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
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
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.