CYP1, a hypovirus-regulated cyclophilin, is required for virulence in the chestnut blight fungus.

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TitleCYP1, a hypovirus-regulated cyclophilin, is required for virulence in the chestnut blight fungus.
Publication TypeJournal Article
Year of Publication2011
AuthorsChen, M-M, Jiang, M, Shang, J, Lan, X, Yang, F, Huang, J, Nuss, DL, Chen, B
JournalMol Plant Pathol
Volume12
Issue3
Pagination239-46
Date Published2011 Apr
ISSN1364-3703
KeywordsAmino Acid Sequence, Ascomycota, Blotting, Southern, Cloning, Molecular, Cyclophilins, Fungal Proteins, Gene Deletion, Gene Expression Regulation, Fungal, Gene Knockout Techniques, Heterotrimeric GTP-Binding Proteins, Hippocastanaceae, Molecular Sequence Data, Phenotype, Plant Diseases, RNA Viruses, RNA, Messenger, Sequence Alignment, Signal Transduction, Virulence
Abstract

Cyclophilins are peptidyl-prolyl cis-trans isomerases that are highly conserved throughout eukaryotes and are the cellular target of the immunosuppressive drug cyclosporin A (CsA). We cloned cyp1, a cyclophilin A-encoding gene in the phytopathogenic fungus Cryphonectria parasitica, and showed that this gene was downregulated following infection by a virulence-attenuating hypovirus. The function of cyp1 was further investigated by construction of a cyp1 deletion mutant. Although the wild-type C. parasitica strain EP155 was sensitive to CsA, the Δcyp1 strain was highly tolerant to CsA, indicating that CYP1 was the target of CsA. Deletion of cyp1 resulted in reduced virulence when inoculated to chestnut stems. Transcriptional analysis revealed that deletion of cyp1 also reduced transcript levels for genes encoding key components of the heterotrimeric guanosine triphosphate-binding protein signalling pathway that are essential for sensing environmental cues and are involved in C. parasitica development and virulence.

DOI10.1111/j.1364-3703.2010.00665.x
Alternate JournalMol. Plant Pathol.
PubMed ID21355996
PubMed Central IDPMC3313458
Grant ListGM55981 / GM / NIGMS NIH HHS / United States
R01 GM055981-16 / GM / NIGMS NIH HHS / United States