At Least Six Avirulence Genes Are Clustered on a 90-Kilobase Plasmid in Xanthomonas campestris pv. malvacearum. Robert De Feyter. Plant Pathology Department, University of Florida, Gainesville 32611. Dean W. Gabriel. Plant Pathology Department, University of Florida, Gainesville 32611.. MPMI 4:423-432. Accepted 29 May 1991. Copyright 1991 The American Phytopathological Society.

A total genomic library of a strain of Xanthomonas campestris pv. malvacearum with multiple avirulence genes was introduced into strains of X. c. pv. malvacearum that are virulent on cotton lines containing the blight resistance genes B₂, B₄, b₆, b₇, or B_In. Fourteen cosmid clones that conferred host gene-specific avirulence on at least one of the virulent strains were isolated. Eight of the clones carried more than one avirulence activity. Restriction analyses and DNA hybridization studies showed that all of the cloned fragments overlapped, and all were derived from a 90-kb plasmid in X. c. pv. malvacearum strain H (XcmH). Subcloning experiments resulted in the separation and partial localization of four avirulence genes, designated avrB4, avrb6, avrb7, and avrBIn. These four appeared to interact in a gene-for-gene manner with the corresponding resistance genes, but these were not exclusive interactions. Subcloning also demonstrated the presence of two additional avirulence genes, designated avrB101 and avrB102, on the XcmH plasmid. All six avr genes in X. c. pv. malvacearum induced a strong hypersensitive response on cotton cultivar 101-102B (contains B,₂ B,₃ and B_Sm) and all but avrBIn in X. c. pv. malvacearum induced a weak hypersensitive response on cultivar Acala-B2. These observations represent possible exceptions to the gene-for-gene hypothesis. Genes avrb6 and avrb7 increased the ability of some X. c. pv. malvacearum strains to water soak the susceptible cultivar Acala-44. Spontaneous Avrb6‾ mutants of X. c. pv. malvacearum were reduced in water-soaking ability, suggesting a possible role of at least one of the avr genes in conditioning virulence of the pathogen on a susceptible host.