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- Author or Editor: R.O. Hampton x
Cowpea cultivars Early Ramshorn and Dixie Queen, reported to be resistant to cucumber mosaic virus (CMV) by Sinclair and Walker in 1955, were reexamined for the existence of individual CMV-resistant genotypes within seedling populations. CMV-inoculated populations of these two cultivars became CMV-infected at rates of 60% and 80%, respectively, as determined by DAS-ELISA. CMV-free plants were grown to maturity, seeds from these sources were planted, and second-generation seedlings were inoculated again with CMV. Rates at which these seedlings became CMV-infected were 10% and 24%, respectively. The complementary 90% and 76% of these populations remained completely free of ELISA-detectable CMV and were saved to maturity. Evaluations of third-generation populations are being performed. Twenty additional cultivars and breeding lines also are being evaluated. Seedlings of 14 of the 22 cultivars/lines became 95% to 100% infected when inoculated with CMV. Results from eight of the 22 suggested that seedling populations contain CMV-susceptible and -resistant plants. Near isogeneic sublines of susceptible and resistant plants per cultivar/line are being conveyed to cowpea breeders for genetic analyses and breeding purposes.
Resistance to white lupin mosaic virus (WLMV), a recently characterized member of the potyvirus group, was found in pea (Pisum sativum L.) plant introductions from Ethiopia (PI 193835) and India (PI 347485). In cross and backcross populations between plants of resistant PI 193835 with those of susceptible `Bonneville' and PP-492-5, this resistance was demonstrated to be governed by a single recessive gene. This gene was distinct from other genes previously found in PI 193835 and PP-492-5 (from PI 347492, India) conferring resistance to clover yellow vein virus (CYVV) and three strains of pea seedborne mosaic virus (PSbMV). Indirect evidence suggests that this newly recognized viral resistance gene, wlv, is a member of a cluster of closely linked genes located on chromosome 6. This gene cluster includes sbm-1, sbm-3, and sbm-4, which govern resistance to three PSbMV pathotypes, and cyv-2, which governs resistance to CYVV.
The inheritance of tolerance to infection by bean leaf roll luteovirus (BLRV) in Pisum sativum L. was studied in the cross of cv. Parlay (sensitive to BLRV infection) × cv. Oregon Sugarpod II (BLRV tolerant). The parents, reciprocal F1, back-crosses, F2, and 234 random F3 families were screened in 1986 and 1987 in the field at Twin Falls, Idaho, under natural BLRV inoculation by aphids. Overall disease index scores for the F1, F2, and F3 were about intermediate between indices of the parents, with the F1 usually slightly higher than midparent values. Backcross disease indices were intermediate between the F1 and the respective parent involved. Distribution of individual F3 family indices was continuous and semi-normal. BLRV-sensitivity ranges within parents and selected cultivars, as well as segregating populations showed continuous variation and differed between the 2 years, suggesting that expression of a major gene was significantly influenced by natural variation in BLRV inoculation pressure and timing. An apparent “additive gene action” was probably an artifact of nonuniform timing and levels of infection within plant populations. Chi-square analyses of segregating populations indicated that a major recessive gene, called lrv, conferred BLR disease tolerance.
Pea seedborne mosaic virus (PSbMV) is of concern to breeders and seedsmen, especially in the Pacific Northwest where most of the pea (Pisum sativum L.) seed used in the U.S. is produced (4). Resistance to PSbMV is the best means to remove the threat of seed stock contamination and reduce the need for costly and restrictive assay programs and quarantines.
Commercial pea (Pisum sativum L.) cultivars, plant introduction (PI) lines, and Oregon State Univ. (OSU) breeding lines were tested for resistance to pathotype P2 (lentil strain) and pathotype P1 (type strain) of pea seedborne mosaic virus (PSbMV) and to bean yellow mosaic virus (BYMV) to assess the relative proportion of resistant and susceptible pea genotypes. Of the 161 commercial cultivars tested, 117 (73%) were resistant and 44 were susceptible to PSbMV-P2. Of these PSbMV-P2-resistant cultivars, 115 were tested for resistance to BYMV and all were resistant. Of the 44 PSbMV-P2-susceptible cultivars, 43 were tested for BYMV susceptibility and all were infected except two, `Quincy' and `Avon', both of which were susceptible to a BYMV isolate in another laboratory. Of 138 commercial cultivars inoculated with PSbMV-P1, all were susceptible. All PI lines and OSU breeding lines that were resistant to PSbMV-P1 were resistant also to PSbMV-P2. The high percentage of commercial cultivars resistant to PSbMV-P2 was probably attributable to the close linkage of genes sbm-2 and mo and the widespread use by breeders of BYMV-resistant `Perfection' and `Dark Skin Perfection' in developing new pea cultivars. Segregation ratios in progenies of three separate crosses between PSbMV-P2-resistant and PSbMV-P2-susceptible cultivars closely fit the expected 3 susceptible: 1 resistant ratio expected for resistance conferred by a single recessive gene.
The inheritance of resistance in beans (Phaseolus vulgaris L.) to typical bean yellow mosaic virus (BYMV) was compared to the severe strain (BYMV-S). When F3 families of BYMV resistant ‘Great Northern UI 31’ (GN31) × susceptible ‘Dwarf Horticultural’ were tested for resistance to each virus strain, occurrence of homozygous resistant families was conditioned by 3 recessive genes for BYMV and 2 recessive genes for BYMV-S. Of the 132 families tested, 122 were susceptible to both BYMV and BYMV-S, 6 were resistant to BYMV-S and susceptible to BYMV, 4 were susceptible to BYMV-S and resistant to BYMV, and none were resistant to both. This ratio closely fits a theoretical 945:63:15:1, indicating that resistance to BYMV and to BYMV-S are inheritied independently. When GN31 was crossed with breeding line Sl-5, also resistant to both virus strains, F3 progenies included families susceptible to one or both virus strains, possibly through the complimentary interaction of modifiers. Chi square tests indicated independent inheritance of resistances to BYMV and BYMV-S in GN31 × S1-5 progenies.
Pea cultivars may be severely or mildly affected (susceptible), or completely symptomless (resistant) when infected with an Oregon isolate of PSV. Infected plants of susceptible and resistant cultivars contained substantial virus concentrations which were not consistently related to symptom severity. The severity of symptoms in inoculated plants and the numbers of plants showing symptoms differed in various tests, apparently in response to changes in environment and the virulence of the virus. When apparent maximum symptom expression occurred, it was shown that the highest degree of resistance was due to a single recessive gene. Deviations from the expected ratio of 3 susceptible: 1 resistant (symptomless) were always the result of excess symptomless plants, probably because of combinations of effects of the environment, modifying genes from one or both parents, and in the later phases of the study, a reduced virus virulence. Observations and limited tests suggested that symptom development was promoted by conditions which were unfavorable for optimum plant growth.