ABSTRACT
ABSTRACT Culture filtrate from Pyrenophora tritici-repentis race 1 isolate 78-62 contained a genotype-specific toxin which elicited extensive chlorosis on sensitive wheat genotypes. This toxin was partially purified using gel filtration, ion exchange, and reversed-phase chromatography. The chlorosis toxin was found to be a polar, nonionic, low-molecular-weight molecule. Wheat genotypes infiltrated with crude culture filtrate and partially purified chlorosis toxin exhibited the same chlorotic symptoms seen with conidial inoculations of isolate 78-62. All tested wheat genotypes that exhibited extensive chlorosis to the toxin also exhibited extensive chlorosis to conidial inoculations, and all wheat genotypes insensitive to the toxin did not exhibit extensive chlorosis to conidial inoculations. The recombinant inbred population derived from the cross W-7984 x Opata 85 segregated for chlorosis induction from infiltration with partially purified chlorosis toxin from isolate 78-62. The locus identified by the marker XGli1, associated with resistance to conidial inoculations from race 1 isolates Pti2 and 78-62 and race 3 isolate D308, also was associated with insensitivity to infiltration of crude culture filtrate and partially purified chlorosis toxin. The marker XGli1, located on the short arm of chromosome 1A, is linked to the insensitivity locus within 5.7 cM. We propose that this chlorosis toxin be designated Ptr ToxC.
ABSTRACT
ABSTRACT Resistance to the chlorosis factor of tan spot of wheat, caused by the ascomycete Pyrenophora tritici-repentis, has been reported to be quantitative and a single quantitative trait loci (QTL), QTsc.ndsu-1A, explained 35% of the variation for resistance to a single isolate in seedlings of recombinant inbred (RI) lines derived from the cross W-7984/Opata 85. The objectives of this study were to determine the number and locations of genes conditioning resistance to the same isolate in adult plants of this population and three isolates in seedlings of wheat RI lines derived from the cross W-7976/Trenton. An extensive restriction fragment length polymorphism map exists for the W-7984/Opata 85 population, and markers significantly associated (P < 0.01) with resistance to tan spot were selected to analyze the W-7976/Trenton population. A multiple regression model accounted for 49% of the variation for resistance in adult plants with QTsc.ndsu-1A, explaining 26% of the variation. QTsc.ndsu-1A explained 47, 58, and 64% of the variation for resistance in seedlings to isolates Pti2, 78-62, and D308, respectively. These results showed that the QTL for tan spot resistance on chromosome 1AS was effective in both seedlings and adult plants and against isolates from different races of P. tritici-repentis.
ABSTRACT
ABSTRACT The fungus Pyrenophora tritici-repentis produces a toxin (Ptr ToxA) that causes rapid cell necrosis in sensitive wheat genotypes. A single recessive gene (tsn1) on chromosome 5BL in common wheat confers insensitivity to this toxin. Our objectives were to analyze the allelic relationships of genotypes that have shown insensitivity to a P. tritici-repentis necrosis-inducing toxin, map the gene for insensitivity to the necrosis-inducing factor produced by P. tritici-repentis in a durum wheat population, and determine the reaction to P. tritici-repentis of aneuploid genotypes that do not contain the gene. Greenhouse-grown plants of seven populations from crosses of insensitive genotypes; an F(2) population of durum wheat; and 'Chinese Spring' aneuploid, substitution, and deletion lines were infiltrated with Ptr ToxA. All crosses involving insensitive genotypes failed to produce sensitive progeny, indicating that the same gene is present in these genotypes. The gene for insensitivity in the durum population was mapped to the same region on 5BL as in common wheat using restriction fragment length polymorphism markers. 'Chinese Spring', its homoeologous group 5 nullisomic-tetrasomic stocks, and 5BL deletion lines were insensitive to the toxin. Substitution of a 5B chromosome from sensitive genotypes into 'Chinese Spring' resulted in sensitivity. Therefore, insensitivity is not conferred by a gene product per se, but rather conferred by absence of a gene for sensitivity.
