Intergenerational adaptations to stress are evolutionarily conserved, stress-specific, and have deleterious trade-offs

Abstract

Despite reports of parental exposure to stress promoting physiological adaptations in progeny in diverse organisms, there remains considerable debate over the significance and evolutionary conservation of such multigenerational effects. Here, we investigate four independent models of intergenerational adaptations to stress in C. elegans (bacterial infection, eukaryotic infection, osmotic stress and nutrient stress) across multiple species. We found that all four intergenerational physiological adaptations are conserved in at least one other species, that they are stress-specific, and that they have deleterious trade-offs in mismatched environments. By profiling the effects of parental bacterial infection and osmotic stress exposure on progeny gene expression across species we established a core set of 279 highly conserved genes that exhibited intergenerational changes in expression in response to stress in all species tested and provide evidence suggesting that presumed adaptive and deleterious intergenerational effects are molecularly related at the gene expression level. By contrast, we found that these same stresses did not elicit any similarly conserved transgenerational changes in progeny gene expression three generations after stress exposure. We conclude that intergenerational responses to stress play a substantial and evolutionarily conserved role in regulating animal physiology and that the vast majority of the effects of parental stress on progeny gene expression are reversible and not maintained transgenerationally.

Co-opted Genes of Algal Origin Protect C. elegans against Cyanogenic Toxins

“…2c). CYSL-1 and CYSL-2 are cysteine synthase-like proteins and have been implicated in hydrogen sulfide and cyanide detoxification 14,15,20,23,24 . While CYSL-2 can enzymatically convert cyanide to nontoxic β-cyanoalanine 14 , the essential role of CYSL-1 in cysl-2 p::GFP activation by amygdalin suggests CYSL-1 acts as a transcriptional regulator rather than a cysteine synthase or an enzyme to detoxify cyanide 15 .…”

“…We treated cysl-2p::GFP animals with each of these amygdalin-derived molecules and found prunasin and cyanide (as in potassium cyanide) activated cysl-2p::GFP as amygdalin did, but others had no detectable effect (Figure 2C). CYSL-1 and CYSL-2 are cysteine synthase-like proteins and have been implicated in hydrogen sulfide and cyanide detoxification 16,17,22,24,25 . While CYSL-2 can enzymatically convert cyanide to nontoxic βcyanoalanine 16 , the essential role of CYSL-1 in cysl-2p::GFP activation by amygdalin suggests CYSL-1 acts as a transcriptional regulator rather than a cysteine synthase or an enzyme to detoxify cyanide 17 .…”

“…2c). CYSL-1 and CYSL-2 are cysteine synthase-like proteins and have been implicated in hydrogen sulfide and cyanide detoxification 14,15,20,23,24 .…”

Cold shock induces a terminal investment reproductive response in C. elegans

“…Indeed, the progeny of C. elegans submitted to various stressors demonstrate improvements in stress survival to the same and other types of stress. Recently, a study by Burton et al [7] examined multigenerational responses to a number of stressors including nutrient deprivation and pathogenic stress and found that multiple Caenorhabditis species regulate gene expression in the F1 generation in a stress-specific manner to benefit survival upon exposure to the same. These studies highlight the evolutionary advantage of provisioning offspring for what is perceived to be a likely future.…”

“…The nematode Caenhorhabditis elegans recently arose as an ideal model for investigating stress-induced parental progeny investment. Several studies have detailed molecular tactics by which worms modify and provision gametes and embryos in response to dietary restriction, infection by pathogenic pseudomonads and microsporidia, and osmotic stress [4][5][6][7]. Among an array of environmentally-relevant stressors, though, the reproductive impacts of thermal stress (specifically cold stress) on C. elegans have not been closely assessed.…”