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Autophagy facilitates mitochondrial rebuilding and developmental recovery after acute heat-stress

Organisms are exposed to variations of the environmental temperature and should manage to preserve their cellular homeostasis in heat stress conditions. Depending on its severity, heat stress could affect very differently the cellular response, ranging from a beneficial to a lethal effect. Autophagy, a mechanism for degrading and recycling of cellular constituents, is one of the main response induced by heat stress.

Using the model animal Caenorhabditis elegans, Renaud Legouis’ laboratory has developed a new paradigm for studying its adaptation to a non lethal acute heat-stress (aHS). This stress results in transitory fragmentation of mitochondria, formation of aggregates in the matrix and the decrease of mitochondrial respiration. Moreover, an active autophagy flux associated to mitophagy events is triggered in many tissues and enables the rebuilding of the mitochondrial network and the developmental recovery, showing that the autophagic response is protective to the animal.

Using genetic and cellular approaches, the authors have shown that the mitochondria are a major site for autophagosome biogenesis in the epidermis, both in standard and heat stress conditions. They identified the dynamin related protein DRP-1, involved in mitochondrial fission, as an important actor for the autophagy process and the adaptation to aHS. They propose that DRP-1 is involved in coordinating mitochondrial fission and autophagosomes biogenesis in stress conditions.

Reference :
Chen Y, Leboutet R, Largeau C, Zentout S, Lefebvre C, Delahodde A, Culetto E*, Legouis R.*
Autophagy facilitates mitochondrial rebuilding after acute heat stress via a DRP-1-dependent process. J Cell Biol. 2021 Apr 5 ;220(4):e201909139.
doi : 10.1083/jcb.201909139.
PMID : 33734301.

Contact : legouis i2bc.paris-saclay.fr

par Communication - publié le