PFP1 , a Gene Encoding an Epc-N Domain-Containing Protein, Is Essential for Pathogenicity of the Barley Pathogen Rhynchosporium commune

Scald caused by Rhynchosporium commune is an important foliar disease of barley. Insertion mutagenesis of R. commune generated a nonpathogenic fungal mutant which carries the inserted plasmid in the upstream region of a gene named PFP1 . The characteristic feature of the gene product is an Epc-N dom...

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Published inEukaryotic cell Vol. 13; no. 8; pp. 1026 - 1035
Main Authors Siersleben, Sylvia, Penselin, Daniel, Wenzel, Claudia, Albert, Sylvie, Knogge, Wolfgang
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.08.2014
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ISSN1535-9778
1535-9786
1535-9786
DOI10.1128/EC.00043-14

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Summary:Scald caused by Rhynchosporium commune is an important foliar disease of barley. Insertion mutagenesis of R. commune generated a nonpathogenic fungal mutant which carries the inserted plasmid in the upstream region of a gene named PFP1 . The characteristic feature of the gene product is an Epc-N domain. This motif is also found in homologous proteins shown to be components of histone acetyltransferase (HAT) complexes of fungi and animals. Therefore, PFP1 is suggested to be the subunit of a HAT complex in R. commune with an essential role in the epigenetic control of fungal pathogenicity. Targeted PFP1 disruption also yielded nonpathogenic mutants which showed wild-type-like growth ex planta , except for the occurrence of hyphal swellings. Complementation of the deletion mutants with the wild-type gene reestablished pathogenicity and suppressed the hyphal swellings. However, despite wild-type-level PFP1 expression, the complementation mutants did not reach wild-type-level virulence. This indicates that the function of the protein complex and, thus, fungal virulence are influenced by a position-affected long-range control of PFP1 expression.
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Present address: Sylvie Albert, Agropolis International, Montpellier, France.
ISSN:1535-9778
1535-9786
1535-9786
DOI:10.1128/EC.00043-14