Related Experiment Video
Updated: Dec 24, 2025
08:03
Unveiling Xenobiotic Transport and Effects in Isolated Mitochondria: Insights from Respirometric and Enzymatic Assays
Published on: March 7, 2025
868
Quantitative proteomics reveals that tea tree oil effects Botrytis cinerea mitochondria function
Nan Wang1, Xingfeng Shao1, Yingying Wei1
1College of Food and Pharmaceutical Sciences, Ningbo University, Ningbo 315800, China.
Pesticide Biochemistry and Physiology
|April 15, 2020
Summary
Tea tree oil (TTO) disrupts vital mitochondrial functions in Botrytis cinerea, inhibiting growth by altering key metabolic pathways. This research reveals TTO
Area of Science:
- Agricultural Science
- Biochemistry
- Mycology
Background:
- Botrytis cinerea is a significant plant pathogen causing grey mold disease.
- Tea tree oil (TTO) exhibits antifungal properties, including inhibition of spore germination and mycelial growth.
- Mitochondrial dysfunction is implicated in the antifungal mechanism of TTO against B. cinerea.
Purpose of the Study:
- To investigate the specific effects of TTO on mitochondrial proteins in Botrytis cinerea.
- To identify the metabolic pathways affected by TTO treatment at the proteomic level.
Main Methods:
- Label-free quantitative proteomics was employed to analyze protein expression changes.
- Differentially expressed proteins (DEPs) were identified and quantified.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed.
Main Results:
- A total of 85 DEPs were identified between TTO-treated and control samples.
- Proteomic analysis revealed significant alterations in mitochondrial pathways, including inhibition of the tricarboxylic acid cycle, pyruvate metabolism, and amino acid metabolism.
- Sphingolipid metabolism was found to be promoted by TTO treatment.
Conclusions:
- Tea tree oil induces mitochondrial dysfunction in Botrytis cinerea by inhibiting essential metabolic processes.
- The observed metabolic perturbations, particularly the promotion of sphingolipid metabolism, may contribute to TTO's fungicidal activity and accelerate fungal cell death.
