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Functional analysis of an extracellular catalase of Botrytis cinerea
Author(s) -
Schouten Alexander,
Tenberge Klaus B.,
Vermeer Joop,
Stewart Jenny,
Wagemakers Lia,
Williamson Brian,
Van Kan Jan A. L.
Publication year - 2002
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1046/j.1364-3703.2002.00114.x
Subject(s) - botrytis cinerea , biology , catalase , extracellular , mutant , mycelium , microbiology and biotechnology , pathogen , virulence , superoxide dismutase , wild type , oxidative stress , botany , gene , biochemistry
Summary There is evidence that the necrotrophic fungal pathogen Botrytis cinerea is exposed to oxidative processes within plant tissues. The pathogen itself also generates active oxygen species and H 2 O 2 as pathogenicity factors. Our aim was to study how the pathogen may defend itself against cellular damage caused by the accumulation of H 2 O 2 and the role of an extracellular catalase in its detoxification during the infection of tomato and bean plants by B. cinerea .  Chloronaphthol staining followed by light microscopy showed that H 2 O 2 accumulates in the infection zone in tomato and bean leaves. An extracellular catalase gene (denominated Bccat 2) was cloned from B. cinerea . Exposure of mycelium to H 2 O 2 in liquid culture resulted in increased Bccat 2 mRNA levels in a concentration‐dependent manner. Bccat 2 mRNA was detected at early stages of tomato leaf infection, suggesting that B. cinerea experiences oxidative stress. Bccat 2‐deficient mutants were generated by transformation‐mediated gene disruption. Mutants were more sensitive then the wild‐type strain to H 2 O 2 in vitro , but they partly compensated for the absence of BcCAT2 by activating other protective mechanisms in the presence of H 2 O 2 . Bccat 2‐deficient mutants did not display a consistent reduction of virulence on bean and tomato leaves. Cerium chloride staining of infected leaf tissue for ultrastructural studies showed that Bccat 2‐deficient mutants were exposed to H 2 O 2 comparably to the wild‐type. The results suggest that B. cinerea is a robust pathogen adapted to growing in hostile oxidizing environments in host tissues.

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