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pH dependency of sclerotial development and pathogenicity revealed by using genetically defined oxalate‐minus mutants of S clerotinia sclerotiorum
Author(s) -
Xu Liangsheng,
Xiang Meichun,
White David,
Chen Weidong
Publication year - 2015
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.12818
Subject(s) - sclerotinia sclerotiorum , biology , virulence , oxalic acid , mutant , oxalate , pathogenicity , microbiology and biotechnology , host (biology) , botany , genetics , biochemistry , gene , chemistry , organic chemistry
Summary The devastating plant pathogen S clerotinia sclerotiorum produces copious (up to 50 mM) amounts of oxalic acid, which, for over a quarter century, has been claimed as the pathogenicity determinant based on UV ‐induced mutants that concomitantly lost oxalate production and pathogenicity. Such a claim was made without fulfilling the molecular K och's postulates because the UV mutants are genetically undefined and harbour a developmental defect in sclerotial production. Here, we generated oxalate‐minus mutants of S . sclerotiorum using two independent mutagenesis techniques, and tested the resulting mutants for growth at different pHs and for pathogenicity on four host plants. The oxalate‐minus mutants accumulated fumaric acid, produced functional sclerotia and have reduced ability to acidify the environment. The oxalate‐minus mutants retained pathogenicity on plants, but their virulence varied depending on the pH and buffering capacity of host tissue. Acidifying the host tissue enhanced virulence of the oxalate‐minus mutants, whereas supplementing with oxalate did not. These results suggest that it is low pH , not oxalic acid itself, that establishes the optimum conditions for growth, reproduction, pathogenicity and virulence expression of S . sclerotiorum . Exonerating oxalic acid as the primary pathogenicity determinant will stimulate research into identifying additional candidates as pathogenicity factors towards better understanding and managing Sclerotinia diseases.