Oxalic acid, a pathogenicity factor for Sclerotinia sclerotiorum, suppresses the oxidative burst of the host plant.
Effective pathogenesis by the fungus Sclerotinia sclerotiorum requires the secretion of oxalic acid. Studies were conducted to determine whether oxalate aids pathogen compatibility by modulating the oxidative burst of the host plant. Inoculation of tobacco leaves with an oxalate-deficient nonpathogenic mutant of S. sclerotiorum induced measurable oxidant biosynthesis, but inoculation with an oxalate-secreting strain did not. Oxalate inhibited production of H(2)O(2) in tobacco and soybean cultured cell lines with a median inhibitory concentration of approximately 4 to 5 mM, a concentration less than that measured in preparations of the virulent fungus. Several observations also indicate that the inhibitory effects of oxalate are largely independent of both its acidity and its affinity for Ca(2)+. These and other data demonstrate that oxalate may inhibit a signaling step positioned upstream of oxidase assembly/activation but downstream of Ca(2)+ fluxes into the plant cell cytosol.
Cessna
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Department of Chemistry, Purdue University, 1393 Brown Building, West Lafayette, Indiana 47904-1393, USA.
Sears
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Dickman
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Low
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D001203:Ascomycota / Q000378:metabolism / Q000472:pathogenicity*; D019815:Oxalic Acid / Q000378:metabolism*; D010947:Plants, Toxic; D016897:Respiratory Burst; D013025:Glycine max / Q000378:metabolism* / Q000382:microbiology; D014026:Nicotiana / Q000378:metabolism* / Q000382:microbiology; D014774:Virulence
D019815:Oxalic Acid