A quantitative bioassay for necrosis toxin from Pyrenophora tritici-repentis based on electrolyte leakage

Pyrenophora tritici-repentis, the causal agent of tan spot of wheat, produces a cultivar-specific toxin (Ptr necrosis toxin) closely associated with the disease symptomatology. We initiated studies aimed at the mode-of-action of Ptr necrosis toxin and, as a first step, report here a bioassay for tox...

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Bibliographic Details
Published inPhytopathology Vol. 86; no. 12; pp. 1360 - 1363
Main Authors Kwon, C.Y. (North Dakota State University, Fargo.), Rasmussen, J.B, Francl, L.J, Meinhardt, S.W
Format Journal Article
LanguageEnglish
Published St. Paul, MN American Phytopathological Society 01.12.1996
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Summary:Pyrenophora tritici-repentis, the causal agent of tan spot of wheat, produces a cultivar-specific toxin (Ptr necrosis toxin) closely associated with the disease symptomatology. We initiated studies aimed at the mode-of-action of Ptr necrosis toxin and, as a first step, report here a bioassay for toxin based on electrolyte leakage. Toxin exposures of 4 h or more caused enhanced electrolyte leakage from wheat line ND495 (toxin sensitive), but not cv. Erik (toxin insensitive), relative to water-treated controls. Electrolyte leakage increased with exposure times up to 12 h the longest time tested, when toxin concentration and leaching time were held constant. Electrolyte leakage increased with toxin concentration between 1 and 20 microgram ml-1, when exposure and leaching times were constant. All toxin-sensitive wheats tested (based on toxin-induced necrosis) showed enhanced electrolyte leakage, and all insensitive wheats did not. A toxin exposure of 4 h permitted completion of the assay in 1 day. We used this rapid assay to demonstrate that incubation of ND495 seedlings at 30 degrees C for 24 h prior to toxin exposure causes a loss of toxin sensitivity. Enhanced electrolyte leakage is the most rapid response to toxin observed to date. However, the toxin exposure times required for leakage to develop (4 h or longer) suggest that effects on the plasmalemma are secondary and occur relatively late in the development of necrosis
Bibliography:9730140
F30
H20
ISSN:0031-949X
1943-7684