Induction of a Cryphonectria parasitica cellobiohydrolase I gene is suppressed by hypovirus infection and regulated by a GTP-binding-protein-linked signaling pathway involved in fungal pathogenesis.

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TitleInduction of a Cryphonectria parasitica cellobiohydrolase I gene is suppressed by hypovirus infection and regulated by a GTP-binding-protein-linked signaling pathway involved in fungal pathogenesis.
Publication TypeJournal Article
Year of Publication1995
AuthorsWang, P, Nuss, DL
JournalProc Natl Acad Sci U S A
Volume92
Issue25
Pagination11529-33
Date Published1995 Dec 5
ISSN0027-8424
KeywordsAmino Acid Sequence, Ascomycota, Base Sequence, Blotting, Southern, Cellulose 1,4-beta-Cellobiosidase, Cloning, Molecular, Enzyme Induction, Gene Expression Regulation, Fungal, Genes, Fungal, Glycoside Hydrolases, GTP-Binding Proteins, Molecular Sequence Data, RNA Precursors, Sequence Homology, Amino Acid, Signal Transduction, Suppression, Genetic, Transcription, Genetic, Trees, Virulence
Abstract

Extracellular cellulase activity is readily induced when the chestnut blight fungus Cryphonectria parasitica is grown on cellulose substrate as the sole carbon source. However, an isogenic C. parasitica strain rendered hypovirulent due to hypovirus infection failed to secrete detectable cellulase activity when grown under parallel conditions. Efforts to identify C. parasitica cellulase-encoding genes resulted in the cloning of a cellobiohydrolase (exoglucanase, EC 3.2.1.91) gene designated chb-1. Northern blot analysis revealed an increase in cbh-1 transcript accumulation in a virus-free virulent C. parasitica strain concomitant with the induction of extracellular cellulase activity. In contrast, induction of cbh-1 transcript accumulation was suppressed in an isogenic hypovirus-infected strain. Significantly, virus-free C. parasitica strains rendered hypovirulent by transgenic cosuppression of a GTP-binding protein alpha subunit were also found to be deficient in the induction of cbh-1 transcript accumulation.

Alternate JournalProc. Natl. Acad. Sci. U.S.A.
PubMed ID8524797
PubMed Central IDPMC40435