Toxin ofPyrenophora tritici-repentis: Host-Specificity, Significance in Disease, and Inheritance of Host Reaction

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Abstract
Pyrenophora tritici-repentis differentially induces combinations of tan necrosis and extensive chlorosis in individual susceptible wheat cultivars. Crude and dialyzed culture filtrates from isolates of P. tritici-repentis contained a heat-labile (121 C for 20 min) toxin(s), which induced necrosis only on fungus-susceptible, tan necrosis-expressing cultivars within the genus Triticum. Cultivars resistant to the fungus as well as cultivars susceptible to extensive chlorosis-inducing isolates were insensitive. Segregation of F2 populations from four different crosses between cultivars resistant and susceptible to tan necrosis indicated that susceptibility to the fungus and sensitivity to the toxin were controlled by the same dominant gene. Toxin production by the pathogen was associated with the ability of individual isolates to induce tan necrosis (nec+) in necrosis-expressing cultivars. Isolates that induced extensive chlorosis but not necrosis (nec-chl+) did not produce toxin in vitro. The toxic differentiated two near-isogenic lines from the cultivar Columbus. When inoculated with a nec+ isolate, only the toxin-sensitive line (Col+) developed tan necrosis. The toxin(s) of P. tritici-repentis is cultivar-specific, involved in the induction of necrosis in the host, and appears to be a pathogenicity factor. Its designation as Ptr necrosis toxin is proposed.