Evolution of populations of Leptosphaeria maculans, a fungal pathogen of oilseed rape, under resistance selection pressure: insights from two decades of surveys in France

National audience; Leptosphaeria maculans is responsible for the stem canker, a major disease of oilseed rape (Brassica napus). Specific resistance genes are used in commercial varieties to control the disease. The effectiveness of a given resistance gene is a function of the frequency of the corresponding avirulent allele in field populations of the pathogen. After the release of the oilseed rape resistance gene Rlm1 in the 1990’s in France, a very rapid increase in the frequency of isolates virulent towards this gene was observed [1]. More recently, a new resistance gene, Rlm7, was introduced into commercial hybrid varieties, at a time when most (>99.5%) of the L. maculans isolates possessed the corresponding avirulent allele AvrLm7 [2]. Since 2000, the frequency of isolates virulent against Rlm7 has been monitored in populations of L. maculans in either experimental fields with increased selection pressure, or at a national scale in more standard agronomic situations. While a rapid increase in frequency of virulent isolates was observed in an experimental field at Grignon that had minimum tillage and continuous oilseed rape cropping (36% of isolates virulent after 3 years; [3]), the breakdown of the Rlm7 gene appeared much less rapid than that observed previously for Rlm1 at the national level in France (less than 20% of isolates virulent after 10 years of widespread use of Rlm7. Among the possible reasons for this unexpected durability of Rlm7, the role of the negative interaction between AvrLm7 and AvrLm3 [4] was explored here. A detailed knowledge of molecular mechanisms responsible for virulence against Rlm3 and Rlm7 was obtained and suggested that pyramiding of the two resistance genes could have a negative impact on Rlm7 durability while the use of both resistance genes in different varieties could have slowed down the breakdown. These population and molecular information are currently used in an epidemiological model to test our hypotheses. References [1] Rouxel T, et al (2003). Eur J Plant Pathol 109:871-881. [2] Balesdent MH, et al (2006). Eur J Plant Pathol 114:53-65. [3] Daverdin G, et al (2012).. PLoS Pathog 8: e1003020. [4] Plissonneau C, et al (2016) New Phytol 209:1613-1624