Open AccessAutophagy facilitates mitochondrial rebuilding after acute heat stress via a DRP-1–dependent process
Author(s) -
Yanfang Chen,
Romane Leboutet,
Céline Largeau,
Siham Zentout,
Christophe Lefebvre,
Agnès Delahodde,
Emmanuel Culetto,
Renaud Legouis
Publication year - 2021
Publication title -
the journal of cell biology/the journal of cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.414
H-Index - 380
eISSN - 1540-8140
pISSN - 0021-9525
DOI - 10.1083/jcb.201909139
Subject(s) - mitophagy , autophagy , biology , microbiology and biotechnology , mitochondrion , parkin , autophagosome , pink1 , mitochondrial fission , organelle , caenorhabditis elegans , mitochondrial biogenesis , biochemistry , apoptosis , gene , medicine , disease , pathology , parkinson's disease
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.