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Variation among strains of Xanthomonas campestris pv. campestris, the causal organism of black rot of crucifers, was studied. The relationship between symptoms associated with selected strains, their epidemiological fitness in misted seedbeds, the presence of a gene associated with severe symptoms in these strains, and a pathovar-specific surface antigen was examined. Strains with blight induction capacity spread more rapidly in misted seedbeds. These blight strains all hybridized with a 5.4-kb DNA fragment isolated from the type strain of X. c. campestris (Xcc528T ). This fragment in pJC41 was previously reported to confer blight symptom induction in cabbage when mobilized to a closely related leaf spot pathogen X. c. armoraciae. The relationship between this 5.4-kb DNA fragment and blight symptom induction was studied by marker-exchange mutagenesis of Xcc528T at the pJC41 region. Loss of the fragment did not destroy the systemicity and blight induction capability of the wild type. However, in pathogenicity studies strains of X. c. campestris that hybridized with pJC41 generally caused strong blight in cabbage. Thus, it is likely that other gene(s) with similar functions exist on the genome. A positive reaction to the monoclonal antibody (MAb) All was associated with strains that produced blight. The hypothesis that the antigen reactivity with this MAb plays a role in blight induction was tested by mutagenizing a blight strain of X. c. campestris (CAMI9) at a gene locus that is necessary for the production of this antigen. Although the two A11-negative mutants (NTG901 and NTG2230) which were obtained were avirulent or had reduced virulence, the restoration of antigenicity by complementation did not result in simultaneous restoration of virulence. Thus, although the antigen for MAb All is a useful marker associated with blight-causing strains, it does not play a role in blight symptom induction or pathogenicity. In summary, blight strains of X. c. campestris are distinct from the more typical black rot strains in symptom induction and epidemiological capability. They usually, but not always, hybridize with pJC41 and react with MAb A11. It is suspected that blight induction is controlled by multiple genes.