The emergence of tan spot disease caused by toxigenic Pyrenophora tritici-repentis in Australia is not associated with increased deployment of toxin-sensitive cultivors.

Authors: OLIVER, RICHARD - MURDOCH UNIVERSITY; LORD, MARYN - MURDOCH UNIVERSITY; RYBAK, KASIA - MURDOCH UNIVERSITY; Faris, Justin; SOLOMON, PETER - MURDOCH UNIVERSITY

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/23/2007
Publication Date: 5/1/2008
Citation: Oliver, R.P., Lord, M., Rybak, K., Faris, J.D., Solomon, P.S. 2008. The emergence of tan spot disease caused by toxigenic Pyrenophora tritici-repentis in Australia is not associated with increased deployment of toxin-sensitive cultivors.. Phytopathology. 98:488-191

Interpretive Summary: The wheat disease tan spot was first described in 1941 in the USA. It was first noted in Australia in 1953 and only became a serious disease in the 1970s. The tan spot pathogen produces a host-selective toxin (HST) known as Ptr ToxA, which contributes to disease development wheat lines that contain the Tsn1 gene. Although the emergence and spread of tan spot had been attributed to the adoption of minimum tillage practices, we wished to test the alternative idea that the planting of Tsn1 wheat lines may have contributed to the establishment of the pathogen in Australia. To do this, wheat cultivars released in Australia from 1911 to 1986 were tested for reaction to ToxA. Prior to 1941, 16 percent of wheat cultivars were ToxA-insensitive and hence, all other factors being equal, would be more resistant to the disease. Surprisingly, only one of the cultivars released since 1940 was ToxA insensitive. The area planted to ToxA-insensitive cultivars varied from 0 to 14 percent in New South Wales, peaking in the 1960s and 1970s. The emergence of tan spot in Australia occurred when only one ToxA-insensitive cultivar was in widespread use and coincided with a peak of its adoption. We therefore conclude that the spread of tan spot in Australia cannot be causally linked to the deployment of cultivars with Tsn1.

Technical Abstract: The wheat disease tan (or yellow leaf) spot, caused by Pyrenophora tritici-repentis, was first described in 1941 in the USA. It was first noted in Australia in 1953 and only became a serious disease in the 1970s. The recent emergence of this disease has been attributed to the acquisition by P. tritici-repentis of the ToxA gene from the wheat leaf and glume blotch pathogen, Stagonospora nodorum. ToxA encodes a host-specific toxin that interacts with the product of the wheat gene Tsn1. Interaction of ToxA with the dominant allele of Tsn1 causes host necrosis. P. tritici-repentis races lacking ToxA give minor indistinct lesions on wheat lines, and wheat lines expressing Tsn1 are significantly more susceptible to the disease. Whilst the emergence and spread of tan spot had been attributed to the adoption of minimum tillage practices, we wished to test the alternative idea that the planting of Tsn1 wheat lines may have contributed to the establishment of the pathogen in Australia. To do this, wheat cultivars released in Australia from 1911 to 1986 were tested for their sensitivity to ToxA. Prior to 1941, 16% of wheat cultivars were ToxA-insensitive and hence, all other factors being equal, would be more resistant to the disease. Surprisingly, only one of the cultivars released since 1940 was ToxA insensitive. The area planted to ToxA-insensitive cultivars varied from 0 to 14% in New South Wales, peaking in the 1960s and 1970s. The emergence of tan spot in Australia occurred when only one ToxA-insensitive cultivar was in widespread use and coincided with a peak of its adoption. We therefore conclude that the spread of P. tritici-repentis in Australia cannot be causally linked to the deployment of ToxA-sensitive cultivars.