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Genetic relationships between race-nonspecific and race-specific interactions in the wheat–Pyrenophora tritici-repentis pathosystem
- Kariyawasam, Gayan K., Carter, Arron H., Rasmussen, Jack B., Faris, Justin, Xu, Steven S., Mergoum, Mohamed, Liu, Zhaohui
- Theoretical and applied genetics 2016 v.129 no.5 pp. 897-908
- Pyrenophora tritici-repentis, Triticum aestivum, breeding, chlorosis, conidia, epistasis, fungi, genes, genetic relationships, genetic resistance, loci, quantitative trait loci, races, wheat
- We identified a major QTL conferring race-nonspecific resistance and revealed its relationships with race-specific interactions in the wheat– Pyrenophora tritici - repentis pathosystem. Tan spot, caused by the fungus Pyrenophora tritici-repentis (Ptr), is a destructive disease of wheat worldwide. The disease system is known to include inverse gene-for-gene, race-specific interactions involving the recognition of fungal-produced necrotrophic effectors (NEs) by corresponding host sensitivity genes. However, quantitative trait loci (QTLs) conferring race-nonspecific resistance have also been identified. In this work, we identified a major race-nonspecific resistance QTL and characterized its genetic relationships with the NE-host gene interactions Ptr ToxA-Tsn1 and Ptr ToxC-Tsc1 in a recombinant inbred wheat population derived from the cross between ‘Louise’ and ‘Penawawa.’ Both parental lines were sensitive to Ptr ToxA, but Penawawa and Louise were highly resistant and susceptible, respectively, to conidial inoculations of all races. Resistance was predominantly governed by a major race-nonspecific QTL on chromosome arm 3BL for resistance to all races. Another significant QTL was detected at the distal end of chromosome arm 1AS for resistance to the Ptr ToxC-producing isolates, which corresponded to the known location of the Tsc1 locus. The effects of the 3B and 1A QTLs were largely additive, and the 3B resistance QTL was epistatic to the Ptr ToxA-Tsn1 interaction. Resistance to race 2 in F₁ plants was completely dominant; however, race 3-inoculated F₁ plants were only moderately resistant because they developed chlorosis presumably due to the Ptr ToxC-Tsc1 interaction. This work provides further understanding of genetic resistance in the wheat-tan spot system as well as important guidance for tan spot resistance breeding.