The role of resistance breeding in the intergrated control of downy mildew (Bremia lactucae) in protected lettuce

Summary

Over the last 30 years, six resistance alleles (Dm2, Dm3, Dm6, Dm7, Dm11 andDm16) located in two linkage groups, have contributed to the control of downy mildew in lettuce crops grown under protection (glass or polythene) in northern Europe. More recently, an as yet genetically uncharacterised resistance factor, R18, has also begun to assume importance. The occurrence of the various combinations of these resistance alleles that exist in commercial cultivars has been dictated by the pathotypes ofBremia lactucae used in their selection but also restricted by linkage in repulsion. In the UK, a pathotype ofB. lactucae insensitive to phenylamide fungicides, such as metalaxyl, emerged in 1978 and became prevalent throughout lettuce production areas in subsequent years. The specific virulence of this pathotype was identical to the previously described phenylamide sensitive pathotype NL10 and cultivars carryingDm11, Dm16 or R18 were resistant. Consequently, an integrated control strategy based on the utilisation of metalaxyl on cultivars carryingDm11 provided effective control in UK until 1987 when a new phenylamide insensitive pathotype began to cause problems. The specific virulence of this second pathotype, which was first reported in the Netherlands and France, was identical to the previously described phenylamide sensitive pathotype NL15. Cultivars carryingDm6, Dm16 or R18, but notDm11, were resistant to NL15; consequently an appropriate change in the cultivar recommendations for use in the integrated control strategy was successfully promulgated. It is predicted that variations of this integrated control strategy involving the use of appropriately selectedDm gene combinations may prove effective for some time. This prediction is based on studies of the status of the avirulence loci in the two phenylamide insensitive pathotypes and of the specific virulence characteristics of phenylamide sensitive components of the pathogen population.