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Autophagy and the Mitochondrial Lon1 Protease Are Necessary for Botrytis cinerea Heat Adaptation

Summary

Researchers studied how a common plant-damaging fungus called Botrytis cinerea survives high temperatures. They found that two cellular cleanup systems—autophagy (which recycles damaged components) and a mitochondrial protease called Lon1—work together to help the fungus survive heat stress. When either system was disabled, the fungus was much more sensitive to heat and showed increased cell death, suggesting these processes are essential for the fungus’s survival strategy.

Background

Botrytis cinerea is a necrotrophic fungal plant pathogen that causes gray mold disease and switches to survival mode at elevated temperatures. Heat adaptation involves coordinated cellular responses including autophagy and mitochondrial proteostasis. ATP-dependent proteases like Lon1 are established in heat stress responses across prokaryotic and eukaryotic organisms.

Objective

To investigate the roles of autophagy and the mitochondrial Lon1 protease in heat adaptation of Botrytis cinerea. To determine whether deletion of bclon1 and blocking of autophagy affect fungal survival under heat stress and identify the coordinated mechanisms between these pathways.

Results

Deletion of bclon1 induced earlier and more intense autophagy under heat stress with increased mitochondrial malfunction and ROS accumulation. The bcatg1/lon1 double mutant showed intensified growth arrest, cell death, and mitochondrial damage compared to single mutants. Blocking autophagy affected mycelia growth, spore germination, nuclei division and spore morphology independently of bclon1 deletion.

Conclusion

Both autophagy and mitochondrial Lon1 protease are necessary for B. cinerea heat adaptation through coordinated activity. Autophagy serves a cytoprotective role downstream of mitochondria-driven death signals and promotes growth arrest to help remove damaged cellular components during heat stress.
  • Published in:Molecular Microbiology,
  • Study Type:Experimental Research,
  • Source: PMID: 40682260, DOI: 10.1111/mmi.70014
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