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Clubroot Resistance and Linkage in Brassica campestris. R. V. James, Former graduate research assistant, Department of Plant Pathology, University of Wisconsin, Madison 53706, Present address of senior author: Department of Plant Pathology, Cornell University, Ithaca, NY 14853; P. H. Williams, professor, Department of Plant Pathology, University of Wisconsin, Madison 53706. Phytopathology 70:776-779. Accepted for publication 24 February 1980. Copyright 1980 The American Phytopathological Society. DOI: 10.1094/Phyto-70-776.

The genetics of resistance in Brassica campestris to Plasmodiophora brassicae race 6 (defined with the Williams differential set) and possible linkage of genes for resistance with genes controlling phenotypic markers were investigated with rapidly flowering stocks. Two B. campestris members of the European Clubroot Differential (ECD) host series and stocks derived from B. campestris ssp. pekinensis ‘Michihili’ were sources of clubroot resistance genes. The resistant reaction in Michihili stocks was due to a single dominant gene, designated Pb1. The resistant reaction in ECD stocks was due to more than one independent dominant gene in each stock. The two single dominant genes Pb2 and Pb3 were identified from ECD 02 and 03, respectively. Pb1, Pb2, and Pb3 were unlinked. Four recessive marker genes were not closely linked with any of the three genes for resistance although loose linkage may occur between PB3 and pk1, and Pb2 and ro.