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The pH signalling transcription factor PacC controls virulence in the plant pathogen Fusarium oxysporum
Author(s) -
Caracuel Zaira,
Roncero M. Isabel G.,
Espeso Eduardo A.,
GonzálezVerdejo Clara I.,
GarcíaMaceira Fe I.,
Di Pietro Antonio
Publication year - 2003
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2003.03465.x
Subject(s) - biology , fusarium oxysporum , virulence , pathogen , microbiology and biotechnology , transcription factor , virulence factor , botany , genetics , gene
Summary Gene expression in fungi by ambient pH is regulated via a conserved signalling cascade whose terminal component is the zinc finger transcription factor PacC/Rim1p. We have identified a pacC orthologue in the vascular wilt pathogen Fusarium oxysporum that binds the consensus 5′‐GCCAAG‐3′ sequence and is proteolytically processed in a similar way to PacC from Aspergillus nidulans. pacC transcript levels were elevated in F. oxysporum grown in alkaline conditions and almost undetectable at extreme acidic growth conditions. PacC +/– loss‐of‐function mutants displayed an acidity‐mimicking phenotype resulting in poor growth at alkaline pH, increased acid protease activity and higher transcript levels of acid‐expressed polygalacturonase genes. Reintroduction of a functional pacC copy into a pacC +/– mutant restored the wild‐type phenotype. Conversely, F. oxysporum merodiploids carrying a dominant activating pacC c allele had increased pacC transcript and protein levels and displayed an alkalinity‐mimicking phenotype with reduced acid phosphatase and increased alkaline protease activities. PacC +/– mutants were more virulent than the wild‐type strain in root infection assays with tomato plants, whereas pacC c strains were significantly reduced in virulence. We propose that F. oxysporum PacC acts as a negative regulator of virulence to plants, possibly by preventing transcription of acid‐expressed genes important for infection.