations to abiotic and biotic stresses osmotic anxiety (Burton et al., 2017), nutrient pressure (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 those 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 had been conserved in 4 diverse species of Caenorhabditis (C. briggsae, C. elegans, C. kamaaina, and C. tropicalis) that shared a final typical ancestor approximately 30 million years ago and have diverged towards the point of possessing ACAT2 web roughly 0.05 substitutions per web site in the nucleotide level (Figure 1A; Cutter, 2008). These species have been selected since they represent numerous independent branches from the Elegans group (Figure 1A) and simply because we could probe the conservation of underlying mechanisms making use of established genetics approaches. We exposed parents of all four species to P. vranovensis and subsequently studied their offspring’s survival rate in response to future P. vranovensis exposure. We discovered that parental exposure towards the bacterial pathogen P. vranovensis protected offspring from future infection in both C. elegans and C. kamaaina (Figure 1B) and that this adaptive intergenerational effect in C. kamaaina necessary exactly 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 via a equivalent and potentially conserved mechanism. By contrast, we found that naive C. briggsae animals have been additional resistant to P. vranovensis than any in the other species tested, but exposure of C. briggsae parents to P. vranovensis caused 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 several added wild isolates of both species (Figure 1–figure Caspase 6 supplier supplement 1A-C). Parental exposure to P. vranovensis had no observable effect on offspring response to infection in C. tropicalis
