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30 results for “Heat-stress”

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dryad36/100

Data for: Excess labile carbon promotes diazotroph abundance in heat-stressed octocorals

Constant nitrogen limitation is the foundation of a stable coral-algal symbiosis. Diazotrophs, i.e., prokaryotes capable of fixing N2 into ammonia, are key players in coral holobionts. Recent studies on reef-building corals have shown that labile dissolved organic carbon (DOC) enrichment or heat stress stimulated the growth and activity of diazotrophs, resulting in excess nitrogen availability. However, the (a)biotic drivers of diazotrophs in octocorals are still poorly understood. We investigated diazotroph abundance (assessed via relative quantification of nifH gene copy numbers) in two symbiotic octocorals, the more mixotrophic soft coral Xenia umbellata and the more autotrophic gorgonian Pinnigorgia flava, under a) labile DOC enrichment for 21 days, followed by b) combined labile DOC enrichment and heat stress for 24 days. In the absence of heat stress, relative diazotroph abundances in X. umbellata and P. flava were unaffected by DOC enrichment. During heat stress, DOC enrichment (higher than 20 mg glucose L-1) increased the relative abundances of diazotrophs by 6-fold in X. umbellata and 4-fold in P. flava, compared to their counterparts without excess DOC. Our data suggest that labile DOC enrichment and concomitant heat stress could disrupt the nitrogen limitation in octocorals through stimulating diazotroph proliferations. Reducing labile DOC loading may effectively help octocorals cope with future ocean warming scenarios.

opencc-zeroFeb 2023View details →

dryad36/100

Exploring the connection between autophagy and heat-stress tolerance in Drosophila melanogaster

Mechanisms aimed at recovering from heat-induced damages are closely associated with the ability of ectotherms to survive exposure to stressful temperatures. Autophagy, a ubiquitous stress-responsive catabolic process, has recently gained renewed attention as one of these mechanisms. By increasing the turnover of cellular structures as well as the clearance of long-lived protein and protein aggregates, the induction of autophagy has been linked to increased tolerance to a range of abiotic stressors in diverse ectothermic organisms. However, whether a link between autophagy and heat-tolerance exists in insect models remains unclear despite broad ecophysiological implications thereof. Here, we explored the putative association between autophagy and heat-tolerance using Drosophila melanogaster as a model. We hypothesized that (i) heat-stress would cause an increase of autophagy in flies' tissues, and (ii) rapamycin exposure would trigger a detectable autophagic response in adults and increase their heat-tolerance. In line with our hypothesis, we report that flies exposed to heat-stress present signs of protein aggregation and appear to trigger an autophagy-related homoeostatic response as a result. We further show that rapamycin feeding causes the systemic effect associated with target of rapamycin (TOR) inhibition, induces autophagy locally in the fly gut, and increases the heat-stress tolerance of individuals. These results argue in favour of a substantial contribution of autophagy to the heat-stress tolerance mechanisms of insects.

opencc-zeroSep 2023View details →

dryad36/100