Background
Yellow spot (YS) also known as yellow leaf spot or tan spot is caused by the fungus Pyrenophora tritici-repentis (Ptr) and is an important foliar disease of wheat worldwide. There has been an increased prominence of the disease in recent years due to implementation of new farm management practices such as minimum tillage, reduced stubble burning, increased wheat-after-wheat cropping and use of susceptible varieties.
In Australia, it is estimated to cause losses at an average of $212 million per annum (despite the use of $150M of fungicides) and the present value of controlling YS lies at $464M per annum (Murray and Brennan 2009). On the basis of present importance of various wheat diseases, yellow spot ranks highest nationally and in the western and northern regions (Murray and Brennan 2009).
Disease cycle
The fungus P. tritici-repentis survives as mycelium in crop stubble and plant debris for up to two years, although relatively poorly after 18 months. In autumn/winter this mycelium develops sexual fruiting bodies (pseudothecia), which appear as black, pinhead-sized, raised structures with hair-like projections. These fruiting bodies are particularly common around the stem nodes. Primary infection is mostly initiated by sexual spores (ascospores) that are shot out of the pseudothecia, infecting young plants adjacent to the infected stubble. Secondary spread within the crop occurs under moist conditions. This is initiated by the production of conidia spores on dead leaf tissue. Conidia travel long distances on the wind and are responsible for developing later infections within the crop canopy, as well as infecting distant crops and stubbles.
Development and adoption of resistant varieties is regarded as the most economically effective, comprehensive and environmentally safe means of controlling YS. Although good progress has been made internationally to understand YS resistance, relatively few resistance genes have been identified and mapped in Australian germplasm and only one (tsn1 on chromosome 5BL) is in general and known use in Australian breeding programs, supported by molecular marker based selection.
Although tsn1 is an important YS resistance gene, it doesn’t explain the full spectrum of resistance in the Australian germplasm. Furthermore, Faris et al. (2012) have shown that the amount of variation explained by tsn1 can vary considerably (5-30%).
The pathogen produces at least three host specific toxins (HST) that interact with specific host sensitivity genes to cause necrosis. Among the identified HST, Ptr ToxA, a well-characterised HST was shown to be responsible for the development of necrosis. It appears that all YS isolates in Australia produce ToxA. Sensitivity to Ptr ToxA is conditioned by a single dominant gene named Tsn1 on 5BL. However, the wheat–yellow spot pathosystem is more complicated than previously thought and resistance can be inherited both qualitatively (Gamba and Lamari, 1998; Lamari and Bernier, 1989) and quantitatively (Elias et al., 1989; Friesen and Faris, 2004).
Several qualitative race-specific toxin sensitivity genes such as tsn1, tsn2, tsn3, tsn4, tsn5, tsn6, and tsn-syn1 and a dominant gene, Tsn-syn2, are known to confer resistance to necrosis (Anderson et al., 1999; Singh et al., 2006, 2008; Tadesse et al., 2006a, 2006b, 2010), and the recessive genes tsc1 and tsc2 condition resistance to chlorosis (Abeysekara et al., 2010; Effertz et al., 2002; Friesen and Faris, 2004).
On the other hand, there have been several reports of non-race specific quantitative trait loci (QTL) associated with YS resistance residing on chromosomes 1BS and 3BL (Faris and Friesen, 2005); 2AS, 4AL and 5AL (Chu et al.; 2008); 3AS, 3BL, 5AL and 7BL (Chu et al., 2010); 1A, 1D, 2B, 2D, 6A, and 7A (Patel et al, 2010); 5DL, 7BS and 7DS (Faris et al 2012); 3AS and 4BL (Singh et al. 2012); 1AS and 2BS (Sun et al. 2010) and 1A, 2BS, 3BS, 3D, 6A, 7A, and 7D (Li et al. 2011).
Incorporating both qualitative and quantitative resistance is essential to develop cultivars with high levels of durable resistance. There is a significant opportunity to enhance expression of YS resistance in the Australian germplasm through identification of resistance factors other than tsn1.