Transcriptomic data for: Social context prevents heat hormetic effects againstmutagens during ?sh development

Climate change increases both the frequency and duration of heat events. Direct negative effects of such heat stress may be exacerbated through heat-induced stress propagation (via stress metabolites) between aquatic animals. Whilst early life stages are vulnerable to stress-induced damage, they also deploy cellular mechanisms to protect cells against their naturally mutagenic environment. Little is known about the fate and performance of fish embryos which have experienced direct or indirect heat stress in a mutagenic environment. Natural environmental mutation rates are typically low which poses an observational challenge. To circumvent this, the present study exposed zebrafish embryos to three treatments consisting of direct heat stress, indirect heat-induced stress metabolites, and combined heat + heat-induced metabolites before undergoing a UVB/UVA damage/repair assay to mimic a mutagenic environment. Indirect heat stress led to expression of keratin and cell structuring-related genes in receivers, associated with longer embryos displaying over-developed pericardial widths and behavioural hypoactivity. Heat stress had a hormetic effect by stimulating the cellular stress response, and presumably facilitating DNA repair, which protected and/or rescued embryos from subsequent UV damage and improved their fitness. However, heat stress combined with stress metabolites emitted by heat-stressed conspecifics overwhelmed embryos, which annihilated the hormetic effect, introduced RNA mutations, and lowered overall fitness indicators. Whilst generated in the laboratory, these findings provide an important baseline for understanding the consequences of thermal stress history in natural environments, where direct and indirect heat stress co-occur. Overall design: Zebrafish embryos were exposed for 24 hours to thermal stress (TS) and stress metabolites (SM) released by heat-stressed zebrafish embryos, in a two-way factorial design (TSxSM), yielding four experimental treatments: fresh medium at 27°C (control C), fresh medium with thermal stress (TS), medium containing stress metabolites at 27°C (SM), and medium containing stress metabolites with thermal stress (TS+SM). After 24 hours of exposure to C, TS, SM, and TS+SM, embyros were exposed to a DNA damage/repair assay (6 min of DNA damage with UVB and 15 min of UVA-induced photorepair), resulting in four treatments: C+UV, TS+UV, SM+UV, and TS+SM+UV. 1-dpf embryos were processed for RNA-sequencing directly following the DNA damage/repair assay. Each treatment contains n = 3 biological replicates, each representing the pooled gene expression from 20 individual embryos.