Quantitative proteomics reveals that tea tree oil effects Botrytis cinerea mitochondria function

Pestic Biochem Physiol. 2020 Mar:164:156-164. doi: 10.1016/j.pestbp.2020.01.005. Epub 2020 Jan 21.

Abstract

Tea tree oil (TTO) inhibits the spore germination and mycelial growth of Botrytis cinerea, and induces mitochondrial dysfunction of B. cinerea. To further determine the effects of TTO on mitochondria in B. cinerea, label-free quantitative proteomics analysis was performed. A total of 85 differentially expression proteins (DEPs) were identified; Among them 51 were more abundant in TTO-treated samples, and 34 were less abundant. DEPs were then annotated and classified into 34 functional groups based on Gene Ontology analysis. Subsequent Kyoto Encyclopedia of Genes and Genomes analysis linked identified DEPs to 83 different pathways. This study suggests that TTO inhibits the tricarboxylic acid cycle, pyruvate metabolism, amino acid metabolism, and membrane-related pathways in mitochondria, and also promotes sphingolipid metabolism, which may accelerate cell death in B. cinerea.

Keywords: Botrytis cinerea; Label-free quantitation; Mitochondria; Proteomic; Tea tree oil.

MeSH terms

  • Botrytis*
  • Citric Acid Cycle
  • Mitochondria
  • Proteomics
  • Tea Tree Oil*

Substances

  • Tea Tree Oil