1887

Abstract

Using a gene disruption strategy, we generated mutants in the locus of the plant-beneficial fungus that were no longer capable of producing gliotoxin. Phenotypic assays demonstrated that the -disrupted mutants grew faster, were more sensitive to oxidative stress and exhibited a sparse colony edge compared with the WT strain. In a plate confrontation assay, the mutants deficient in gliotoxin production were ineffective as mycoparasites against the oomycete, , and the necrotrophic fungal pathogen, , but retained mycoparasitic ability against . Biocontrol assays in soil showed that the mutants were incapable of protecting cotton seedlings from attack by , against which the WT strain was highly effective. The mutants, however, were as effective as the WT strain in protecting cotton seedlings against . Loss of gliotoxin production also resulted in a reduced ability of the mutants to attack the sclerotia of compared with the WT. The addition of exogenous gliotoxin to the sclerotia colonized by the mutants partially restored their degradative abilities. Interestingly, as in , an opportunistic human pathogen, gliotoxin was found to be involved in pathogenicity of against larvae of the wax moth, . The loss of gliotoxin production in was restored by complementation with the gene from . We have, thus, demonstrated that the putative cluster of is responsible for the biosynthesis of gliotoxin, and gliotoxin is involved in mycoparasitism and biocontrol properties of this plant-beneficial fungus.

Funding
This study was supported by the:
  • USDA (Award 2008-35319-04470)
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2014-10-01
2024-04-26
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