Infection of soybean plants with Soybean mosaic virus (SMV), which is transmitted by aphids and through seed, can cause significant reductions in seed production and quality. Because seedborne infections are the primary sources of inoculum for SMV infections in North America, host-plant resistance to seed transmission can limit the pool of plants that can serve as sources of inoculum. To examine the inheritance of SMV seed transmission in soybean, crosses were made between plant introductions (PIs) with high (PI88799), moderate (PI60279), and low (PI548391) rates of transmission of SMV through seed. In four F₂ populations, SMV seed transmission segregated as if conditioned by two or more genes. Consequently, a recombinant inbred line population was derived from a cross between PIs 88799 and 548391 and evaluated for segregation of SMV seed transmission, seed coat mottling, and simple sequence repeat markers. Chromosomal regions on linkage groups C1 and C2 were significantly associated with both transmission of isolate SMV 413 through seed and SMV-induced seed coat mottling, and explained ≈42.8 and 46.4% of the variability in these two traits, respectively. Chromosomal regions associated with seed transmission and seed coat mottling contained homologues of Arabidopsis genes DCL3 and RDR6, which encode enzymes involved in RNA-mediated transcriptional and posttranscriptional gene silencing.

Soybean mosaic virus (SMV) is an aphid- and seed-transmitted virus that infects soybean (Glycine max) plants and causes significant yield losses. Seed-borne infections are the primary sources of inoculum for SMV infections. The strain specificity of SMV transmission through seed and SMV-induced seed-coat mottling were investigated in field experiments. Six soybean plant introductions (PIs) were inoculated with eight SMV strains and isolates. Transmission of SMV through seed ranged from 0 to 43%, and isolate-by-soybean line interactions occurred in both transmission rates and percentages of mottled seeds. For example, SMV 746 was transmitted through 43% of seed in PI 229324, but was not transmitted through seed of PIs 68522, 68671, or 86449. In contrast, SMV 413 was transmitted through seed from all PIs. SMVs that were transmitted poorly by the Asian soybean aphid, Aphis glycines, also were transmitted poorly through seed. No predicted amino acid sequences within the helper-component protease or coat protein coding regions differentiated the two groups of SMV strains. The loss of aphid and seed transmissibility by repeated mechanical transmission suggests that constant selection pressure is needed to maintain the regions of the SMV genome controlling the two phenotypes from genetic drift and loss of function.

Transgenic soybean (Glycine max) plants expressing Soybean mosaic virus (SMV) helper component-protease (HC-Pro) showed altered vegetative and reproductive phenotypes and responses to SMV infection. When inoculated with SMV, transgenic plants expressing the lowest level of HC-Pro mRNA and those transformed with the vector alone initially showed mild SMV symptoms. Plants that accumulated the highest level of SMV HC-Pro mRNA showed very severe SMV symptoms initially, but after 2 weeks symptoms disappeared, and SMV titers were greatly reduced. Analysis of SMV RNA abundance over time with region-specific probes showed that the HC-Pro region of the SMV genome was degraded before the coat protein region. Transgenic soybean plants that expressed SMV HC-Pro showed dose-dependent alterations in unifoliate leaf morphologies and seed production where plants expressing the highest levels of HC-Pro had the most deformed leaves and the lowest seed production. Accumulation of microRNAs (miRNAs) and mRNAs putatively targeted by miRNAs was analyzed in leaves and flowers of healthy, HC-Pro-transgenic, and SMV-infected plants. Neither expression of SMV HC-Pro nor SMV infection produced greater than twofold changes in accumulation of six miRNAs. In contrast, SMV infection was associated with twofold or greater increases in the accumulation of four of seven miRNA-targeted mRNAs tested.

Soybean mosaic virus (SMV) helper component protease (HC-Pro), a suppressor of post-transcriptional gene silencing, was evaluated for its ability to enhance production of soybean hygromycin-resistant somatic embryos (HR-SEs), and stabilize transgene expression. Immature soybean cotyledonary explants were co-cultured with Agrobacterium tumefaciens strain KYRT1 harboring either pCAMBIA1302, carrying a hygromycin phosphotransferase gene (hpt) and a gene encoding green fluorescent protein; pCAMBIA1305.1, carrying hpt and β-glucuronidase (uidA) genes; pG2-HC-Pro, a derivative of pCAMBIA1305.1 containing SMV G2 HC-Pro; or pG5-HC-Pro, a derivative of pCAMBIA1305.1 containing SMV G5 HC-Pro, but lacking uidA. Significantly (ρ < 0.02) higher numbers of HR-SEs were obtained from explants transformed with Agrobacterium harboring either pG2-HC-Pro or pG5-HC-Pro than with either of the vector controls (pCAMBIA1302 or pCAMBIA1305.1). β-glucuronidase (GUS) expression was significantly (P < 0.003) higher in 50-day-old transgenic plants expressing GUS along with SMV-HC-Pro and in SMV-infected GUS transgenic plants than in transgenic plants expressing GUS alone. Together, these data suggest that SMV-HC-Pro enhanced recovery of HR-SEs by suppressing silencing of the hygromycin phosphotransferase gene.

Fifty-two North American (NA) ancestral soybean [Glycine max (L.) Merr.] lines were screened for resistance to Bean pod mottle virus (BPMV), Soybean mosaic virus (SMV) strains G1 and G5, Tobacco ringspot virus (TRSV), and Tobacco streak virus (TSV). Seven ancestors, ‘CNS’, ‘Haberlandt’, ‘Ogden’, ‘Peking’, PI 71506, PI 88788, and ‘Tokyo’, were resistant to SMV-G1. Sixteen entries, ‘A.K. (Harrow)’, ‘Capital’, CNS, FC 33243, Haberlandt, ‘Illini’, ‘Improved Pelican’, ‘Laredo’, ‘Lincoln’, ‘Mandarin’, ‘Mandarin (Ottawa)’, Ogden, ‘Palmetto’, Peking, PI 88788, and Tokyo were resistant to SMV-G5. All ancestral lines tested were susceptible to BPMV and TRSV. Only one ancestor, ‘Tanner’, was resistant to TSV. On the basis of cultivar registration articles through 2002, there were 15 public soybean cultivars with reported resistance to SMV. The possible donors of resistance for each were identified. Two soybean ancestors, CNS and Ogden, were the most important possible sources of SMV resistance genes in U.S. commercial soybean cultivars, as the pedigree of 75 and 56% of the reported resistant cultivars contained CNS and Ogden, respectively. In most of the cultivar registration articles, reactions to SMV were not reported. With the relatively high frequency of SMV resistance in major ancestral lines, SMV resistance in U.S. cultivars may be more common than expected.

Soybean mosaic virus (SMV) is one of the most common soybean viruses worldwide. The resistance or susceptibility of most commercial soybean cultivars to SMV is not known. The objectives of this study were to evaluate resistance to SMV strains G1 and G5 of current soybean cultivars, isogenic lines with different Rsv genes and alleles in ‘Williams’ or ‘Williams 82’ background, and selected soybean lines with reported or observed SMV resistance. Commercial and precommercial soybean cultivars were screened for resistance to SMV strains G1 and G5. Based on multiple tests, 1.5% and 6.7% of the 850 cultivars were resistant to SMV-G1 and SMV-G5, respectively. No cultivars were resistant to both strains. Expression of different SMV resistance genes in Williams isogenic lines inoculated with both SMV strains indicated that lines with Rsv1-y from ‘Dorman’, or unnamed resistance genes from ‘Kosamame’, and ‘Sodendaizu’, were resistant to G1 and susceptible to G5. Lines with Rsv1 alleles from PI 96983, ‘Marshall’, or ‘Ogden’ were resistant to both strains, and lines with Rsv1 alleles from ‘Raiden’, ‘SS 74185’ (PI486355), or ‘Suweon 97’ were resistant to G1 and produced a systemic necrosis reaction with G5. Lines with Rsv3-h from ‘Hardee’ were susceptible to G1 and resistant to G5. Isogenic lines with SMV resistance genes from ‘Buffalo’ showed either a resistant–resistant or resistant–susceptible reaction to the two SMV strains, suggesting the presence of more than one SMV resistance gene. Ten selected lines with reported or observed resistance to SMV were inoculated with the two SMV strains. Some lines were resistant to either G1 or G5, and some were resistant to both strains.