Journal of Heredity Advance Access originally published online on September 21, 2006
Journal of Heredity 2006 97(5):429-437; doi:10.1093/jhered/esl024
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Genetic Analysis of Resistance to Soybean Mosaic Virus in J05 Soybean
From the Department of Crop, Soil, and Environmental Sciences, University of Arkansas, Fayetteville, AR 72701 (Zheng and Chen); and Department of Plant Pathology, University of Arkansas, Fayetteville, AR 72701 (Gergerich)
Address correspondence to P. Chen at the address above, or e-mail: pchen{at}uark.edu.
Soybean cultivar J05 was identified to be resistant to the most virulent strain of soybean mosaic virus (SMV) in northeastern China. However, the reaction of J05 to SMV strains in the United States of America is unknown, and genetic information is needed to utilize this germplasm in a breeding program. The objectives of this study were to determine the reaction of J05 to all US strains of SMV (G1–G7), the inheritance of SMV resistance in J05, and the allelic relationship of resistance genes in J05 with other reported resistance genes. J05 was crossed with susceptible cultivar Essex (rsv) to study the inheritance of SMV resistance. J05 was also crossed with PI 96983 (Rsv1), L29 (Rsv3), and V94-5152 (Rsv4) to test the allelism of resistance genes. F2 populations and F2:3 lines from these crosses were inoculated with G1 or G7 in the greenhouse. Inheritance and allelism studies indicate that J05 possesses 2 independent dominant genes for SMV resistance, one at the Rsv1 locus conferring resistance to G1 and necrosis to G7 and the other at the Rsv3 locus conditioning resistance to G7 but susceptibility to G1. The presence of both genes in J05 provides resistance to G1 and G7. J05 is unique from the previous sources that carry 2 genes of Rsv1Rsv3 and will be useful in breeding for SMV resistance.
Soybean mosaic virus (SMV) is one of the most destructive viral diseases in soybean (Glycine max (L.) Merr.). Various strains and isolates of SMV that cause different symptoms on soybean have been identified worldwide. Symptoms of infection by SMV on soybean include mosaic and necrosis. Symptoms associated with mosaic include light and dark green areas of mild mottling or severe mosaic, chlorosis, leaf rugosity, and leaf curl. There are 3 types of necrotic reactions: local necrosis, systemic necrosis, and stem-tip necrosis. The local necrosis is a hypersensitive reaction, and necrotic lesions are restricted to the initial infection sites on the inoculated leaves. Symptom of systemic necrosis includes necrotic lesions on both inoculated and noninoculated leaflets, petioles, and stems. Symptoms associated with stem-tip necrosis include local necrosis, systemic necrosis, bud blight, severe plant stunting and defoliation, and eventually plant death.
Cho and Goodman (1979) classified 98 isolates of SMV from seeds in the US Department of Agriculture Soybean Germplasm Collection into 7 strain groups (G1–G7) based on their virulence on infecting a set of 8 differential soybean cultivars. G1, the least virulent strain, did not infect any of the resistant cultivars. G7, the most virulent strain, infected all cultivars tested and caused necrosis in Marshall, Ogden, Kwanggyo, and Buffalo and mosaic symptoms on Davis and York soybean. This classification system has been used in SMV strain identification and differentiation of SMV-resistance alleles (Chen et al. 1991, 1993, 1994, 2001, 2002; Ma et al. 1995, 2003; Gunduz et al. 2001, 2002, 2004).
Three independent loci, Rsv1, Rsv3, and Rsv4, have been reported so far for SMV resistance in soybean in the United States of America. Nine resistance alleles (Rsv1, Rsv1-t, Rsv1-y, Rsv1-m, Rsv1-k, Rsv1-r, Rsv1-h, Rsv1-s, and Rsv1-n) have been identified at the Rsv1 locus in PI 96983, Ogden, York, Marshall, Kwanggyo, Raiden, Suweon 97, LR1, and PI 507389, respectively. Two alleles for SMV resistance have been reported at the Rsv3 locus: one was identified in the OX686 soybean line derived from the cultivar Columbia (Buzzell and Tu 1989) and the other was found in L29 soybean derived from the cultivar Hardee (Buss et al. 1999). The Rsv3 gene provides resistance to more virulent strains (G5–G7) but not to G1–G4. The Rsv4 locus was identified in a breeding line V94-5152 derived from PI 486355 x Essex and was shown to confer an early resistance but a late susceptibility to SMV strains G1–G7 (Chen et al. 1993; Ma et al. 1995, 2002; Buss et al. 1997; Gunduz et al. 2004). OX670, Tousan 140, Hourei, and Zao 18 soybean were shown to possess 2 genes, Rsv1 and Rsv3 (Gunduz et al. 2001, 2002; Liao et al. 2002), conferring resistance to G1–G7.
Soybean cultivar J05 was developed by the Institute of Crop Breeding and Cultivation, Chinese Academy of Agricultural Science, in China. J05 was reported to be resistant to the most virulent strains of SMV in northeastern China (Zheng et al. 2000). The reaction of J05 to SMV strains identified in the United States of America has not been tested yet. The objectives of this study were 1) to examine the reaction of J05 to all US strains of SMV (G1–G7), 2) to investigate the inheritance of SMV resistance in J05, and 3) to determine the allelic relationship of resistance genes in J05 with the 3 reported resistance loci.
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Virus Strains
SMV stains G1–G3 and G5–G7 were used in this study and were provided by S. Tolin of Virginia Tech. The SMV strains were maintained by mechanical inoculation in Essex soybean (for G1–G3) and York soybean (for G5–G7) in the greenhouse. Some of these SMV strains have been deposited in the American Type Culture Collection (Rockville, MD) (Chen et al. 1994). SMV-G4 strain was not available to us and was not included in this study. A sample of leaf tissue infected with each SMV strain was also stored at –80 °C as backup cultures for our study. Strain identity was checked regularly by inoculation on a set of differential soybean genotypes including V94-5152, L29, PI 96983, PI 507389, Marshall, Ogden, Kwanggyo, York, Essex, and Suweon 97 (Cho and Goodman 1979; Chen et al. 2002; Ma et al. 2003). The differential genotypes were also included in each experiment to confirm the identity and purity of the strain used.
Plant Materials
J05 seeds were obtained from the Institute of Crop Germplasm Resources, Chinese Academy of Agricultural Sciences, Beijing, China. J05 was mechanically inoculated with SMV strains G1–G3 and G5–G7 to determine the disease reaction in the greenhouse. Soybean plants were grown in 20-cm-diameter plastic pots containing the Redi-Earth commercial soil mix (Scotts-Sierra Horticultural Products Co., Marysville, OH) in the greenhouse maintained at 20–28 °C and 14-h photoperiod. Plants in 2 pots (8 plants per pot) were inoculated with each strain, and plants in the third pot were left uninoculated as control. J05 was crossed with SMV-susceptible cultivar Essex to study the inheritance of resistance. J05 was also crossed with SMV-resistant lines PI 96983 (Kiihl and Hartwig 1979), L29 (Buss et al. 1999), and V94-5152 (Buss et al. 1997), which possess Rsv1, Rsv3, and Rsv4, respectively, to determine genetic allelism. All F1 plants were grown in the field and harvested individually. An average of 200 F2 plants per population and 30 F2:3 plants from each of the 80–100 F2:3 lines derived from each cross were inoculated with G1 or G7 in the greenhouse. Parental lines were also inoculated with G1 and G7 as a control. Differential soybean cultivar/lines were used in each inoculation test for SMV strain verification.
Mechanical Inoculation
Systemically infected leaves of Essex or York soybean were ground in 0.05 M potassium phosphate buffer (pH 7.2) with a mortar and pestle (1 g leaf tissue:10 ml buffer). Inoculum was applied with cheesecloth pads to both unifoliolate soybean leaves (V1 stage) of each plant that had been previously dusted with 600-mesh carborundum (Zheng et al. 2005). Plants were gently rinsed with tap water after inoculation. Inoculated soybean plants were monitored for symptom expression on a regular basis for 6–8 weeks.
Test for Virus Infection
Leaf sap of test plants were extracted using a tissue extractor (Erich Pollahne, West Germany) and tested for SMV by a protein-A enzyme-linked immunosorbent assay (ELISA) (Edwards and Cooper 1985) using an anti-SMV rabbit polyclonal antiserum. Samples of the leaf extracts were tested at a dilution of 1:10 in phosphate-buffered saline–Tween. Absorbance values were determined spectrophotometrically 30 min after substrate addition at a wavelength of 405 nm using a microplate reader (Model 7250, Cambridge Technology Inc., Cambridge, MA). Samples were considered positive for SMV if ELISA absorbance values were three or more times than those of healthy plant extracts.
Data Analysis
Individual plant reactions were classified as resistant (R, symptomless), necrotic (N, stem-tip necrosis), or susceptible (S, mosaic symptom) (Figure 1). F2:3 lines were classified as all R, all N, all S, or segregating (3:1, 15:1, 12:3:1). 
2 tests were used to determine the goodness-of-fit of observed segregations (F2 populations, individual F2:3 lines, and all F3 populations) to expected genetic ratios.
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Genetic models were proposed based on inheritance of single, independent, dominant genes at 3 separate loci. The inheritance of each locus was based on the results of F2 and F2:3 segregation ratios when inoculated with G1 or G7. The SMV reaction of Rsv1 is characterized by resistance to G1 and necrosis or mosaic to G7. Rsv1 is also partially dominant and confers necrotic reaction in the heterozygous state when paired with a susceptible allele. The Rsv3 typically confers resistance to G7 but susceptibility to G1, whereas Rsv4 conditions resistance to both G1 and G7 at the early seedling stage and a delayed mosaic reaction 3 weeks later (Ma et al. 2002).
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Inheritance of Resistance to SMV-G1 and -G7 in J05
J05 exhibited a resistant reaction to SMV strains G1–G3 and G5–G7. No virus was detected in the inoculated plants by ELISA (data not shown). Based on these results, it appears that J05 is a good source of SMV resistance and a valuable germplasm for breeding. Essex, a universally susceptible cultivar, showed a mosaic reaction to G1–G3 and G5–G7. PI 96983 carrying Rsv1 was resistant to strains G1–G6 but necrotic to G7. L29 contains Rsv3 giving rise to resistance to G5–G7 but susceptibility to G1–G3. V94-5152, carrying Rsv4, was resistant to G1–G7 at the seedling stage.
The segregation of the F2 population from J05 (R) x Essex (S) showed an acceptable fit to a 3(R + N):1S ratio when inoculated with G1 and 15(R + N):1S when inoculated with G7 (Table 1 and Figure 1). These results indicate that J05 possesses 1 dominant resistance gene for resistance to G1 and 2 dominant genes for resistance to G7.
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A number of necrotic plants were observed in the F2 population from J05 x Essex inoculated with either G1 or G7 (Table 1 and Figure 1). However, necrosis appeared earlier in J05 x Essex after inoculation with G7 (Figure 1B) than with G1 (Figure 1A). These necrotic plants, although lower than the expected frequency, are most likely the heterozygotes and were combined with the resistant class for the
2 test. The expression of necrosis was apparently the result of the incomplete dominance nature of the resistance gene under the assumption that necrosis is associated with heterozygosity. Some of the necrotic plants exhibited chimeric symptoms of necrosis and mosaic when inoculated with G7, whereas others recovered from the stem-tip necrosis and produced new leaves with mosaic symptoms at the top of the plant (Figure 1B). When the F2:3 lines derived from J05 x Essex were inoculated with G1, a ratio with a good fit to 1(all R):2[3(R + N):1S]:1(all S) was observed (Table 2). When the F2:3 lines from this cross were inoculated with G7, a ratio of 4(all R):2(3R:1N):1(all N):4(12R:3N:1S):2(3N:1S):2(3R:1S):1(all S) was observed (Table 3). These results confirm that J05 carries 1 dominant gene for resistance to G1 and 2 dominant resistance genes for reaction to G7. The presence of necrotic plants in segregating F2:3 lines also supports the assumption that the necrotic F2 plants are heterozygotes (Table 1).
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Allelic Relationship of the Resistance Genes in J05 with Rsv1
No susceptible plants were observed in the F2 population and F2:3 lines from PI 96983 (R, Rsv1) x J05 (R) when inoculated with G1 (Tables 1 and 2). The complete absence of susceptible segregants in this cross with G1 inoculation indicates that J05 has a resistance gene at the Rsv1 locus. When the F2 population and F2:3 lines from PI 96983 (N, Rsv1) x J05 (R) were inoculated with G7, the F2 population segregated in a ratio of 3R:1N (Table 1) and the F2:3 lines segregated in a ratio of 1(all R):2(3R:1N):1(all N) (Table 4). These results suggest that there is another gene (in addition to the Rsv1 allele) segregating in the cross for reaction to G7.
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Allelic Relationship of the Resistance Genes in J05 with Rsv3
When the F2 population and F2:3 lines from J05 (R) x L29 (R, Rsv3) were inoculated with G7, no susceptible plants were found (Tables 1 and 2). These results indicate that J05 carries a resistance gene that is allelic to Rsv3. When the F2 population from J05 (R) x L29 (S, Rsv3) was inoculated with G1, the phenotypic segregation provided a good fit to 3R:1S, indicating that there is one gene (a non-Rsv3 gene) segregating in the cross for SMV reaction. This gene appears to be allelic to Rsv1 because Rsv3 does not provide resistance to G1. The F2:3 lines from the same cross exhibit a segregation of 1(all R):2[3(R + N):1S]:1(all S), confirming one gene (Rsv1) segregation for G1 reaction in the cross. Because the Rsv3 gene in L29 confers resistance to G7 but susceptibility to G1, the Rsv3 gene in both L29 and J05 is overcome by G1. Therefore, segregation of only one gene (Rsv1) is observed in the progenies of J05 (R) x L29 (S, Rsv3) when inoculated with G1.
Based on the F2 and F2:3 data of J05 x Essex inoculated with G1 and G7, we concluded that J05 carries 1 dominant gene for resistance to G1 and 2 dominant genes for resistance to G7. According to the allelic test with Rsv1 and Rsv3, we confirmed that J05 contains 2 resistance genes, Rsv1 and Rsv3. Rsv1 confers resistance to G1–G3, and Rsv3 confers resistance to G5–G7. The presence of both Rsv1 and Rsv3 in J05 gives rise to resistance to all SMV strains tested.
Allelic Relationship of the Resistance Genes in J05 with Rsv4
When the F2 population from J05 (R, Rsv1Rsv3) x V94-5152 (R, Rsv4) were inoculated with G1, a digenic (Rsv1 and Rsv4) segregation ratio of 15(R + N):1S was obtained (Table 1) because Rsv3 is nonfunctional against G1. However, 3-gene segregation with a ratio of 63(R + N):1S was observed in the F2 population from this cross when inoculated with G7. The F2:3 lines from J05 x V94-5152 segregated in a ratio of 7(all R):4[3(R + N):1S]:4[15(R + N):1S]:1(all S) when inoculated with G1 (Table 5) and 28(all R):4(15R:1N):4(3R:1N):1(all N):8[63(R + N):1S]:12[15(R + N):1S]:4[3(R + N):1S]:2(3N:1S):1(all S) when inoculated with G7 (Table 6). These results indicated that neither of the 2 genes in J05 is allelic to the Rsv4 locus. Apparently, when G1 is used for inoculation, the Rsv3 gene in J05 is not expressed; likewise, the Rsv1 gene in J05 is overcome when G7 is used for inoculation. Therefore, the progenies from the cross of J05 (R) x V94-5152 (R, Rsv4) exhibited digenic segregation for G1 reaction but a 3-gene segregation for G7 reaction. These results also provide support for the conclusion that J05 contains 2 dominant genes, Rsv1 and Rsv3, for SMV resistance.
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Inheritance and Allelism of Resistance to SMV in J05
In this study, we have investigated the inheritance of resistance in J05 to SMV and tested the allelism of the resistance genes in J05 with the 3 reported genes, Rsv1, Rsv3, and Rsv4. The results clearly indicate that J05 carries 2 dominant genes for SMV resistance. One of the genes is at the Rsv1 locus and confers resistance to G1 and necrosis to G7. The other resistance gene is located at the Rsv3 locus, which confers resistance to G7 but susceptibility to G1. Therefore, the presence of both genes in J05 confers resistance to G1 and G7. Similar research findings have been reported for Zao 18 (Liao et al. 2002), OX670, Tousan 140, and Hourei soybean (Gunduz et al. 2001, 2002), all of which carry 2 genes for SMV resistance, Rsv1 and Rsv3. In addition, Columbia soybean was shown to carry 2 genes, Rsv3 and Rsv4, for resistance to SMV G1–G3 and G5–G7 (Ma et al. 2002).
There are 9 resistance alleles reported at the Rsv1 locus, and their reactions to differential SMV strains follow different patterns (Chen et al. 2002). From our results, Rsv1 in J05 confers resistance to G1 and necrosis to G7, which is similar to the reaction of PI 96983 (Kiihl and Hartwig 1979). The Rsv1 in Zao 18 (Liao et al. 2002) and Tousan 140 (Gunduz et al. 2002) confers resistance to G1 but susceptibility to G7, which is similar to the reaction of York. Rsv1 in OX670 (Gunduz et al. 2001) was derived from Raiden and confers resistance to G1–G4 and G7 but necrosis to G5–G6. The Rsv1 allele in Hourei also conditions resistance to G1 and G7 (Gunduz et al. 2002). Therefore, the Rsv1 allele in J05 is different from the Rsv1 alleles in Zao 18, Tousan 140, Hourei, and OX670.
The 2 resistance alleles in J05, Rsv1 and Rsv3, have contrasting genetic specificities when interacting with specific SMV strains. Rsv1 confers resistance to G1, whereas Rsv3 provides resistance to G7, which are the typical characteristics of alleles at these 2 reported loci (Cho and Goodman 1979; Buss et al. 1999; Gunduz et al. 2001, 2004; Chen et al. 2002; Ma et al. 2003; Zheng et al. 2005a, 2005b). Because of these specific interactions between resistance genes and SMV strains, the cross J05 (Rsv1 Rsv3) x Essex (rsv1 rsv3) exhibited monogenic segregation when screened with G1 as the Rsv3 gene was defeated by G1. However, when this cross was inoculated with G7, a digenic ratio was obtained because Rsv1 conditions a necrotic reaction rather than susceptibility and only the double-recessive genotypes (1/16 in frequency) would be susceptible. Therefore, in the allelism tests, the cross J05 (Rsv1 Rsv3) x PI 96983 (Rsv1 rsv3) showed no segregation to G1 inoculation but a monogenic segregation to G7 inoculation. In contrast, the cross J05 (Rsv1 Rsv3) x L29 (rsv1 Rsv3) exhibited no segregation to G7 inoculation but a monogenetic segregation to G1 inoculation. In the cross of J05 (Rsv1 Rsv3) x V94-5152 (Rsv4), however, a digenic and a trigenic segregation were expected for G1 and G7 inoculation, respectively, due to the differential responses of Rsv3 to G1 and G7.
Proposed Genetic Models for the Cosegregation of 2 Genes in J05
Based on the inheritance study and allelism test results, we proposed 4 genetic models (Tables 7–10) to explain the interaction of the 2 genes in J05 with Essex (rsv), PI 96983 (Rsv1), L29 (Rsv3), and V94-5152 (Rsv4) when challenged with G1 or G7 inoculation. Five theoretical genotypes were proposed in this study: Rsv1JRsv1JRsv3JRsv3J (referred as R1JR1JR3JR3J hereafter) for J05, Rsv1Rsv1rsv3rsv3 (R1R1r3r3 hereafter) for PI 96983, rsv1rsv1Rsv3Rsv3 (r1r1R3R3 hereafter) for L29, rsv1rsv1rsv3rsv3Rsv4Rsv4 (r1r1r3r3R4R4 hereafter) for V94-5152, and rsv1rsv1rsv3rsv3 (r1r1r3r3 hereafter) for Essex.
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In the cross of J05 x Essex, the F2 population exhibited a 3(R + N):1S segregation ratio when inoculated with G1 and a 12R:3N:1S ratio when inoculated with G7. The F2:3 lines of this cross should segregate in a ratio of 1(all R):2[3(R + N):1S]:1(all S) for G1 reaction and 4(all R):2(3R:1N):1(all N):4(12R:3N:1S):2(3N:1S):2(3R:1S):1(all S) for G7 reaction. Our observations for the phenotypic segregation in F2 population and F2:3 lines fit well with the expected genotypic segregation from the proposed genetic model (Tables 1–3, 7 and Figure 1). It is important to point out that genotypes heterozygous for Rsv1rsv1 would exhibit necrosis regardless of the Rsv3 gene with G1 inoculation due to the partial dominance nature of Rsv1. In contrast, genotypes homozygous for Rsv1Rsv1 would show necrosis in the absence of the Rsv3 gene when challenged by G7 but resistance to G1 regardless of Rsv3. The difference between this model and the one developed for Zao 18 is that the Rsv1 allele in J05 confers necrosis (Table 7), whereas the Rsv1 allele in Zao 18 conditions susceptibility in the absence of Rsv3 (Liao et al. 2002).
In the cross of J05 x PI 96983, because both R1J and R1 confer resistance to G1 (Table 8), no susceptible segregation is expected in F2 and F2:3 when inoculated with G1. When this cross is inoculated with G7, however, the F2 population would segregate in a ratio of 3R:1N because one-fourth of the population would have the genotype of Rsv1Rsv1rsv3rsv3 and exhibit a necrotic reaction. When inoculated with G7, the F2:3 lines derived from F2 plants with homozygous Rsv3 genotype should be resistant regardless of Rsv1 because Rsv3 confers resistance to G7, whereas F2:3 lines from F2 plants with genotype of homozygous Rsv1Rsv1 would be all necrotic in the absence of Rsv3. F2:3 lines from F2 plants heterozygous for Rsv3 would segregate in a ratio of 3R:1N in response to G7 inoculation. Our results of the F2 populations and F2:3 lines from J05 x PI 96983 inoculated with G1 and G7 fit satisfactorily to the proposed genetic model (Tables 1, 2, 4, and 8). This model is different from the ones proposed for Zao 18 (Liao et al. 2002) and OX670 (Gunduz et al. 2001) in reactions to G7. In the absence of Rsv3, the Rsv1 allele in J05 confers necrosis, whereas the Rsv1 alleles in Zao 18 and OX670 confer susceptibility and resistance, respectively.
In the cross of J05 x L29, no susceptible segregation in both F2 and F2:3 would be anticipated when inoculated with G7 because of the presence of Rsv3 in both parents (Table 9). However, when inoculated with G1, the F2 populations and F2:3 lines would segregate in a ratio of 3(R + N):1S and 1(all R):2[3(R + N):1S]:1(all S), respectively. The heterozygous genotypes for the Rsv1 gene would exhibit either resistant or necrotic response in F2 plants and 3(R + N):1S segregation in F2:3 lines. Because Rsv3 confers susceptibility to G1, homozygous recessive rsv1 gene would result in complete susceptibility in F2 plants and F2:3 lines regardless of Rsv3. Our results (Tables 1 and 2) were in agreement with the proposed genetic model (Table 9), which is identical to the model for Zao 18 (Liao et al. 2002).
In the cross of J05 x V94-5152, the F2 populations should segregate in a ratio of 15(R + N):1S and 63(R + N):1S when inoculated with G1 and G7, respectively. There are interactions involving all 3 genes, Rsv1, Rsv3, and Rsv4, in this cross. Both Rsv1 and Rsv4 condition resistance to G1, whereas Rsv3 confers susceptibility to G1. Therefore, F2 plants with the genotype of both homozygous recessive rsv1 and rsv4 regardless of Rsv3 would give rise to susceptibility to G1 and the derived F2:3 lines would all be homogeneously susceptible. F2 plants with heterozygous Rsv1 genotype in the absence of Rsv4 regardless of Rsv3 would exhibit either resistance or necrosis when inoculated with G1, and the derived F2:3 lines would segregate in a ratio of 3(R + N):1S. F2:3 lines derived from F2 plants with heterozygous Rsv4 genotype in the absence of Rsv1 and regardless of Rsv3 would also segregate in a 3(R + N):1S ratio when inoculated with G1. F2:3 lines derived from F2 plants with the genotype of both heterozygous Rsv1 and Rsv4 regardless of Rsv3 would segregate in a ratio of 15(R + N):1S when inoculated with G1.
When inoculated with G7, only F2 plants with the genotype of r1r1r3r3r4r4 would exhibit susceptibility and the derived F2:3 lines should all be susceptible. Because both Rsv3 and Rsv4 confer resistance to G7 and Rsv1 confers necrosis to G7, F2 plants with the genotype of R1JR1Jr3r3r4r4 and R1Jr1r3r3r4r4 would exhibit necrosis to G7 and the derived F2:3 lines would exhibit all N and 3N:1S, respectively. F2 plants with the genotype of heterozygous Rsv4 or Rsv3 regardless of Rsv1 would exhibit either resistant or necrotic response to G7. F2:3 lines derived from the F2 plants with the genotype of R1JR1JR3Jr3R4r4 would segregate in 15R:1N. F2:3 lines derived from the F2 plants with the genotype of R1JR1JR3Jr3r4r4 and R1JR1Jr3r3R4r4 would segregate in a ratio of 3R:1N. F2:3 lines derived from the F2 plants with genotype of 3 heterozygous genes would segregate in a 63(R + N):1S ratio. F2:3 lines derived from the F2 plants with genotype of 2 heterozygous genes would segregate in a 15(R + N):1S ratio. F2:3 lines derived from the F2 plants with the genotype of 1 heterozygous resistance gene of Rsv3 or Rsv4 in the absence of Rsv1 would segregate in a ratio of 3(R + N):1S. F2:3 lines derived from the F2 plants with the genotype of homozygous Rsv3 or Rsv4 regardless of Rsv1 would exhibit all R response, whereas F2 plants and F2:3 lines without any of the 3 genes would all be susceptible. Our results (Tables 1, 5, and 6) are in good agreement with the proposed genetic model (Table 10).
In summary, J05 carries 2 dominant genes for SMV resistance, one is at the Rsv1 locus, which confers resistance to G1 but necrosis to G7, and the other gene is allelic to Rsv3, which confers resistance to G7 but susceptibility to G1. The combination of both Rsv1 and Rsv3 in J05 provides resistance to all SMV strains (G1–G7). Soybean genotypes with resistance to all SMV strains are rare, and most commercial soybean cultivars are susceptible to SMV. Therefore, identification of new soybean genotypes such as J05 with resistance to all SMV strains is valuable in breeding for SMV resistance.
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Corresponding Editor: Reid Palmer
Received January 29, 2006
Accepted July 26, 2006
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