INHERITANCE OF RESISTANCE TO POTYVIRUSES IN PHASEOLUS-VULGARIS L .2. LINKAGE RELATIONS AND UTILITY OF A DOMINANT GENE FOR LETHAL SYSTEMIC NECROSIS TO SOYBEAN MOSAIC-VIRUS

Citation
Mm. Kyle et R. Provvidenti, INHERITANCE OF RESISTANCE TO POTYVIRUSES IN PHASEOLUS-VULGARIS L .2. LINKAGE RELATIONS AND UTILITY OF A DOMINANT GENE FOR LETHAL SYSTEMIC NECROSIS TO SOYBEAN MOSAIC-VIRUS, Theoretical and Applied Genetics, 86(2-3), 1993, pp. 189-196
Citations number
39
Categorie Soggetti
Genetics & Heredity
ISSN journal
00405752
Volume
86
Issue
2-3
Year of publication
1993
Pages
189 - 196
Database
ISI
SICI code
0040-5752(1993)86:2-3<189:IORTPI>2.0.ZU;2-Y
Abstract
A single dominant factor, Hss, that conditions a rapid lethal necrotic response to soybean mosaic virus (SMV) has been identified in Phaseol us vulgaris L. cv. 'Black Turtle Soup', line BT-1. Inoculated plants c arrying this factor developed pinpoint necrotic lesions on inoculated tissue followed by systemic vascular necrosis and plant death within a bout 7 days, regardless of ambient temperature. BT-1 also carries domi nant resistance to potyviruses attributed to the tightly linked or ide ntical factors, I, Bcm, Cam, and Hsw, so linkage with Hss was evaluate d. No recombinants were identified among 381 F3 families segregating f or potyvirus susceptibility, thus if Hss is a distinct factor, it is t ightly linked to I, Bcm, Cam, and Hsw. BT-1 was also crossed reciproca lly with the line 'Great Northern 1140' ('GN 1140') in which the domin ant gene, Smv, for systemic resistance to SMV was first identified. Sm v and Hss segregated independently and are co-dominant. The ('GN 1140' x BT-1) F1 populations showed a seasonal shift of the codominant phen otype. Evaluation of the ('GN 1140' x BT-1) F2 population under condit ions where Smv is partially dominant allowed additional phenotypic cla sses to be distinguished. Pathotype specificity has not been demonstra ted for either Smv or Hss. Genotypes that are homozygous for both domi nant alleles are systemically resistant to the virus and in addition s how 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 crea te an improved resistant phenotype.