Project description:The body temperature of Drosophila melanogaster depends on the extrinsic temperature. Numerous studies show that environmental temperature influences metabolism, lifespan, and starvation resilience. We have previously shown that Chameau (Chm), a MYST-domain acetyltransferase, promotes aging but also increases starvation resilience. Strikingly, the metabolic increase associated with a 2°C temperature rise was sufficient to bypass the requirement for Chm in starvation resilience, suggesting that Chm modulates metabolism in a temperature-dependent manner. The increase in temperature also rescued the dampened expression of genes involved in starvation response, the weight loss, and the misregulation of trehalose, which we observed in chm mutants at 23°C. Thus, Chm regulates starvation at ≤23°C but becomes obsolete at higher temperatures, likely because of efficient acetyl-CoA generation ensuring similar acetylation despite lower Chm. Supporting this, citrate supplementation increased starvation resilience of chm mutants at lower temperatures. Our finding that a gene's role manifests only under specific environments has important implications in light of global climate change
Project description:<p>Viral studies of Drosophila melanogaster typically involve virus injection with a small needle, causing post-injury a wounding/wound healing response, in addition to the effects of viral infection. However, the metabolic response to the needle injury is understudied, and many viral investigations neglect potential effects of this response. Furthermore, the wMel strain of the endosymbiont bacterium Wolbachia pipientis provides anti-viral protection in Drosophila. Here we used NMR-based metabolomics to characterise the acute wounding response in Drosophila and the relationship between wound healing and the Wolbachia strain wMel. The most notable response to wounding was found on the initial day of injury and lessened with time in both uninfected and Wolbachia infected flies. Metabolic changes in injured flies revealed evidence of inflammation, Warburg-like metabolism and the melanisation immune response as a response to wounding. In addition, at five days post injury Wolbachia infected injured flies were metabolically more similar to the uninjured flies than uninfected injured flies were at the same time point, indicating a positive interaction between Wolbachia infection and wound healing. This study is the first metabolomic characterisation of the wound response in Drosophila and its findings are crucial to the metabolic interpretation of viral experiments in Drosophila in both past and future studies.</p>
Project description:Organisms in the wild constantly encounter fluctuations in temperature and food availability, pathogens, and other stressors that disrupt their physiological balance. To counteract these disruptions, organisms initiate stress responses that vary in nature depending on the intensity and duration of the stressor. While severe stress can be harmful or even fatal, moderate stress can activate adaptive mechanisms, a phenomenon known as hormesis. Hormesis enhances resilience to stress and has been associated with improved aging, immunity, and metabolism. Short-term exposures to mild stress, such as heat or oxidative stress, have been shown to extend Drosophila lifespan and promote cross-tolerance to other stressors. Among various environmental stressors, starvation poses a significant and recurring challenge that has driven the evolution of energy-conserving strategies essential for survival. Prior exposure to starvation has been shown to influence longevity, resilience to starvation, physiological status and stress tolerance. However, the mechanisms underlying these hormetic effects remain poorly understood. In this study, we investigate how short-term starvation enhances resistance to prolonged food deprivation in Drosophila. Our findings reveal that metabolic rewiring, including changes in energy utilization, insulin signaling, and transcriptomic profiles underpins this adaptive plasticity. These insights will improve our understanding of the molecular and metabolic mechanisms driving hormesis, with broader implications for stress resilience and organismal health.