Abstract

Tan spot is a devastating foliar disease of wheat caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis. Much has been learned during the past two decades about the genetics of wheat-P. tritici-repentis interactions. Research has shown that the fungus produces at least three host-selective toxins (HSTs), known as Ptr ToxA, Ptr ToxB, and Ptr ToxC, that interact directly or indirectly with the products of the dominant host genes Tsn1, Tsc2, and Tsc1, respectively. The recent cloning and characterization of Tsn1 provided strong evidence that the pathogen utilizes HSTs to subvert host resistance mechanisms to cause disease. However, in addition to host-HST interactions, broad-spectrum, race non-specific resistance QTLs and recessively inherited qualitative 'resistance' genes have been identified. Molecular markers suitable for marker-assisted selection against HST sensitivity genes and for race non-specific resistance QTLs have been developed and used to generate adapted germplasm with good levels of tan spot resistance. Future research is needed to identify novel HSTs and corresponding host sensitivity genes, determine if the recessively inherited resistance genes are HST insensitivities, extend the current race classification system to account for new HSTs, and determine the molecular basis of race non-specific resistance QTLs and their relationships with host-HST interactions at the molecular level. Necrotrophic pathogens such as P. tritici-repentis are likely to become increasingly significant under a changing global climate making it imperative to further characterize the wheat-P. tritici-repentis pathosystem and develop tan spot resistant wheat varieties.

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