Genetic Dissection of Blackleg Resistance Loci in Rapeseed (Brassica napus L.)

Blackleg disease caused by the heterothallic ascomycete fungus Leptosphaeria maculans (Desm.) Ces. et de Not. (anamorph: Phoma lingam Tode ex Fr.), is the major disease of Brassica crops such as turnip rape (Brassica rapa L. syn. B. campestris; 2n = 2x = 20, genome AA), cabbage (B. oleracea L.; 2n = 2x = 18, genome CC), rapeseed (syn. canola or oilseed rape B. napus L.; 2n = 4x = 38, genome AACC), and B. juncea L. (Indian or brown mustard; 2n = 4x = 36, genome AABB) grown in temperate regions of the world. It was recorded for the first time on stems of red cabbage [1]. B. napus originated as a result of natural interspecific hybridization and genome doubling between the monogenomic diploid species, B. rapa and B. oleracea, in southern Europe approximately 10,000–100,000 years ago [2, 3]. However, it was selected and grown as an oilseed crop only 300-500 years ago [4, 5]. B. napus originally evolved as a spring or semi-winter type under the Mediterranean climates, and spread rapidly from southern to northern Europe after the development of winter B. napus varieties [6]. Both spring and winter types are affected by blackleg disease, particularly in Australia, Europe and North America. Currently B. napus is the world’s third most important oilseed crop, grown on an area of over 23 million hectares and produce almost 53.3 million tonnes annually [7]. Increase in B. napus production has been attributed to the development and release of high yielding superior varieties including hybrids having traits such as high oil content, improved protein quality and herbicide resistance for better crop management.