Submitted to: Australasian Plant Pathlogy Society
Publication Type: Proceedings
Publication Acceptance Date: 10/21/2007
Publication Date: 11/1/2007
Citation: Goodwin, S.B. 2007. Back to basics and beyond: increasing the level of resistance to Septoria tritici blotch in wheat. Australasian Plant Pathlogy Society. 36:532-538.
Technical Abstract: Septoria tritici blotch (STB), caused by the ascomycete Mycosphaerella graminicola (anamorph: Septoria tritici), is one of the most ubiquitous and important diseases of wheat worldwide. Losses to STB can range from 30 to 50% in disease-conducive climates. Little progress was made in increasing the level of resistance to STB in wheat prior to 1990, due to a variety of factors, including slow growth of the pathogen in culture, long latent period of the disease, the need for specific environmental conditions for infection, and variability in symptom expression that complicated the scoring of inoculated plants. To identify and map genes for resistance to STB in the wheat genome, to understand how they function in their interactions with the pathogen and, ultimately, to increase the level of resistance so that the disease can be managed without extensive use of fungicides, crosses between parents differing in response to STB were made or obtained from collaborators for the resistance genes Stb1, Stb2, Stb3, Stb4 and Stb8. Plants were grown and inoculated with one or more isolates of M. graminicola in a greenhouse. The five targeted resistance genes Stb1-Stb4 and Stb8 were mapped to wheat chromosomes 5BL, 3BS, 6DS, 4DS, and 7BL, respectively. All of the genes had at least one linked microsatellite locus, and two of them (Stb2 and Stb8) were mapped between flanking microsatellites. These experiments plus those in other laboratories worldwide have determined the map locations for 12 genes for resistance to STB in wheat. Most of these genes have associated molecular markers that will be useful for future marker-assisted selection. However, there is still a great need for more markers and additional mapped genes, and for a better understanding of defence responses to STB.