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Inheritance of resistance to potyviruses in Phaseolus vulgaris L. II. Linkage relations and utility of a dominant gene for lethal systemic necrosis to soybean mosaic virus

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Summary

A single dominant factor, Hss, that conditions a rapid lethal necrotic response to soybean mosaic virus (SMV) has been identified in Phaseolus vulgaris L. cv. ‘Black Turtle Soup’, line BT-1. Inoculated plants carrying this factor developed pinpoint necrotic lesions on inoculated tissue followed by systemic vascular necrosis and plant death within about 7 days, regardless of ambient temperature. BT-1 also carries dominant resistance to potyviruses attributed to the tightly linked or identical factors, I, Bcm, Cam, and Hsw, so linkage with Hss was evaluated. No recombinants were identified among 381 F3 families segregating for potyvirus susceptibility, thus if Hss is a distinct factor, it is tightly linked to I, Bcm, Cam, and Hsw. BT-1 was also crossed reciprocally with the line ‘Great Northern 1140’ (‘GN 1140’) in which the dominant gene, Smv, for systemic resistance to SMV was first identified. Smv and Hss segregated independently and are co-dominant. The (‘GN 1140’ x BT-1) F1 populations showed a seasonal shift of the codominant phenotype. Evaluation of the (‘GN 1140’ x BT-1) F2 population under conditions where Smv is partially dominant allowed additional phenotypic classes to be distinguished. Pathotype specificity has not been demonstrated for either Smv or Hss. Genotypes that are homozygous for both dominant alleles are systemically resistant to the virus and in addition show undetectable local viral replication or and no seed transmission. This work demonstrates that a gene which conditions a systemic lethal response to a pathogen may be combined with additional gene(s) to create an improved resistant phenotype.

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Communicated by G. S. Khush

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Kyle1, M.M., Provvidenti, R. Inheritance of resistance to potyviruses in Phaseolus vulgaris L. II. Linkage relations and utility of a dominant gene for lethal systemic necrosis to soybean mosaic virus. Theoret. Appl. Genetics 86, 189–196 (1993). https://doi.org/10.1007/BF00222078

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