Abstract
Heat adaptation is a multilayered universal process involving a coordinated response of general and heat-specific cellular systems and processes. Here, we demonstrate that adaptation of the plant pathogenic fungus Botrytis cinerea to mild heat stress requires both autophagy and the mitochondrial Lon1 protease. Deleting bclon1 or blocking autophagy by deleting the bcatg1 autophagy-regulating gene did not affect fungal survival at optimal temperature. Under heat stress, deletion of bclon1 induced earlier and more intense autophagy, mitochondrial malfunction, and accelerated fungal cell death. These phenomena were intensified in a bcatg1/lon1 double mutant, indicating coordinated activity of both pathways in heat adaptation. Blocking autophagy, but not bclon1, also affected mycelia growth, spore germination, as well as nuclei division and spore morphology. Our results support a cytoprotective role for autophagy downstream of mitochondria-driven death signals, possibly as a mechanism that promotes growth arrest and helps remove damaged cellular components.