Autophagy facilitates mitochondrial rebuilding after acute heat stress via a DRP-1–dependent process

Author:

Chen Yanfang1,Leboutet Romane12,Largeau Céline12,Zentout Siham1ORCID,Lefebvre Christophe12ORCID,Delahodde Agnès1,Culetto Emmanuel12ORCID,Legouis Renaud12ORCID

Affiliation:

1. Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), 91198, Gif-sur-Yvette, France.

2. INSERM U1280, Gif-sur-Yvette, France

Abstract

Acute heat stress (aHS) can induce strong developmental defects in Caenorhabditis elegans larva but not lethality or sterility. This stress results in transitory fragmentation of mitochondria, formation of aggregates in the matrix, and decrease of mitochondrial respiration. Moreover, active autophagic flux associated with mitophagy events enables the rebuilding of the mitochondrial network and developmental recovery, showing that the autophagic response is protective. This adaptation to aHS does not require Pink1/Parkin or the mitophagy receptors DCT-1/NIX and FUNDC1. We also find that mitochondria are a major site for autophagosome biogenesis in the epidermis in both standard and heat stress conditions. In addition, we report that the depletion of the dynamin-related protein 1 (DRP-1) affects autophagic processes and the adaptation to aHS. In drp-1 animals, the abnormal mitochondria tend to modify their shape upon aHS but are unable to achieve fragmentation. Autophagy is induced, but autophagosomes are abnormally elongated and clustered on mitochondria. Our data support a role for DRP-1 in coordinating mitochondrial fission and autophagosome biogenesis in stress conditions.

Funder

Agence Nationale de la Recherche

Association pour la Recherche contre le Cancer

Ligue contre le Cancer

Publisher

Rockefeller University Press

Subject

Cell Biology

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