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Genetics

Mapping Loci Controlling Brassica napus Resistance to Leptosphaeria maculans under Different Screening Conditions. M. E. Ferreira, Department of Agronomy and Plant Pathology, University of Wisconsin, Madison 53706, Current address: EMBRAPA/CENARGEN, C.P. 0.2372, CEP 70770, Brasília, DF, Brazil; S. R. Rimmer(2), P. H. Williams(3), and T. C. Osborn(4). (2)Department of Plant Science, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada; (3)Department of Plant Pathology, University of Wisconsin, Madison 53706; (4)Department of Agronomy, University of Wisconsin, Madison 53706. Phytopathology 85:213-217. Accepted for publication 2 November 1994. Copyright 1995 The American Phytopathological Society. DOI: 10.1094/Phyto-85-213.

Leptosphaeria maculans, the causal agent of blackleg of crucifers, is a major threat to rapeseed (Brassica napus) production throughout the world. Genes controlling blackleg resistance in B. napus were mapped using an F₁-derived doubled haploid (DH) population of 105 lines and 138 restriction fragment length polymorphism (RFLP) markers. The host-pathogen interaction phenotype was assessed qualitatively and by several quantitative measurements using different environments and plant developmental stages. A single major locus controlling blackleg resistance (LEM1) was mapped to linkage group 6 based on qualitative scores of the interaction phenotype on inoculated cotyledons. This resistance locus was also identified by interval mapping using quantitative measurements of the interaction phenotype on cotyledon- and stem-inoculated plants. Four other genomic regions were significantly associated with quantitative measurements of resistance on cotyledon and stem, among them a marker locus interval in linkage group 17 that included a pathogenesis related gene (PR2). Two genomic regions associated with resistance in field-evaluated plants were different from those identified in cotyledon- and stem-evaluated plants. The use of different environments and plant developmental stages for mapping disease resistance loci is discussed.