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Robust anti‐oxidant defences in the rice blast fungus Magnaporthe oryzae confer tolerance to the host oxidative burst
Author(s) -
Samalova Marketa,
Meyer Andreas J.,
Gurr Sarah J.,
Fricker Mark D.
Publication year - 2014
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.12530
Subject(s) - appressorium , reactive oxygen species , glutathione , biology , oxidative stress , respiratory burst , magnaporthe grisea , pathogen , mitochondrion , mitochondrial ros , microbiology and biotechnology , spore germination , oxidative phosphorylation , pathosystem , hypha , biochemistry , spore , oryza sativa , enzyme , gene
Summary Plants respond to pathogen attack via a rapid burst of reactive oxygen species ( ROS ). However, ROS are also produced by fungal metabolism and are required for the development of infection structures in Magnaporthe oryzae . To obtain a better understanding of redox regulation in M. oryzae , we measured the amount and redox potential of glutathione ( E GSH ), as the major cytoplasmic anti‐oxidant, the rates of ROS production, and mitochondrial activity using multi‐channel four‐dimensional ( x,y,z,t ) confocal imaging of Grx1‐ro GFP 2 and fluorescent reporters during spore germination, appressorium formation and infection. High levels of mitochondrial activity and ROS were localized to the growing germ tube and appressorium, but E GSH was highly reduced and tightly regulated during development. Furthermore, germlings were extremely resistant to external H 2 O 2 exposure ex planta . E GSH remained highly reduced during successful infection of the susceptible rice cultivar CO 39. By contrast, there was a dramatic reduction in the infection of resistant ( IR 68) rice, but the sparse hyphae that did form also maintained a similar reduced E GSH . We conclude that M. oryzae has a robust anti‐oxidant defence system and maintains tight control of E GSH despite substantial oxidative challenge. Furthermore, the magnitude of the host oxidative burst alone does not stress the pathogen sufficiently to prevent infection in this pathosystem.