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A novel mitochondrial membrane protein, O hmm, limits fungal oxidative stress resistance and virulence in the insect fungal pathogen B eauveria bassiana
Author(s) -
He Zhangjiang,
Zhang Suhong,
Keyhani Nemat O.,
Song Yulin,
Huang Shuaishuai,
Pei Yan,
Zhang Yongjun
Publication year - 2015
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.12713
Subject(s) - biology , oxidative stress , virulence , conidiation , microbiology and biotechnology , biochemistry , gene
Summary The H og1 mitogen‐activated protein ( MAP ) kinase regulates environmental stress responses and virulence in the entomopathogenic fungus B eauveria bassiana . To further characterize this pathway, we constructed a subtraction library enriched for genes regulated by H og1. One targeted gene, encoding a novel membrane protein, O hmm (oxidative homeostasis membrane‐protein–mitochondria), was uniquely identified as being downregulated in the Δ H og1 background during growth under non‐stress and osmotic stress conditions, but upregulated under oxidative stress. O hmm was an experimentally validated flavin‐binding protein and targeted to the mitochondria. Deletion of O hmm resulted in increased oxidative stress resistance, whereas overexpression caused an opposite phenotype. The Δ O hmm showed accumulation of reactive oxygen species with alterations in cell wall composition and compatible solute accumulation evident as compared with the wild type parent. Conidiation was reduced > 80%; however, conidia produced by the Δ O hmm strain germinated significantly faster than wild type cells. Insect bioassays using the greater wax moth revealed increased virulence for the Δ O hmm strain in both topical and intrahemocoel injection assays, indicating a negative effect of the presence of O hmm with respect to pathogenesis. As predicted from our characterization, deletion of O hmm in a Δ Hog 1 background rescued its oxidative sensitivity phenotype, confirming that O hmm acts downstream of the Hog 1 MAP ‐kinase.