The Journal of Heredity 2001:92(1)
© 2001 The American Genetic Association 92:51-55
Inheritance and Allelism Tests of Raiden Soybean for Resistance to Soybean Mosaic Virus
From the Department of Crop and Soil Environmental Sciences (Chen, Ma, Buss, and Gunduz) and Department of Plant Pathology, Physiology, and Weed Science (Roane and Tolin), Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.
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Abstract |
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The gene symbol Rsv2 was previously assigned to the gene in the soybean [Glycine max (L.) Merr.] line OX670 for resistance to soybean mosaic virus (SMV). The Rsv2 gene was reported to be derived from the Raiden soybean (PI 360844) and to be independent of Rsv1. Accumulated data from our genetic experiments were in disagreement with this conclusion. In this study, Raiden and L88-8431, a Williams BC5 isoline with SMV resistance derived from Raiden, were crossed with two SMV-susceptible cultivars to investigate the mode of inheritance of SMV resistance in Raiden. They were also crossed with five resistant cultivars to examine the allelomorphic relationships of the Raiden gene with other reported genes at the Rsv1 locus. F1 plants, F2 populations, and F2-derived F3 (F2:3) lines were tested with SMV strains G1 or G7 in the greenhouse or in the field. The individual plant reactions were classified as resistant (R, symptomless), necrotic (N, systemic necrosis), or susceptible (S, mosaic). The F2 populations from R x S crosses segregated in a ratio of 3 (R + N):1 S and the F2:3 lines from Lee 68 (S) x Raiden (R) exhibited a segregation pattern of 1 (all R):2 segregating:1 (all S). The F2 populations and F2:3 progenies from all R x R crosses did not show any segregation for susceptibility. These results demonstrate that the resistance to SMV in Raiden and L88-8431 is controlled by a single dominant gene and the gene is allelic to Rsv1. The heterozygous plants from R x S and R x N crosses exhibited systemic necrosis when inoculated with SMV G7, indicating a partial dominance nature of the resistance gene. Raiden and L88-8431 are both resistant to SMV G1–G4 and G7, but necrotic to G5, G6, and G7A. Since the resistance gene in Raiden is clearly an allele at the Rsv1 locus and it exhibits a unique reaction to the SMV strain groups, assignment of a new gene symbol, Rsv1-r, to replace Rsv2 would seem appropriate. Further research is ongoing to investigate the possible existence of the Rsv2 locus in OX670 and its relatives.
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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Resistance to soybean mosaic virus (SMV) in soybean [Glycine max (L.) Merr.] is usually controlled by a single dominant gene. Most of the resistance genes identified previously are at the same locus, Rsv1. Six resistance alleles, Rsv1 (PI96983), Rsv1-y (York), Rsv1-m (Marshall), Rsv1-t (Ogden), Rsv1-k (Kwanggyo), and Rsv1-s (PI486355), have been reported at this common locus (Chen et al. 1991; Kiihl and Hartwig 1979; Ma et al. 1995a,b). Most of these SMV resistance sources were found to be resistant to some, but not all seven strain groups (G1–G7) described by Cho and Goodman (1979).
Buzzell and Tu (1984) crossed a resistant breeding line, OX670, with L78-379 to study the genetics of SMV resistance. OX670 carries SMV resistance reportedly inherited from Raiden. L78-379 is an isogenic line of Williams with the SMV resistance gene Rsv1 derived from PI 96983. The inoculated F2 population exhibited a 15 resistant:1 susceptible segregation. Based on that result, they assigned the gene symbol Rsv2 for the resistance gene derived from Raiden. The gene symbol Rsv3 was assigned to a gene conferring stem-tip necrosis that was derived from the cultivar Columbia (Buzzell and Tu 1989). Resistance genes at loci other than Rsv1 have also been reported from various sources, but no gene symbols were assigned because of the lack of complete allelism tests with named loci (Bowers et al. 1992; Ma et al. 1995b; Shigemori 1988).
In the process of our allelism tests in which Raiden was used as an Rsv2 source, we observed genetic segregations contradictory to the conclusion given by Buzzell and Tu (1984). The objectives of this study were to clarify the inheritance of SMV resistance in Raiden and to test the allelic relationship of the Raiden gene with Rsv1.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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Raiden (PI 360844) and L88-8431 [Williams (6) x Raiden], a Williams isoline with SMV resistance derived from Raiden (Bernard et al. 1991), were crossed with SMV-susceptible cultivars Lee 68 or Essex and with five resistant genotypes (PI 96983, Ogden, York, Marshall, and Kwanggyo) possessing the Rsv1 alleles (Chen et al. 1991). Seeds of Raiden and L88-8431 were provided by Dr. R. L. Bernard, formerly the curator of the USDA Soybean Germplasm Collection at the University of Illinois.
To advance genetic populations to the F2 and F3 generations, F1 plants were grown in the greenhouse and F2 populations were planted in a field free of SMV at Warsaw, Virginia. All F1 and F2 plants were harvested and threshed individually. F1 individuals, F2 populations, and F2:3 progenies were inoculated with SMV G1 in the greenhouse or in the field nursery at Blacksburg, Virginia. Various numbers of F1 and F2 plants were screened for SMV reactions depending on the availability of seeds. Approximately 20 plants from each F2:3 progeny were inoculated with virus and scored for reaction. The sources of the virus strains, maintenance of virus cultures, inoculation procedures, greenhouse conditions, and field plot techniques were the same as described previously (Chen et al. 1991, 1994; Ma et al. 1995b).
F1 individuals and F2 populations from the crosses of L88-8431 x Lee 68, PI 96983 x L88-8431, Raiden x PI 96983, and Marshall x Raiden were also tested with SMV G7 in the greenhouse. Raiden and L88-8431 were also evaluated in the greenhouse for reactions to all SMV strains (G1–G7 and G7A) which were originally characterized by Cho and Goodman (1979). Parents of each cross and a set of SMV-strain differentials were included as checks in the greenhouse and field inoculations for verification of strain identification.
Individual plant reactions were evaluated regularly for symptom expression by visual examinations until about 4 weeks after inoculation and were classified as three distinct reaction types: resistant (R, no systemic symptoms), systemic necrotic (N), or susceptible (S, mosaic). For SMV G1, necrotic plants in segregating populations were combined with resistant plants as a resistant class for genetic analysis, whereas for SMV G7, necrotic plants were treated as a separate class. The F2:3 lines were classified as all resistant, segregating, or all susceptible, based on actual plant counts.
Chi-squared tests were used to determine the goodness-of-fit of observed segregations to expected genetic ratios. A chi-squared test for heterogeneity was also performed to examine whether different populations from the same type of cross displayed similar genetic behavior.
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Results and Discussion |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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When inoculated with SMV G1, the F2 populations from the crosses of Raiden and L88-8431 with susceptible cultivars Lee 68 or Essex showed a good fit to a ratio of 3 (R + N):1 S, which is expected for a single gene segregation (Table 1). The heterogeneity test indicated that all three populations had homogeneous segregation patterns. The necrotic plants were combined with resistant ones as a resistant class for the chi-squared tests, as has been done in many previous studies, because necrosis has been observed to be the expression of some heterozygotes of resistance genes (Bowers et al. 1992; Buss et al. 1989; Chen et al. 1991, 1994; Kiihl and Hartwig 1979; Ma et al. 1995a,b; Shigemori 1988).
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The overall segregation of the F2:3 progenies from Lee 68 x Raiden showed a good fit to a ratio of 1 (all R):2 [3 (R + N): 1 S]:1 (all S), confirming the presence of a single dominant gene in Raiden for SMV resistance (Table 2). The numbers of plants in segregating F2:3 progenies also exhibited good fits to the 3 (R + N):1 S ratio. The fact that no F2:3 progenies had all systemic necrotic plants indicated that systemic necrosis was not the expression of any homozygous genotype in this cross. Instead, the necrotic segregants in segregating rows represent the heterozygous genotype. These results demonstrate that Raiden has a single dominant gene for resistance to SMV G1 and the resistance gene in L88-8431 is the same as the one in its donor parent, Raiden.
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When the F2 populations from R x R crosses of Raiden and L88-8431 with the resistant cultivars possessing Rsv1 alleles were tested with SMV G1 in the greenhouse or in the field, no susceptible segregants were observed in any of the six populations (Table 3), although a few systemic necrotic plants were occasionally found. A very low percentage of necrotic plants in R x R crosses involving the resistance genes at the Rsv1 locus were also observed in previous studies and were shown not to be the result of genetic segregation (Chen et al. 1991; Ma et al. 1995b). The absolute absence of segregation for susceptibility in the R x R crosses indicates that the gene in Raiden shares a common locus with other Rsv1 alleles.
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In Table 4 are the results from F2:3 lines of R x R crosses involving Raiden and L88-8431 as one parent, with four resistant cultivars having Rsv1 alleles when inoculated with SMV G1 in the greenhouse or in the field. No susceptible segregants were observed in any of the crosses, although occasional necrotic plants were noticed in only a few progenies. The few necrotic plants observed in these populations did not appear to represent genetic segregation, since no F2:3 progenies from the four crosses were homogeneously necrotic (Table 4). The complete lack of segregation for susceptibility in these R x R crosses (2006 F2 plants and 5999 F3 plants) provides strong evidence that the resistance gene from Raiden is allelic to Rsv1 rather than independent of Rsv1.
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When inoculated with SMV G7 in the greenhouse, all the F1 individuals from the R x S cross of L88-8431 x Lee 68 were systemic necrotic and the F2 population from the same cross gave a good fit to a 1 R:2 N:1 S ratio, as expected from a single gene segregation (Table 5). Obviously, heterozygotes of the resistance gene from L88-8431 with the susceptible allele rsv1 from Lee 68 showed systemic necrosis, indicating the partial dominance nature of the resistance gene.
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In contrast, when inoculated with SMV G1, F1 individuals from the same cross were resistant rather than necrotic and the F2 populations from the three R x S crosses contained much less than 50% of necrotic plants (64 N/484 total = 13% N) (Table 1), suggesting that the phenotypic expression of the heterozygotes depends on the virus strains. The low percentage of necrotic phenotype of the heterozygotes may also be attributed to the influence of environmental conditions such as temperature (Cho et al. 1977; Tu and Buzzell 1987). Although the F1 individuals from L88-8431 x Lee 68 were resistant (no systemic symptoms) to SMV G1, all those plants showed pinpoint necrotic spots on the inoculated leaves which are considered to be a typical hypersensitive reaction of the heterozygous genotype. Such necrotic spots were not observed on L88-8431 when inoculated with SMV G1.
PI96983 and Marshall each carry an allele of Rsv1, conferring systemic necrosis to SMV G7 (Chen et al. 1991, 1994). When they were crossed with L88-8431 or Raiden, the F2 populations showed a 1 R:3 N single gene segregation with the heterozygotes being necrotic in reaction to SMV G7 inoculation (Table 5). The heterogeneity test indicated a homogeneous segregation pattern for all the R x N F2 populations, although the Marshall x Raiden cross had a slight deficiency of resistant plants. No susceptible segregants were observed in any of these R x N crosses, indicating that the necrotic and resistant reactions are conditioned by alleles at the same locus. If two separate genes controlled resistance and necrosis, the R x N F2 populations should contain 1/16 susceptible segregants (double homozygous recessives). The complete lack of susceptibles confirms that the gene in Raiden and L88-8431 is allelic to Rsv1.
Our observation in the present investigation that the resistance gene from Raiden is allelic to Rsv1 contradicts the conclusion of Buzzell and Tu (1984). One possible reason for the discrepancy could be that OX670, which Buzzell and Tu (1984) used in their allelism test, might contain another resistance gene from an ancestor line other than Raiden. We have preliminary evidence that OX670 may have inherited two resistance genes from its ancestors, one from Raiden (resistant to G1–G4) and the other from Harosoy (resistant to G5–G7). This research finding will be reported separately. The other possibility for the discrepancy is that Buzzell and Tu (1984) classified necrotic plants as susceptible, as such plants often express much more severe symptoms than the typical mosaic of the susceptible response. Although they did not specifically mention the classification in their article, they stated that L78-379 (a Williams isoline with Rsv1) was "susceptible to two isolates of G7." However, this gene consistently produces a systemic necrotic reaction to our isolate of SMV G7, in agreement with Cho and Goodman (1979). From this we have deduced that at least some, and possibly all, of the plants they classified as susceptible were actually necrotic.
All the SMV strains (G1–G7 and G7A) used in this study were the same pathotype cultures as those used previously (Chen et al. 1991, 1994) and were originally described by Cho and Goodman (1979). Data from our greenhouse and field inoculations show that Raiden and L88-8431 are resistant to SMV G1–G4 and G7, but necrotic to SMV G5, G6, and G7A (Table 6). Using the OX670 line in their study, Buzzell and Tu (1984) reported that the gene Rsv2, presumably from Raiden, conferred resistance to all SMV strains G1–G7 and the isolate G7A. Their result, however, was based on reactions of OX615, one of the parental lines of OX670, rather than Raiden itself. Therefore their implication that the Rsv2 gene in Raiden confers resistance to all seven SMV strains is not accurate. We used SMV G1 and G7 for our allelism test in the present investigation instead of SMV G6, which Buzzell and Tu (1984) used for their allelism test, because our isolate of G6-induced systemic necrosis on both Raiden and L88-8431.
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Both Raiden and L88-8431 showed conspicuous pinpoint necrotic spots on the inoculated leaves when inoculated with SMV G7, but no systemic symptoms were observed on subsequent leaves. SMV G7 is the most virulent strain among the seven (G1–G7) groups identified in the United States and is capable of defeating all the reported Rsv1 alleles, causing systemic mosaic or necrosis symptoms. The lack of systemic symptoms in Raiden and L88-8431 induced by SMV G7 indicated a potential advantage of the Raiden gene for preventing infection by severe strains of SMV.
Figure 1 shows the pedigree of OX670, as constructed from Buzzell and Tu (1984). The SMV reactions of the parents are summarized from Buzzell and Tu's report and from our experiments. Buzzell and Tu (1984) reported that OX615 is resistant to SMV G1–G7. We found that OX670 and OX615 are both resistant to SMV strains that we tested, namely, G1, G5, G6, and G7. We have also found that Harosoy is susceptible to SMV G1, which is considered to be the least virulent strain of SMV for the Rsv1 alleles (Cho and Goodman 1979), but is resistant to SMV G5, G6, and G7 which are more virulent strains for the Rsv1 alleles. It is clear, by following the resistance to SMV G1, that the resistance gene in Raiden was passed to OX670 via OX615 and OX315. Since nearly all of the remaining pedigree of OX670 is derived from Harosoy or Harcor, the SMV resistance to G5–G7 could have come through any route from the donor parents Harosoy or Harcor.
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Harosoy was also reported to be resistant to SMV strains A, C, and D in Japan (Hashimoto 1986). No genetic study on the SMV resistance of Harosoy has yet been reported. It is very likely, however, that Harosoy contains an SMV resistance gene at a locus different from Rsv1, based on its unique reactions to SMV G1 and G7. We have also observed that Corsoy and Harcor, which were derived from Harosoy and appeared several times in the pedigree (Figure 1), showed similar SMV reactions to those of Harosoy. It is highly likely that Harcor inherited its SMV resistance from Harosoy based on the pedigree information [Harcor = Corsoy x (Corsoy x Harosoy 73) and Corsoy = Harosoy x Capital].
Reactions of OX670 to SMV strains are distinctly different from those of either Raiden and Harosoy or Harcor and appear to be the result of a combination of the resistant reactions from both Raiden and Harosoy. It is very likely that the resistance of Raiden to SMV G1 and G7 was combined with the resistance in Harosoy via Harcor to SMV G5, G6, and G7 in the process of crossbreeding and selection. Therefore the progeny lines OX315 and OX615 are resistant to SMV G1–G7. Evidently there is a complementary action of the resistance genes from Raiden and Harosoy giving rise to resistance to SMV strains G1–G7 in OX315, OX615, and OX670. It appears that the combined resistance of Raiden and Harosoy/Harcor was passed from OX315 to OX615 and then to OX670.
Although Buzzell and Tu (1984) reported that OX670 carried only one resistance gene, they used virulent strains G7 and G7A, which could produce necrotic reactions in plants heterozygous for the Raiden gene, as shown in the present study with SMV G7. When systemic necrosis was classified as susceptibility, as possibly was done in Buzzell and Tu's (1984) study, two-gene segregation ratios, for example, 13 resistant:2 necrotic:1 susceptible or 13 resistant:1 necrotic, could appear to fit a single gene ratio of 3 resistant:1 susceptible (actually N + S). This particular misclassification and then misinterpretation could readily happen when no F2:3 progeny and only relatively small F2 populations were tested for an inheritance study like Buzzell and Tu's.
For the allelism test with Rsv1, Buzzell and Tu (1984) inoculated the F2 population from OX670 (R) x L78-379 (R, Rsv1) with SMV G6. If OX670 contains one resistance gene from Raiden, which confers systemic necrosis, and another independent gene from Harosoy, which is resistant to SMV G6, the F2 population would be expected to fit a ratio of 15 resistant:1 necrotic (only 1/16 of the genotypes with homozygous dominant alleles from Raiden and homozygous recessive alleles from Harosoy would show necrosis). Buzzell and Tu reached their conclusion that OX670 had only one resistance gene that is independent of Rsv1, based on an F2 population containing 190 resistant and 12 "susceptible" plants. No F2:3 progenies were tested to verify their conclusion.
It is very clear from our present study that the resistance gene from Raiden is an allele at the Rsv1 locus instead of at an independent locus. The Raiden gene confers resistant reactions to the SMV strains G1–G4, and G7, but necrotic to G5, G6, and G7A (Table 6), a unique combination for Rsv1 alleles. The gene from Raiden also shares common characteristics with other Rsv1 alleles since it confers systemic necrosis to at least one SMV strain and exhibits partial dominance with the heterozygotes showing systemic necrosis. Therefore we assign, with the approval of the Soybean Genetics Committee, a new gene symbol, Rsv1-r, to the resistance gene in Raiden. However, we still do not have enough evidence to prove nonexistence of the Rsv2 and therefore cannot eliminate this locus as yet. Further investigations are being undertaken to examine the possible presence of Rsv2 in OX670 and its ancestors. The results of the ongoing research and the outcome of the Rsv2 locus will be reported later.
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Acknowledgments |
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This research was supported in part by a grant from the Virginia Soybean Board and by the Virginia Agricultural Experiment Station.
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Footnotes |
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Address correspondence to Dr. G. R. Buss at the address above or e-mail:gbuss{at}vt.edu.
Corresponding Editor: Prem P. Jauhar
Received March 20, 2000
Accepted October 31, 2000
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References |
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