Ethal odor dose, respectively. b Meals aversion induced by 1 l ccBA of naive and ccBA-preconditioned (1 l for 4 h) animals at distinct time points. c Meals aversion induced by 4 l of ccDA of naive and ccDA-preconditioned (four l for 4 h) animals at diverse time points. d Survival of naive and ccBA-preconditioned worms 14 h just after a 3-h ERK8 web exposure to 8 l ccBA. e Survival of naive and ccDA-preconditioned worms 14 h just after a 3-h exposure to 16 l ccDA. Information are expressed as imply SEM. N, number of independent experiments. p values were obtained by one-way ANOVA with Fisher’s LSD post hoc test. n.s., not substantial; p 0.05; p 0.01; p 0.Hajdet al. BMC Biology(2021) 19:Page 6 ofsurvival decline on ccDA (Fig. 2d, e), representing a protective (hormetic) effect of ccBA as well as a debilitating (distressing) impact of ccDA preconditioning. Hormesis and dimAChR1 Species stress are well-known phenomena in strain biology and recommend efficient or insufficient physiological responses towards the pressure induced by ccBA or ccDA exposures, respectively [17]. These findings are consistent with these on Fig. 1, i.e., comparable survival prices of animals on the respective odors, showing a recovery of ccBA-exposed worms from a transient early paralysis in comparison with the progressive decline just after modest initial paralysis of ccDA-exposed worms (cf. Fig. 1e , two h of exposure). Thus, ccBA preconditioning induces behavioral and physiological stress tolerance, while ccDA preconditioning induces behavioral sensitization and physiological distress. These results suggest that nematodes can mount effective physiological protection against ccBA, but can only engage additional alert behavioral defense by way of sensitization against ccDA.Undiluted benzaldehyde, but not diacetyl, activates certain systemic cytoprotective responsesRNAi, while that of gst-4 was abolished by skn-1 RNAi (Fig. 3c, d). Importantly, ccBA didn’t activate several other stress reporters, including the HSF-1 and DAF-16 target hsp-16.2, the HSF-1 target and endoplasmic reticulum unfolded protein response (UPR) reporter hsp-4, the SKN-1-dependent gcs-1, as well as the DAF-16dependent sod-3 reporter (Additional File 1: Fig. S3c). These findings demonstrate that a distinct tension and detoxification response involving a subset of DAF-16- and SKN-1-activated genes participate in the molecular defense against ccBA toxicity. In contrast, no apparent stress responses had been detected upon ccDA exposure.ccBA-induced cytoprotective responses confer behavioral tolerance to ccBA, but not to ccDANext, we asked if the efficient vs. insufficient physiological protection against ccBA and ccDA exposure may possibly be reflected in the differential mobilization of cellular defense responses to the respective toxic stresses. In agreement with our findings around the toxicity of ccBA, earlier studies demonstrated that BA induced oxidative pressure [26]. Hence, we tested numerous oxidative strain response pathways that might be involved inside the physiological adaptation to ccBA. Applying the TJ356 strain expressing GFP-tagged DAF-16, we observed that the identical ccBA dose utilized for preconditioning induced a strong nuclear translocation of DAF-16 after 30 min, comparable to that induced by heat anxiety. Nonetheless, DAF-16 remained cytosolic in response to ccDA (Fig. 3a and More File 1: Fig. S3a). The shift in DAF-16 localization exhibited a clear BA dose dependence (Extra File 1: Fig. S3b). These congruent ccBA dosedependent adjustments in DAF-16 translocation and meals avoidance (cf.