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

Abstract

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.

Transiently restricting individual amino acids protects Drosophila melanogaster against multiple stressors

“…As TOR is a master regulator of growth, which detects cellular levels of amino acids and is inactivated by low levels of amino acids [83], we assumed that both isoleucine deprivation and rapamycin achieved nicotine resistance through TOR suppression. However, other studies have shown that rapamycin treatment improves the heat tolerance of wild-type flies [84] and can improve the maximum thermal temperature (CTmax) withstood by Drosophila Genetic Reference Panel (DGRP) flies [85]. We therefore anticipated that short-term isoleucine deprivation would also increase heat tolerance in our flies, but it did not.…”