Anti-Therapeutic Action: Deletion of Lon1 protease or autophagy genes increases sensitivity to heat stress and cellular damage

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

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.

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