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Parastagonospora nodorum is a major fungal pathogen of wheat in Australia causing septoria nodorum blotch (SNB). P. nodorum virulence is quantitative and depends to a large extent on multiple effector-host sensitivity gene interactions. The pathogen utilises a series of proteinaceous necrotrophic effectors to facilitate disease development on wheat cultivars that possess appropriate dominant sensitivity loci. Thus far, three necrotrophic effector genes have been cloned. Proteins derived from these genes were used to identify wheat cultivars that confer effector sensitivity. The goal of the study was to determine if effector sensitivity could be used to enhance breeding for SNB resistance. In this study, we have demonstrated that SnTox1 effector sensitivity is common in current commercial Western Australian wheat cultivars. Thirty-three of 46 cultivars showed evidence of sensitivity to SnTox1. Of these, 19 showed moderate or strong chlorotic/necrotic responses to SnTox1. Thirteen were completely insensitive to SnTox1. Disease susceptibility was most closely associated with SnTox3 sensitivity. In addition, we have identified biochemical evidence of a novel chlorosis-inducing protein or proteins in P. nodorum culture filtrates unmasked in strains that lack expression of ToxA, SnTox1 and SnTox3 activities.

Stagonospora nodorum is a major pathogen of wheat in many parts of the world and particularly in Western Australia. The pathosystem is characterised by interactions of multiple pathogen necrotrophic effectors (NE) (formerly host-specific toxins) with corresponding dominant host sensitivity loci. To date, five NE interactions have been reported in S. nodorum. Two proteinaceous NE (ToxA and SnTox3) have been cloned and expressed in microbial systems. The identification of wheat cultivars lacking sensitivity to one or more NE is a promising way to identify cultivars suitable for use in breeding for increased resistance to this economically important pathogen. The prevalence of sensitivity to the NE SnTox3 was investigated in 60 current Western Australian-adapted bread wheat (Triticum aestivum L.) cultivars. Infiltration of SnTox3 into seedling leaves caused a moderate or strong necrotic response in 52 cultivars. Six cultivars were insensitive and two cultivars exhibited a weak chlorotic response. Five of the cultivars that were insensitive or weakly sensitive to SnTox3 were noticeably more resistant to the disease. The 60 cultivars gave a very similar reaction to SnTox3 and to the crude S. nodorum SN15 culture filtrate demonstrating that SnTox3 is the dominant NE in this isolate. We conclude that a simple screen using both SnTox3 and ToxA effectors combined with simple greenhouse disease evaluation, will allow breeders to select cultivars that are more resistant to the disease, allowing them to concentrate resources on other still intractable breeding objectives.

Pyrenophora tritici-repentis, the causal organism of the necrotrophic foliar wheat disease tan spot [also known as yellow (leaf) spot in Australia] is an important disease in Australia and in many parts of the world. North American isolates of the pathogen have been shown to produce combinations of three host-specific toxins, ToxA, ToxB and ToxC. Each toxin interacts with a host sensitivity locus, respectively Tsn1, Tsc2 and Tsc1. The virulence of an isolate is partially correlated with the presence of these toxins and resistance in the host is associated with absence of the sensitivity loci. Breeding for resistance to tan spot can, therefore, be aided by knowledge of the prevalence of the toxin-encoding genes in local pathogen populations. Two of the toxins, A and B, are encoded by known genes and molecular tests for the genes have been developed. We screened a diverse collection of 119 tan spot isolates collected between 1984 and 2008 and from all affected regions of Australia (Queensland, New South Wales, Victoria and Western Australia). In all cases, the gene for ToxA was present and the gene for ToxB was absent. The implications for resistance breeding and epidemiology of the disease are discussed. We also define a diagnostic molecular marker for P. tritici-repentis.

Pyrenophora tritici-repentis, the causal organism of the necrotrophic foliar wheat disease tan spot [also known as yellow (leaf) spot in Australia] is an important disease in Australia and in many parts of the world. North American isolates of the pathogen have been shown to produce combinations of three host-specific toxins, ToxA, ToxB and ToxC. Each toxin interacts with a host sensitivity locus, respectively Tsn1, Tsc2 and Tsc1. The virulence of an isolate is partially correlated with the presence of these toxins and resistance in the host is associated with absence of the sensitivity loci. Breeding for resistance to tan spot can, therefore, be aided by knowledge of the prevalence of the toxin-encoding genes in local pathogen populations. Two of the toxins, A and B, are encoded by known genes and molecular tests for the genes have been developed. We screened a diverse collection of 119 tan spot isolates collected between 1984 and 2008 and from all affected regions of Australia (Queensland, New South Wales, Victoria and Western Australia). In all cases, the gene for ToxA was present and the gene for ToxB was absent. The implications for resistance breeding and epidemiology of the disease are discussed. We also define a diagnostic molecular marker for P. tritici-repentis.

Pyrenophora tritici-repentis, the causal organism of the necrotrophic foliar wheat disease tan spot [alsoknown as yellow (leaf) spot in Australia] is an important disease in Australia and in many parts of the world. NorthAmerican isolates of the pathogen have been shown to produce combinations of three host-specific toxins, ToxA, ToxBand ToxC. Each toxin interacts with a host sensitivity locus, respectively Tsn1, Tsc2 and Tsc1. The virulence of anisolate is partially correlated with the presence of these toxins and resistance in the host is associated with absence ofthe sensitivity loci. Breeding for resistance to tan spot can, therefore, be aided by knowledge of the prevalence ofthe toxin-encoding genes in local pathogen populations. Two of the toxins, A and B, are encoded by known genesand molecular tests for the genes have been developed. We screened a diverse collection of 119 tan spot isolatescollected between 1984 and 2008 and from all affected regions of Australia (Queensland, New South Wales, Victoriaand Western Australia). In all cases, the gene for ToxA was present and the gene for ToxB was absent. Theimplications for resistance breeding and epidemiology of the disease are discussed. We also define a diagnosticmolecular marker for P. tritici-repentis.

A recent survey of worldwide isolates of Stagonospora nodorum showed that all Australian isolates expressed the host-specific toxin ToxA (Stukenbrock and McDonald 2007). In contrast, very few Chinese isolates did. All the Australian Pyrenophora tritici-repentis isolates that were tested expressed ToxA. We therefore postulated that the wheat gene that confers sensitivity to ToxA, Tsn1, would vary in prevalence in wheat cultivars in use in the two countries. Contrary to expectation, 10 out of 21 Chinese cultivars responded to ToxA as did 26 out of 46 Australian cultivars. The result suggests that ToxA has not had a determining effect on the survival of wheat cultivars in either country. They also suggest that despite the widespread use of Tsn1 markers in Australia, sensitive alleles are still commonplace. The removal of sensitive alleles from breeders' lines could be readily achieved and could significantly affect the resistance of wheat to both diseases.

A recent survey of worldwide isolates of Stagonospora nodorum showed that all Australian isolates expressed the host-specific toxin ToxA (Stukenbrock and McDonald 2007). In contrast, very few Chinese isolates did. All the Australian Pyrenophora tritici-repentis isolates that were tested expressed ToxA. We therefore postulated that the wheat gene that confers sensitivity to ToxA, Tsn1, would vary in prevalence in wheat cultivars in use in the two countries. Contrary to expectation, 10 out of 21 Chinese cultivars responded to ToxA as did 26 out of 46 Australian cultivars. The result suggests that ToxA has not had a determining effect on the survival of wheat cultivars in either country. They also suggest that despite the widespread use of Tsn1 markers in Australia, sensitive alleles are still commonplace. The removal of sensitive alleles from breeders' lines could be readily achieved and could significantly affect the resistance of wheat to both diseases.