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Crop Science 41:1785-1791 (2001)
© 2001 Crop Science Society of America

CROP BREEDING, GENETICS & CYTOLOGY

Genetic Analysis of Resistance to Soybean mosaic virus in OX670 and Harosoy Soybean

I. Gunduza, G. R. Buss*,a, G. Mac, P. Chena and S. A. Tolinb

a Department of Crop and Soil Environmental Sciences, Virginia Polytechnic Institute and State Univ., Blacksburg, VA 24061-0404
b Department of Plant Pathology, Physiology, and Weed Sciences, Virginia Polytechnic Institute and State Univ., Blacksburg, VA 24061-0404
c Medtronic Sofamor Danek, 1800 Pyramid Place, Memphis, TN 38132

* Corresponding author (gbuss{at}vt.edu)


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
Soybean mosaic virus (SMV) resistance in the soybean [Glycine max (L.) Merr.] breeding line OX670 previously was postulated to be controlled by a gene derived from the cultivar Raiden and designated as Rsv2. Subsequently, it was shown that Raiden has a single resistance gene at the Rsv1 locus, suggesting that the resistance gene in OX670 was not from Raiden. Most of the remaining ancestry of OX670 is derived from ‘Harosoy’. The objectives of this study were to determine (i) the reaction of Harosoy to SMV-G1 through G7 strains; (ii) the inheritance of SMV resistance in Harosoy and OX670; and (iii) the allelomorphic relationship of resistance genes in these cultivars with previously described resistance genes. OX670 and Harosoy were crossed with the SMV susceptible cultivar Lee 68 to study the inheritance of resistance. OX670 and Harosoy were also crossed with the resistant lines L78-379, L88-8431, PI96983, L29, and V94-5152 to elucidate the allelomorphic relationships between the genes in OX670, Harosoy, and previously reported genes. Our results indicated that Harosoy, which is resistant to SMV-G5 through G7 and susceptible to SMV-G1 through G4, possesses a single partially dominant SMV resistance gene at the Rsv3 locus. Inheritance studies indicated that OX670, which is resistant to SMV-G1 through G7, possesses two independent dominant genes for SMV resistance. One is allelic to the Rsv1 locus and derived from Raiden, while the other is allelic to the Rsv3 locus and derived from Harosoy. Presence of both Rsv1 and Rsv3 in OX670 confers resistance to SMV-G1 through G7. Therefore, the previously proposed Rsv2 locus does not appear to exist in OX670 or its ancestors.

Abbreviations: SMV, soybean mosaic virus • DAI, days after inoculation • R, resistant • N, necrotic • S, susceptible • ELISA, enzyme-linked immunoabsorbent assay


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
THREE INDEPENDENT GENE SYMBOLS, Rsv1, Rsv2, and Rsv3 conferring resistance in soybean [Glycine max (L.) Merr.] to Soybean mosaic virus (SMV) have been assigned. A single dominant gene for SMV resistance in PI96983 was identified and designated as Rsv (later renamed Rsv1) (Kiihl and Hartwig, 1979; Chen et al., 1991). The single resistance genes in ‘Ogden’, ‘York’, ‘Marshall’, and ‘Kwangyo’ were also found to be alleles at the Rsv1 locus and were assigned the gene symbols, Rsv1-t, Rsv1-y, Rsv1-m, and Rsv1-k, respectively (Chen et al., 1991). PI486355 was found to contain two genes for SMV resistance, one of which is at the Rsv1 locus and was designated Rsv1-s (Chen et al., 1993; Ma et al., 1995). These six Rsv1 alleles confer differential reaction to SMV strains G1 through G7 as defined by Cho and Goodman (1979)(1982). The Rsv1 locus maps to linkage group F and has been associated with flanking closely linked markers (Yu et al., 1994).

The gene symbol Rsv2 was assigned to a gene in OX670. Since Raiden was the only parent in the pedigree with known SMV resistance, it was assumed to be the source of resistance in OX670 (Fig. 1) (Buzzell and Tu, 1984). The Rsv3 gene derived from ‘Columbia’ conditions systemic necrosis to SMV-G1 (Buzzell and Tu, 1989). Another Rsv3 allele from ‘Hardee’ confers susceptibility to SMV strains G1 through G4, but resistance to strains G5 through G7 (Buss et al., 1999).



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  		Fig. 1. The pedigree of the soybean line OX670 and ancestral reactions to SMV strains. R, resistant; S, susceptible.

 
As previously mentioned PI486355 possesses two independent resistance genes, one of which is at the Rsv1 locus. The other resistance gene (non-Rsv1) was isolated in the soybean line LR2 and found to be independent of Rsv1 and Rsv3 (Ma et al., 1995). LR2 was a selection from PI486355 x ‘Essex’. V94-5152 is a reselection from LR2 that was registered as resistant germplasm (Buss et al., 1997). Due to the lack of an allelism test with an Rsv2 source, a gene symbol has not been assigned to the non-Rsv1 gene in V94-5152. However, it will be referred to as Rsv4 for reference purposes in this paper.

Buzzell and Tu's (1984) conclusion that OX670 contains Rsv2 was based on the segregation pattern obtained in an F2 population of OX670 (R) x L78-379 (S). Although, they described L78-379 as necrotic to G7, they classified it as susceptible and did not report N and S plants in segregating populations separately. "S" will be used in the remainder of this paper to refer to their data in which N and S plants were combined. The F2 population inoculated with SMV-G7 segregated 3R:1"S", indicating that OX670 possesses a single dominant gene. The F2 population of the same cross OX670 (R) x L78-379 (R, Rsv1) inoculated with the SMV-G6 strain fit a 15R:1"S" segregation ratio indicating that the gene in OX670 is independent of the Rsv1 locus. Therefore, the gene symbol Rsv2 was assigned to the resistance gene in OX670. However, it was later shown that Raiden possesses a single SMV resistance gene at the Rsv1 locus (Chen et al., 2001; Wang et al., 1998). These contradictory results suggest that Rsv2, if present in OX670, was not from Raiden.

A pedigree analysis of OX670 reveals that, except for Raiden, Harosoy or its derivatives were the primary ancestors of OX670 (Fig. 1). Buzzell and Tu (1984) postulated that Harosoy was susceptible, based on its reaction to SMV-G1. Raiden is resistant to SMV-G1 through G4 and G7 and necrotic to SMV-G5 and G6 (Chen et al., 2001). However, OX670 exhibits resistant reactions to SMV-G1 through G7 (Buzzell and Tu, 1984). The inconsistency in the reaction of OX670 and Raiden infer that either the resistance gene in OX670 is not from Raiden or there could be another gene in OX670, possibly from Harosoy, which complements the Raiden gene. The objectives of this study were to determine (i) the reaction of Harosoy to SMV-G1 through G7 strains; (ii) the inheritance of SMV resistance in Harosoy and OX670; and (iii) the allelomorphic relationship of resistance genes in these cultivars with previously described resistance genes.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 REFERENCES
 
OX670 and Harosoy were crossed with the SMV susceptible cultivar, Lee 68, to study the inheritance of resistance. They were also crossed with resistant lines L29 and V94-5152 which contain Rsv3, and Rsv4, respectively, to study the allelomorphic relationships between the resistance genes in OX670, Harosoy, and previously identified genes. L29 is a ‘Williams’ isoline with SMV resistance gene Rsv3 derived from Hardee (Buss et al., 1999). Harosoy was crossed with L78-379 and OX670 was crossed with PI96983 and L88-8431 to study the allelomorphic relationship of resistance genes in OX670 and Harosoy with Rsv1. L78-379 and L88-8431 are Williams isolines with SMV resistance gene Rsv1 derived from PI96983 and Raiden, respectively (Chen et al., 1991, 2001). PI96983 and L78-379 were used interchangeably in this study since they exhibit identical reactions to the SMV strains and have been shown to be genetically equivalent in previous studies (Chen et al., 1991). Pedigree information of OX670 was obtained from Buzzell and Tu (1984) and the National Plant Germplasm System web page (http://www.ars-grin.gov/npgs/).

F1 plants were grown either in the greenhouse or in the field without SMV inoculation at Blacksburg, VA, and harvested individually. F2 plants were grown in the field without virus inoculation either at Blacksburg or Warsaw, VA, and individually harvested. Crosses were distinguished from selfs in the F1 and F2 generations using leaf shape, flower color, pubescence color, and maturity as morphological markers.

Remnant F2 seeds and F2 populations were tested with SMV-G1 in the greenhouse and F2:3 progeny were tested in the greenhouse and field. SMV-G6 and G7 inoculations were conducted only in the greenhouse at Blacksburg. F1 plants and F2 populations were tested with the proper strain in the greenhouse at the same time. An average of five F1 plants, 200 F2 plants, and 50 F2:3 families from each cross were inoculated. Approximately 20 plants were tested in each F2:3 family. Individual plant reactions were examined about 10, 20, 30, and 40 d after inoculation and classified into three distinct groups: resistant (R) (symptomless or local necrotic lesions on inoculated leaves), susceptible (S) (typical mosaic) (Fig. 2) and necrotic (N) (stem tip necrosis that develops into necrotic lesions 3 to 5 mm in diameter on inoculated leaves 5 to 7 d after inoculation and spreads into veins, which frequently results in plant death 10 to 15 d after inoculation) (Fig. 3) .



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  		Fig. 2. Mosaic symptoms of Soybean mosaic virus (SMV) on soybean cultivar Lee 68 17 d after inoculation with SMV-G1.

 


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  		Fig. 3. Necrotic reaction on soybean genotype PI96983, when inoculated with Soybean mosaic virus G7 in the greenhouse 12 d after inoculation.

 
All parents used in this study were tested with SMV-G1 through G7 in the greenhouse to compare their differential reactions (Table 1). The SMV-G1 strain used in this study was originally isolated from ‘Lee’ soybean in Virginia (Hunst and Tolin, 1982) and is analogous to the SMV-G1 of Cho and Goodman (1979)( 1982). Strains SMV-G2 through G7 were originally obtained from Dr. R.M. Goodman in 1984, at the University of Illinois. Cultures of SMV-G1 and SMV-G7 have been deposited as PV-571 and PV-613, respectively, in the American Type Culture Collection (10801 University Boulevard, Manassas, VA 20110-2209, USA). The SMV-G1 through G4 cultures were maintained by continuous passage in Lee 68, while SMV-G5 through G7 were maintained on York.


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  		Table 1. Disease reaction of a set of soybean differential genotypes and cultivars to seven Soybean mosaic virus strain groups.

 
For the greenhouse tests, inocula were prepared from infected trifoliolate leaf tissue homogenized in 0.01 M sodium phosphate buffer solution, pH 7.0, at an approximate rate of 1 g infected tissue per 10 ml buffer. Unifoliolate leaves were inoculated, approximately 10 d after planting at the V1 stage (Fehr and Caviness, 1977). A small amount of 600-mesh carborundum was dusted on the leaves to be inoculated. Both leaves of each plant were rubbed with a pestle dipped in the inoculum. Inoculated leaves were rinsed with tap water. The differential soybean cultivars, York, PI96983, L29, and V94-5152, as well as parents, were included in each set of inoculations to confirm the identity and purity of the strain used. A daylength of approximately 14 h was maintained by using both fluorescent and incandescent supplemental lighting during winter months. Greenhouse temperatures were maintained at 24 to 30°C during daylight hours and 15 to 20°C at night.

The procedure and inoculum preparation used for field inoculation is described by Roane et al. (1983). Inoculum was applied to the underside of a single leaflet per plant by using an artist's air brush. All plants with questionable symptoms, as well as 10 to 20 randomly selected susceptible, symptomless, and necrotic plants from each population were tested to confirm the presence or absence of SMV by dot blot enzyme-linked immunoabsorbent assays (ELISA) (Srinivasan and Tolin, 1992). Symptomless plants that were negative for SMV were classified as resistant. Chi-square tests were performed to determine the goodness-of-fit of observed segregations to expected genetic ratios.


   RESULTS AND DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
REFERENCES
 
All parents and differentials, included in all the inoculations, exhibited reactions in agreement with previous reports (Table 1). Dot blot ELISA results indicated that all sampled susceptible plants were positive for SMV (virus present) and symptomless plants were negative (virus absent). Necrotic plants were strongly positive for SMV if samples were taken in the early stage (7 to 10 d after inoculation) but were only weakly positive in live tissue after that point.

Inheritance and Allelomorphic Relationships of Resistance Gene/Genes in Harosoy
Buzzell and Tu (1984) considered Harosoy to be a susceptible cultivar, probably based on its reaction to SMV-G1. Our results indicate that Harosoy is also susceptible to SMV-G2 through G4, but is resistant to SMV-G5 through G7 (Table 1). F1 plants of Harosoy (R) x Lee 68 (S) exhibited a lethal necrotic reaction to SMV-G7 at 15 to 20 d after inoculation, indicating that the resistance gene in Harosoy was incompletely dominant (Table 2). The segregating F2 population of Harosoy (R) x Lee 68 (S) fit a 1R:2N:1S single gene ratio when the population was inoculated with SMV-G7. Thus, it appears that a single resistance gene is segregating, with the homozygous resistant and heterozygous genotypes being expressed as resistant and necrotic, respectively. The same population was completely susceptible to SMV-G1 strain, verifying the susceptibility of Harosoy to that strain. F2:3 families of the same cross segregated to fit a 1 (all R): 2 [3(R+N):1S]: 1 (all S) genotypic ratio, which verified that Harosoy indeed has a single gene for resistance to SMV-G7 (Table 3).


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  		Table 2. Reaction of F1 plants and F2 populations from crosses between Harosoy, OX670, and susceptible or resistant soybean genotypes, when inoculated with Soybean mosaic virus G1 and G7 in the greenhouse.

 

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  		Table 3. Segregation of F2:3 soybean families when inoculated with Soybean mosaic virus G7 in the greenhouse and G1 in the field.

 
No susceptible plants were observed in the F2 populations and F2:3 families of Harosoy x L29 when inoculated with SMV-G7 (Tables 2 and 3) indicating that the gene in Harosoy is allelic to the gene at the Rsv3 locus. The F2 population of L78-379 (N) x Harosoy (R) inoculated with SMV-G7 fit a digenic ratio of 12R:3N:1S (Table 2). The F2:3 families of the same cross segregated 4 (all R): 2 (3R:1S): 2(3R:1N): 2(3N:1S): 4(12R:3N:1S): 1 (all N): 1 (all S) (Table 4), indicating that the SMV resistance gene in Harosoy is independent of the SMV resistance gene, Rsv1, in L78-379.


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  		Table 4. Segregation of F2:3 soybean families from L78-379 (Rsv1) x Harosoy when inoculated with Soybean mosaic virus G7 in the greenhouse.

 
Segregation in the F2 population of Harosoy (R) x V94-5152 (R) conformed to a 15 (R+N): 1S digenic ratio when tested with SMV-G7 (Table 2). This result was confirmed by the observed 7 (all R): 4[3(R+N):1S]: 4[15(R+N):1S]: 1 (all S) segregation pattern in the F2:3 families (Table 5), and verifies that the single dominant gene in Harosoy is independent of the Rsv4 locus of V94-5152.


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  		Table 5. Segregation of F2:3 families derived from crosses of Harosoy and OX670 with susceptible and resistant soybean genotypes.

 
Inheritance of Resistance to SMV Strains G1 and G7 in OX67O
OX670 exhibits resistant reactions to SMV-G1 through G7 (Table 1). F1 plants from OX670 x Lee 68 were symptomless when inoculated with SMV-G7, and necrotic when inoculated with SMV-G1 (Table 2). Therefore, one of the genes in OX670 confers a necrotic reaction to SMV-G1 in the heterozygous condition. Because of the reaction of the F1 plants to SMV-G1, necrotic (heterozygous resistant) plants were grouped in the resistant class for genetic tests. The association between heterozygosity and necrosis were reported by other investigators, and necrotic plants were combined with the resistant plants for genetic analysis (Kiihl and Hartwig, 1979; Shigemori, 1988; Buss et al., 1989; Bowers et al., 1992; Chen et al., 1991, 1994; Ma et al., 1995). The segregating F2 population from OX670 (R) x Lee 68 (S) fit the single gene ratio of 3(R+N):1S when inoculated with SMV-G1 (Table 2). However, a fit to the digenic ratio of 15(R+N):1S was observed when SMV-G7 was used (Table 2). These results indicate that OX670 has two genes. One is resistant to SMV-G1 and G7, and the other gene is also resistant to SMV-G7 but susceptible to SMV-G1. The overall segregation of the F2:3 families from OX670 (R) x Lee 68 (S) conformed to the 1 (all R): 2 [3(R+N):1S]:1 (all S) ratio expected with SMV-G1 (Table 3) and fit a 7 (all R):4[15(R+N):1S]:4[(3R+N):1S]:1 (all S) ratio when SMV-G7 was used (Table 5). These data verify the presence of two genes in OX670 for SMV resistance.

Although F1 heterozygotes are frequently necrotic, the frequency of necrotic plants in the F2 population and F2:3 families (1% of the total plants) was well below that expected for heterozygotes (Table 2). No homogenous necrotic F2:3 lines were observed, indicating that the necrotic reaction was not expressed by a homozygous genotype. Many investigators have reported the association between heterozygosity and necrotic reaction but still it is not clear why all heterozygous plants in F2 and F2:3 populations do not show the necrotic reaction.

Allelic Relationship of the Resistance Genes in OX670 with Rsv1
No susceptible plants were found in the F2 and F2:3 populations of the cross between PI96983 (Rsv1) and OX670, when inoculated with SMV-G1, G6, and G7 (Tables 2, 3, 6, and 7). The lack of susceptible plants indicates that one of the genes in OX670 is an allele at the Rsv1 locus.


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  		Table 6. Segregation of F2:3 soybean families from PI96983 x OX670 inoculated with Soybean mosaic virus G6 in the greenhouse.

 

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  		Table 7. Segregation of F2:3 soybean families from PI96983 x OX670 inoculated with Soybean mosaic virus G7 in the greenhouse.

 
Necrotic plants were observed in a 15(R):1(N) ratio in the F2 of PI96983 (R) x OX670 (R) inoculated with SMV-G1 (Table 2). Of seventy F2:3 families, eight segregated for the necrotic reaction (Table 3). However, each family had only one or two necrotic plants and no homogeneous necrotic F2:3 families, suggesting that the necrotic plants observed in this population did not appear to represent genetic segregation. Necrotic plants previously have been reported in R(Rsv1) x R (Rsv1) crosses and were assumed not to be the result of genetic segregation (Chen et al., 1994; Ma, 1995).

The F2 population from PI96983 (N) x OX670 (R) inoculated with SMV-G7 segregated to fit a 13(R):3(N) ratio (Table 2), and F2:3 families segregated 7 (all R):2(3R:1N):2(3N:1R): 4(15R:1N):1 (all N) (Table 7), indicating digenic segregation. In contrast, Buzzell and Tu (1984) obtained a 3(R):1"S" monogenic ratio from the F2 population of L78-379("S") x OX670(R) using SMV-G7. The 3:1 ratio is statistically close to the 13(R):3(N), that we obtained from the F2 of PI96983(N) x OX670 (R) (Table 2). But since L78-379 is necrotic to SMV-G7, it is likely that most, if not all, of the "S" plants observed by Buzzell and Tu (1984) were actually necrotic. This hypothesis is supported by the fact that no susceptible plants were found in the segregating populations of PI96983 x OX670 inoculated with SMV-G7 in the present study (Tables 2 and 7).

Segregation of the F2 population of PI96983 (R) x OX670 (R) inoculated with SMV-G6 fits a 15(R):1(N) ratio (Table 2), which supports digenic segregation. Segregating F2:3 families of the same cross fit a 7 (all R):4(3R:1N):4(15R:1N):1 (all N) genotypic ratio (Table 6). Obviously, one of the SMV resistance genes in OX670 produces a necrotic reaction to SMV-G6 in the homozygous condition since homogeneous necrotic F2:3 families were observed. The pedigree of OX670 (Fig. 1) shows that Raiden and Harosoy are possible sources of SMV resistance genes in OX670. Harosoy is resistant to SMV-G6 and possesses an SMV resistance gene at the Rsv3 locus, which does not exhibit necrosis to SMV-G6 (Gunduz et al., 1999). Raiden, however, is necrotic to SMV-G6 and contains an SMV resistance gene at the Rsv1 locus (Buss et al., 1995). Thus, it is logical to assume that the Rsv1 gene in OX670, derived from Raiden, was the source of the necrotic reaction observed in the segregating populations of PI96983(R) x OX670(R) since the Rsv1 allele in PI96983 is resistant to SMV-G6. Moreover, Rsv1 alleles in Raiden and OX670 exhibit identical reactions to SMV-G1 and G7. Raiden exhibits the resistant reaction to SMV-G1 and G7 (Chen et al., 2001). PI96983 x OX670 F2 populations and F2:3 families did not segregate when inoculated with SMV-G1 and G7 (Tables 1, 2, and 7), indicating that the Rsv1 allele in OX670 exhibits a resistant reaction to both strains. Buzzell and Tu (1984) obtained a 15R:1"S" ratio from F2 populations of L78-379(R) x OX670(R) inoculated with SMV-G6 and concluded that the resistance gene in OX670 is independent of Rsv1. If it is assumed that all of the "S" plants observed by Buzzell and Tu were actually necrotic, there is complete agreement between their data and those of the present study. Only the interpretations are different.

L88-8431 is a Williams BC5 isoline with SMV resistance derived from Raiden (Bernard et al., 1991). No susceptible plants, as well as no necrotic plants of consequence, were found in the F2 population and F2:3 families of L88-8431 (R, Rsv1) x OX670 crosses when SMV-G7 was used (Tables 2 and 3), verifying that one of the genes in OX670 is an allele at the Rsv1 locus. The two necrotic plants observed in the F2 (Table 2), probably were either mechanical mixtures of seeds or the result of viral contaminations. A low percentage of necrotic plants in R x R crosses involving resistance alleles at the Rsv1 locus was also observed in a previous study (Chen et al., 1991).

Allelic Relationship of the Resistance Genes in OX670 with Rsv3 and Rsv4
No susceptible plants were observed in the F2 populations of L29 (R, Rsv3) x OX670(R) or OX670(R) x Harosoy (R, Rsv3) when inoculated with SMV-G7 in the greenhouse (Table 2). Nor were any susceptible plants found in the F2:3 families from the same crosses (Table 3), which confirms that one of the genes in OX670 is an allele at the Rsv3 locus. These data and the pedigree information strongly suggest that the Rsv3 gene in OX670 was derived from Harosoy. ‘Harcor’ is a descendent of Harosoy and exhibits the same reaction to G1 and G7 (Table 1). Apparently, Harcor inherited the gene from Harosoy (Fig. 1). The combination of the Harosoy and Raiden genes likely occurred when Raiden was crossed with Harcor (Fig. 1), since OX315 is resistant to SMV-G1 through G7 (Buzzell and Tu, 1984). The genes from the two sources complement each other and make OX315 and OX670 resistant to SMV-G1 through G7, since Harosoy is resistant only to SMV-G5, G6, and G7, and Raiden is necrotic to SMV-G5 and G6 and resistant to the other strains (Table 1). The Rsv3 gene from Harosoy is epistatic to Rsv1 from Raiden in OX670 since it masked expression of necrotic reaction of the Rsv1 gene when SMV-G6 was used (Table 1). Knowledge of complementary action of Rsv1 and Rsv3 can be used to develop soybean cultivars with broad resistance to SMV as seen in OX670.

The segregating F2 population from OX670 (R) x V94-5152 (R, Rsv4) fit a digenic ratio of 15 (R+N):1 (S) when inoculated with SMV-G1 (Table 2). When the F2 population of the same cross was inoculated with SMV-G7, a 63 (R+N):1 (S) trigenic ratio was obtained (Table 2). The observed segregation pattern among F2:3 families from the same cross with SMV-G1 fit a 7 (all R):4[3(R+N):1S]:4[15(R+N):1S]:1 (all S) genotypic ratio expected for two genes (Table 5). When tested with SMV-G7, families segregating 63(R+N):1S were combined with the homozygous resistant class because the number of plants tested for each F2:3 family were insufficient to distinguish between the two classes. Therefore, a 45 [all R or 63(R+N):1S]:12 [15(R+N):1S]:6 [3(R+N):1S]:1 (all S) trigenic ratio was tested against the actual F2:3 segregation with SMV-G7 (Table 8). The good fit indicated that neither of the genes in OX670 is allelic to the gene at the Rsv4 locus.


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  		Table 8. Segregation of F2:3 soybean families from OX670 x V94-5152 inoculated with Soybean mosaic virus G7 in the greenhouse.

 
In general, the disagreement between the conclusion of Buzzell and Tu (1984) and that of the current study regarding genes governing SMV resistance in OX670 can be attributed to the difference in classification of the necrotic plants, including the necrotic reaction of L78-379. Also, Buzzell and Tu (1984) apparently were not aware that Harosoy is resistant to SMV-G5, G6, and G7. It is now known that OX670 also carries a resistance gene from Harosoy, which explains why our PI96983 x OX670 F2 and F2:3 (Table 2, 6, and 7) and the L78-379 x OX670 F2 population of Buzzell and Tu (1984) all exhibited digenic segregation patterns for the necrotic reaction. If we assume that all plants classified as "susceptible" by Buzzell and Tu (1984) were actually necrotic, all observations fit well with the proposed genetic model (Table 9). When inoculated with SMV-G6, only the Rsv1rRsv1rRsv3Rsv3 genotype shows the necrotic reaction. Gene Rsv1r is derived from Raiden, which exhibits the necrotic reaction to SMV-G6 (Chen et al., 2001). When SMV-G6 was used, F2:3 families of PI96983 x OX670 segregated to fit the expected genotypic ratio 7 (all R):4(15R:1N):4(3R:1N):1 (all N) (Table 6). None of the F2:3 families segregated to fit a 3N:1R ratio, indicating that the resistant reaction of Rsv1 in PI96983 is dominant to the necrotic reaction of the resistance gene Rsv1r in Raiden when SMV-G6 is used. According to our genetic model Rsv1Rsv1Rsv3Rsv3 and Rsv1Rsv1r Rsv3Rsv3 genotypes give the necrotic reaction against SMV-G7. In fact, some F2:3 families segregated 3N:1R when SMV-G7 was used (Table 7), indicating that the necrotic reaction of Rsv1 is dominant to the resistant reaction conferred by Rsv1r. Thus, it appears that the resistance allele in PI96983 is dominant to the resistance allele in Raiden, regardless of the SMV strain used.


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  		Table 9. A proposed genetic model for resistance to Soybean mosaic virus in crosses between OX670 and PI96983.

 
Results of this study clearly indicate that OX670 possesses two genes for resistance to SMV. One of the genes in OX670, derived from Raiden, is allelic to Rsv1, and the other, derived from Harosoy, is allelic to Rsv3. The presence of Rsv1 and Rsv3 in OX670 confers resistance to SMV-G1 through G7, combining the resistances of both genes. Therefore, the previously designated Rsv2 locus does not appear to exist in OX670 or its ancestors and thus could not be shown to exist at all.

Received for publication September 18, 2000.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 




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A. Shi, P. Chen, C. Zheng, A. Hou, and B. Zhang
A PCR-based Marker for the Rsv1 Locus Conferring Resistance to Soybean Mosaic Virus
Crop Sci., January 16, 2008; 48(1): 262 - 268.
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Y. Wang, H. A. Hobbs, C. R. Bowen, R. L. Bernard, C. B. Hill, J. S. Haudenshield, L. L. Domier, and G. L. Hartman
Evaluation of Soybean Cultivars, 'Williams' Isogenic Lines, and Other Selected Soybean Lines for Resistance to Two Soybean Mosaic Virus Strains
Crop Sci., November 21, 2006; 46(6): 2649 - 2653.
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C. Zheng, P. Chen, and R. Gergerich
Genetic Analysis of Resistance to Soybean Mosaic Virus in J05 Soybean
J. Hered., September 1, 2006; 97(5): 429 - 437.
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C. Zheng, P. Chen, and R. Gergerich
Characterization of Resistance to Soybean mosaic virus in Diverse Soybean Germplasm
Crop Sci., October 27, 2005; 45(6): 2503 - 2509.
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C. Zheng, P. Chen, and R. Gergerich
Effect of Temperature on the Expression of Necrosis in Soybean Infected with Soybean mosaic virus
Crop Sci., March 28, 2005; 45(3): 916 - 922.
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Y. Wang, H. A. Hobbs, C. B. Hill, L. L. Domier, G. L. Hartman, and R. L. Nelson
Evaluation of Ancestral Lines of U.S. Soybean Cultivars for Resistance to Four Soybean Viruses
Crop Sci., February 23, 2005; 45(2): 639 - 644.
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I. Gunduz, G. R. Buss, P. Chen, and S. A. Tolin
Characterization of SMV Resistance Genes in Tousan 140 and Hourei Soybean
Crop Sci., January 1, 2002; 42(1): 90 - 95.
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