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

Summary

Scientists studied how a fungus that causes gray mold disease adapts to heat stress by examining two key cellular processes: autophagy (cellular cleanup) and a mitochondrial protease called Lon1. They found that both processes work together to help the fungus survive high temperatures by removing damaged cellular components and maintaining healthy mitochondria. When either process was disrupted, the fungus became much more vulnerable to heat and could not survive as well.

Background

Heat adaptation is a multilayered process involving coordinated cellular responses. The plant pathogenic fungus Botrytis cinerea switches to survival mode at higher temperatures and can be primed by moderately high temperatures to better cope with severe heat stress. The roles of ATP-dependent proteases and autophagy in heat adaptation have been established in other organisms but remain understudied in B. cinerea.

Objective

This study investigates the involvement of autophagy and mitochondrial Lon1 protease in the heat stress adaptation of B. cinerea. The researchers aimed to determine whether both autophagy and the mitochondrial Lon1 protease are necessary for fungal tolerance to mild heat stress.

Results

Deletion of bclon1 or blocking autophagy did not affect fungal survival at optimal temperature. Under heat stress, bclon1 deletion induced earlier and more intense autophagy, mitochondrial malfunction, and accelerated cell death. The bcatg1/lon1 double mutant showed intensified mitochondrial damage and growth defects. Blocking autophagy affected mycelia growth, spore germination, nuclei division, and spore morphology independent of temperature.

Conclusion

Both autophagy and the Lon1 protease contribute to B. cinerea heat adaptation in a coordinated manner. Autophagy provides a cytoprotective function downstream of mitochondria-driven death signals and is necessary for proper growth arrest regulation under heat stress. The mitochondrial destabilization caused by Lon1 protease disruption activates autophagy, which helps remove damaged cellular components and promotes cellular survival.
  • Published in:Molecular Microbiology,
  • Study Type:Experimental Study,
  • Source: PMID: 40682260, DOI: 10.1111/mmi.70014
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