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

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 Pinkl/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.

Automated summary

Acute heat stress affects the development of Caenorhabditis elegans larvae without causing lethality or sterility, with mitochondrial fragmentation and autophagic flux playing key roles in developmental recovery. The adaptation to heat stress is independent of specific proteins and receptors, with mitochondria serving as a major site for autophagosome biogenesis. DRP-1 is involved in coordinating mitochondrial fission and autophagosome formation in stress conditions.