Abstract
Abstract Canola/rapeseed is the third largest global vegetable oil source, after soybean and palm oil. Blackleg caused by the fungus Leptosphaeria maculans (Desm.) Ces. & de Not. (anamorph Phoma lingam Tode ex Fr.), is a devastating disease present all over rapeseed/canola‐growing areas except China. The pathogen can infect all parts of the plant, but stem canker is the most serious symptom as it causes plant lodging and yield loss. Populations of blackleg pathogen are a complex of at least two genetically distinct groups, now referred to as two different species, L. maculans (highly virulent, A‐group) and L. biglobosa (weakly virulent, B‐group). According to the interaction phenotype (IP), isolates can be classified into at least five pathogenicity groups (PGs): PG‐1, PG‐2, PG‐3, PG‐4, and PGT. Population genetic diversity of L. maculans that can break down novel resistance sources is mainly derived from three factors: sexual recombination, large population size and a high gene flow through large‐scale dissemination of ascospores. Human activity too may contribute to this. The gene‐for‐gene hypothesis has been proven in Brassica–blackleg pathosystem. To date, nine avirulence (Avr) genes AvrLm1–9 and their corresponding resistance genes have been characterized following genetic studies on both the plant and the pathogen. Two types of the induced resistance, systemic acquired resistance (SAR) and induced systemic resistance (ISR), have been suggested in Brassica–blackleg pathosystem. The disease control methods such as crop rotation, resistant cultivars and seed treatment with fungicide have proven to be effective. However, the most economical and environmentally friendly method of disease control to the farmer is resistance (R‐gene resistance) in the host. This durable resistance against the Blackleg pathogen is sort after by all breeding groups. Although single gene resistance has been effective, with the advent of pathogen strains belonging to different pathotypes and carrying different Avr genes, it has become necessary for most breeding programs to concentrate their efforts on gene pyramiding for multiple R genes in the host. This is effectively achieved by marker‐assisted selection.
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