Journal of Heredity 2003:94(3)
© 2003 The American Genetic Association 94:205-211
Genetic Study of a Lethal Necrosis to Soybean Mosaic Virus in PI 507389 Soybean
From Medtronic Sofamor Danek, 1800 Pyramid Place, Memphis, TN 38132 (Ma); the Department of Crop, Soil, and Environmental Sciences, University of Arkansas, Fayetteville, AR 72701 (Chen); and the Departments of Crop and Soil Environmental Sciences (Buss) and Plant Pathology, Physiology, and Weed Science (Tolin), Virginia Tech, Blacksburg, VA 24061.
Address correspondence to P. Chen at the address above, or e-mail: pchen{at}uark.edu.
 |
Abstract |
|---|
 Top Abstract Materials and MethodsResults and DiscussionReferences |
|---|
PI 507389 soybean [Glycine max (L.) Merr.], a large-seeded line from Japan, exhibits a rapid, lethal, necrotic response to strains G1, G2, G5, and G6 of soybean mosaic virus (SMV). Unlike the hypersensitive necrotic reaction, this stem-tip necrosis can be a serious threat to soybean production. To investigate the genetic basis of lethal necrosis (LN), PI 507389 was crossed with the susceptible (S) cv. Lee 68 and with resistant (R) lines PI 96983, cv. York, and cv. Marshall, which carry single dominant genes for SMV resistance at the Rsv1 locus. F1 plants, F2 populations, and F2:3 lines were inoculated with G1 and G6 in the greenhouse or in the field. Results indicated that LN is controlled by a single gene allelic to Rsv1, and this allele in PI 507389 is recessive to R alleles in PI 96983, York, and Marshall. The LN allele is codominant with the allele for S, for the heterozygotes showed a mixed phenotype of both necrosis (N) and mosaic (M) symptoms (NM). The LN allele becomes recessive to the S allele as the mixed NM shifts to S at a later stage in response to more virulent strains. The gene symbol Rsv1-n is assigned for the allele conferring LN in PI 507389. Rsv1-n is the only allele at the Rsv1 locus conditioning N to G1 and no R to any other SMV strains, and thus a unique genotype for SMV strain differentiation. The phenotypic expression of heterozygotes and the dominance relationships among R, N, and S depend on the virulence of SMV strains, source of alleles, and developmental stage.
Soybean mosaic, caused by soybean mosaic virus (SMV), is an important soybean disease in many areas and distributed worldwide (Dunleavy 1973; Hill 1999). It can cause drastic yield losses and reduce seed quality (Hill et al. 1987; Ross 1983). Cho and Goodman (1979, 1982) classified 98 SMV isolates from seeds in the U.S. Department of Agriculture (USDA) soybean germplasm collection into seven strain groups (G1 to G7), according to symptoms induced in a set of soybean differential cultivars. There are usually three distinct reactions: R (symptomless), N (systemic necrosis), or S (mosaic), depending on the interaction between soybean genotypes and SMV strains (Chen et al. 1994; Cho and Goodman 1979, 1982; Ma et al. 1995).
Necrotic plants are usually severely stunted and eventually die with little or no seed production (Buss et al. 1989; Cho et al. 1977). Occurrence of an N disease, caused by a severe strain of SMV (SMV-N), was reported in Korea (Cho and Chung 1976), and an outbreak of this disease was observed in a large soybean growing area of central Korea (Chung et al. 1973). The N reaction resulted from infection of soybean cultivars that had R to less virulent SMV strains by more virulent strains of the same virus (Chen et al. 1994; Cho et al. 1977; Cho and Goodman 1979, 1982). Therefore, N is considered a serious threat to soybean production in some areas (Cho and Chung 1976; Cho et al. 1977).
Kwon and Oh (1980) crossed R cultivars with S cultivars that actually had the N reaction in response to the SMV-N strain in Korea and found N was conditioned by a single gene. They also demonstrated that the allele for N was dominant to that for R. Chen et al. (1994) reported similar results with more virulent strains of SMV identified in the United States. However, Kiihl and Hartwig (1979) showed that, when inoculated with SMV-1-B, which is equivalent to SMV-G3 in Cho and Goodman's system (1979, 1982), an F2 population from a R x N cross (PI 96983 x cv. Ogden) exhibited a 3R:1N segregation, indicating the dominant nature of R over N. In N x S crosses, N alleles have been reported consistently to be dominant to S alleles (Chen et al. 1994; Kiihl and Hartwig 1979). A temperature-dependent stem-tip N was observed in breeding lines derived from cv. Columbia and exhibited monogenic inheritance with complete dominance (Tu and Buzzell, 1987). Necrosis is also a genotypic expression of heterozygotes with an R allele and an S allele (Bowers et al. 1992; Chen et al. 1991, 1994; Kiihl and Hartwig 1979; Ma et al. 1995).
Several symbols have been assigned to genes for R to SMV. Eight alleles at the Rsv1 locus, Rsv1, Rsv1-t, Rsv1-y, Rsv1-m, Rsv1-k, Rsv1-s, Rsv1-r, and Rsv1-h, have been identified in PI 96983, Ogden, York, Marshall, Kwanggyo, LR1, Raiden, and Suweon 97, respectively. Each of these alleles confers R to different strains of SMV (Chen et al. 1991, 1994, 2001, 2002; Kiihl and Hartwig 1979; Ma et al. 1995). A new locus, Rsv2, was established for a dominant gene derived from Raiden (Buzzell and Tu 1984) but was later eliminated because of its allelism with the Rsv1' locus (Chen et al. 2001). The dominant gene for stem-tip N derived from Columbia was demonstrated to be at an independent locus and was labeled Rsv3 (Buzzell and Tu 1989). A new allele at the Rsv3 locus was later identified in L29, an isoline of cv. Williams with SMV resistance derived from cv. Hardee (Buss et al. 1999). Rsv4 was found in a breeding line, V94-5152, that was derived from PI 486355 (Buss et al. 1997). PI 486355 carries two independent dominant genes, Rsv1-s and Rsv4, and Rsv1-s has been isolated in the breeding line LR1 (Buss et al. 1997; Chen et al. 1993; Ma et al. 1995).
PI 507389 is a large-seeded soybean accession collected from Japan. It consistently shows LN when inoculated with SMV-G1 in the field and in the greenhouse. G1, although the least virulent strain of SMV, is of most concern because it is most prevalent in the field (Cho and Goodman 1979; Hunst and Tolin 1982; Pietersen and Garnett 1992). The infected PI 507389 plants appear to be S to the virus by showing a dark green, rugose, mosaic-like symptom in the early stage, and then the growing tip develops N and trifoliolate leaves gradually become smaller, wrinkled, and yellowish, and eventually drop off, resulting in plant death about two weeks after inoculation. Such rapid N symptoms leading to plant death are referred to as LN. PI 507389 has been widely used in breeding large-seeded soybean varieties for the soyfood market. Lethal necrosis, a serious threat to soybean production, has emphasized the need for investigating the genetic basis of this unique disease response. Objectives of this study were to investigate the inheritance of LN in PI 507389 in response to SMV strains and to test for allelism with R alleles at Rsv1.
|
Materials and Methods |
|---|
|
TopAbstractMaterials and MethodsResults and DiscussionReferences |
|---|
PI 507389 was crossed with S cv. Lee 68 to determine the number of loci conditioning LN. PI 507389 was also crossed to R lines PI 96983, York, and Marshall (containing alleles Rsv1, Rsv1-y, and Rsv1-m, respectively) for allelism tests. F1 plants, F2 populations, and F2:3 lines were inoculated with G1 in the greenhouse, in the field, or in both. For each F2:3 line, 20 seeds were planted for inoculation. In addition, F1 plants and F2 populations from PI 507389 x Lee 68 and PI 96983 x PI 507389, and F2:3 lines from PI 96983 x PI 507389 were inoculated in the greenhouse with G6, which is more virulent than G1. PI 507389 was also tested with G2 through G5 and G7 in the greenhouse.
The sources of virus cultures, inoculation procedures, and greenhouse and field conditions were as described previously (Chen et al. 1991, 1994; Ma et al. 1995). A set of differential cultivars (Table 1) were included with each batch of inoculation to verify the identity of each strain used. Individual plant reactions were evaluated visually for symptom expression from about 10 days to 4 weeks after inoculation and classified into resistant (R, symptomless), lethal necrotic (LN), slow necrotic (SN), necrotic mosaic (NM), and susceptible (S, mosaic). SN and NM were two types of reactions observed in F1 plants and segregating progenies, which were different from those of any parental lines. SN is a delayed N response with N lesions on both inoculated unifoliolate leaves and subsequent trifoliolate leaves. The N symptoms are slow developing and less severe than those of LN. The NM is a mixed phenotype having both N and mosaic symptoms, with N lesions on the inoculated unifoliolate leaves and first trifoliolate leaves and mosaic on upper trifoliolate leaves.
|
According to individual plant reaction and actual plant counts, F2:3 lines were classified as all R, all N, all S, or segregating. Chi-square tests were used in analyzing F2 and F3 data for goodness-of-fit to expected monogenic segregation ratios (3:1, or 1:2:1). A
2 test for heterogeneity was also used to determine whether different F2 populations from the same type of cross display similar genetic behavior. |
Results and Discussion |
|---|
|
TopAbstractMaterials and MethodsResults and DiscussionReferences |
|---|
Reactions of PI 507389 to Different Strains of SMV
PI 507389 reacted with LN to G1, G2, G5, and G6 strains and with S to G3, G4, and G7 strains (Table 1). Necrotic symptoms were very similar, regardless of strain. Infected plants started showing dark green, mosaic-like symptoms on the first trifoliolate leaves about 7 days after inoculation, which then turned into N within 2–3 days. Small N spots were observed on all the inoculated unifoliolate leaves, and large N lesions subsequently developed on upper plant parts (i.e., leaflets, veins, petioles, and stems). Eventually, the N plants turned brownish yellow and died about 2 weeks after inoculation. PI 507389 consistently showed LN when inoculated with G1 in the greenhouse (at a wide range of temperatures) and in the field.
PI 507389 exhibited a different combination of reactions to G1 through G7 as compared to other soybean lines reported to date (Table 1). It had no R to any of seven strains tested, which is an exception to the general observation that N is usually an expression of R genes for a mild strain when challenged by more virulent strains of SMV (Chen et al. 1994; Cho and Goodman 1982; Kwon and Oh 1980). However, it is possible that PI 507389 confers R to strains that have not yet been isolated or tested. This unique LN reaction of PI 507389 can be used in differentiating SMV strains.
LN in PI 507389 differed from N reactions (normal N) induced on other differential cultivars by various SMV strains. Plants with normal N lack the dark green, mosaic-like symptoms (a sign of vast replication and movement of the virus) at the initial stage after inoculation, thus developing N symptoms late as compared to the rapid LN. In addition, development of the normal type of N symptoms is favored by high temperature (Cho and Goodman 1979; Kwon and Oh 1980), whereas LN in PI 507389 was a very stable and temperature-independent response.
Segregation of the Necrotic Reaction to SMV-G1 in F2 Populations and F2:3 Lines
When inoculated with G1, F1 plants from PI 507389 (LN) x PI 96983 (R), PI 96983 (R) x PI 507389 (LN), and PI 507389 (LN) x York (R) were R. The F2 populations from these three crosses and from PI 507389 (LN) x Marshall (R) showed a monogenic segregation with a ratio of 3R:1LN (Table 2). The F2:3 lines from PI 96983 x PI 507389 exhibited a segregation ratio of 1 (all R):2 (segregating 3R:1LN):1 (all LN) and all plants from segregating F2:3 lines gave a good fit to the 3R:1LN ratio (Table 3). These results clearly indicate that there is only one gene segregating in R x LN crosses and that the R allele is dominant to the LN allele.
|
|
F1 plants from PI 507389 (LN) x Lee 68 (S) showed NM, and segregation of the F2 population showed a good fit to a 1LN:2NM:1S ratio when inoculated with G1 (Table 2). The F2:3 lines exhibited a 1(all LN):2 segregating (1LN:2NM:1S):1(all S) segregation pattern, and the combined plants from segregating F2:3 lines gave a good fit to the 1LN:2NM:1S ratio (Table 4). These results suggested that the LN reaction is controlled by a single gene. The mixed NM on heterozygotes can be attributed to the codominant nature of N and S reactions.
|
In F2 populations and F2:3 lines from R x LN crosses of PI 507389 with PI 96983, York, and Marshall, no S segregants were observed (Tables 2 and 3), indicating that the gene conferring LN in PI 507389 is an allele at Rsv1. If LN and R were controlled at separate loci, a digenic segregation pattern would be expected and R x LN F2 populations should contain 1/16 S plants. Likewise, 1/16 of R x LN F2:3 lines should be homogeneous S, and 50% of F2:3 lines should be segregating for S. The complete lack of S segregants in 1,026 F2 plants and 122 F2:3 lines provides strong evidence that the single genes for the LN in PI 507389 and for R in PI 96983, York, and Marshall are alleles at the same locus (Rsv1).
Segregation of Necrotic Reaction to SMV-G6 in F2 Populations and F2:3 Lines
When tested with SMV-G6, F1 plants of PI 507389 (LN) x Lee 68 (S) showed a mixed NM reaction at an early stage (first 2 weeks after inoculation) and then recovered into S plants at 3–4 weeks after inoculation (Table 5). The F2 population showed a 1LN:2NM:1S segregation at the early stage and then developed to be a 1LN:3S segregation when the NM plants recovered into S plants about 3–4 weeks after inoculation. These results indicate that LN in PI 507389 is controlled by a single gene and that the LN allele is codominant with the S allele at the early stage, but recessive to the S allele at a later stage.
|
F1 plants from PI 507389 (LN) x PI 96983 (R) gave a R response at an early stage but showed SN about 3–4 weeks after inoculation with G6 (Table 5). Segregation of the F2 population from PI 96983 x PI 507389 provided a very good fit to a monogenic 3R:1LN ratio at the early stage. However, a portion of the R plants later developed SN and, therefore, the final segregation appeared to be 1R:2SN:1LN, as expected for a monogenic segregation. The results also suggest that the R allele was completely dominant to the LN allele at the early stage, but exhibited partial dominance at a later stage.
When inoculated with G6, F1 plants of PI 96983 (R) x Lee 68 (S) were R at the early stage but turned into SN later (Table 5), indicating a shift of complete to partial dominance of the R allele over time. A portion of F2 plants from the same cross also developed similar SN symptoms at the late stage. Timing and appearance of SN symptoms were very similar to those of F1 plants and those in the F2 population from PI 96983 (R) x PI 507389(LN). These results strongly support the hypothesis that SN of F1 plants and a portion of F2 plants from R x LN and R x S crosses is the expression of heterozygotes of Rsv1, as observed previously (Chen et al. 1991, 1994).
Segregation of F2:3 lines from PI 96983 (R) x PI 507389 (LN) showed a good fit to a monogenic ratio of 1 (all R):2 (segregating):1 (all LN) when inoculated with G6 (Table 6). The combined data for individual F2:3 plants also provided a good fit to a monogenic segregation. SN was observed only in segregating progenies, and no S plants were observed. These results provide further evidence that there is only one gene segregating in the R x LN cross, that SN is associated with the heterozygosity of Rsv1, and that the gene for LN in PI 507389 is allelic to Rsv1.
|
Dominance Relationships Among Resistance, Necrosis, and Susceptibility
Our data demonstrate that the Rsv1 alleles for R are completely dominant to the LN allele when challenged with the mild strain G1 but partially dominant when challenged with the virulent strain, G6 (Tables 2, 3, 5, and 7). The allele for LN shows codominance with the allele for S when interacting with G1. In response to G6, however, the LN allele exhibits codominance with the S allele initially (2 weeks after inoculation), but is recessive to the S allele later (4 weeks after inoculation; Tables 2, 4, 5 and 7). In most previous reports alleles for N appeared to be dominant to those for R and S when more virulent strains were used (Chen et al. 1994; Kwon and Oh 1980; Tu and Buzzell 1987). Kiihl and Hartwig (1979) showed that alleles for N were dominant to alleles for S and recessive to alleles for R in an F2 population inoculated with SMV-1-B, which is equivalent to G3 in the Cho and Goodman system (1979) and is a less virulent isolate of SMV. Evidently, dominance relationships among alleles for R, N, and S depend upon SMV strains and soybean genotypes used.
|
In R x N crosses of previous reports, N conferred by heterozygotes was not distinguished from N of homozygotes, so the alleles for N appeared to be dominant to alleles for R (3N:1R) (Kwon and Oh 1980; Chen et al. 1994; Ma et al. 1995). In the present study LN was clearly different from SN, a phenotypic expression of heterozygotes, which appeared to be strain-dependent. Our results have shown that heterozygotes of Rsv1 from PI 96983 with either the S allele, rsv1, from Lee 68 or the LN allele from PI 507389 developed SN upon inoculation with G6, indicating the partial dominance of Rsv1 (Table 5). However, the allele for R was completely dominant to the allele for LN when inoculated with G1. No SN was observed in F1, F2, and F2:3 from PI 96983 x PI 507389 (Tables 2 and 3). This observation is in agreement with the report by Kiihl and Hartwig (1979) when mild strains G2 and G3 were used. Whether heterozygotes of R genes express SN to a given strain may also depend on the specific R alleles. For example, the Rsv1 allele in PI 96983 exhibits complete dominance for R to G1 (Tables 2 and 3; Kiihl and Hartwig 1979). In contrast, a portion of heterozygotes of the Rsv1-y allele from York showed N (partial dominance) to G1 (Chen et al. 1991; Ma et al. 1995). Eighteen of 118 R plants in the F2 population from York x PI 507389 developed SN at a late stage after the inoculation with G1 (Table 2). These plants could well be the heterozygotes of Rsv1-y Rsv1-1n.
The mixed expression of NM is a unique phenotype of the heterozygous plants from LN x S crosses. This response has not been reported previously in the SMV x soybean system. In most of the genetic studies alleles for N were found to be completely dominant to S alleles (Chen et al. 1994; Kiihl and Hartwig 1979; Kwon and Oh 1980, Tu and Buzzell 1987). The coexistence of N and S reaction in an individual plant (NM) is presumably due to the dual expression of two different alleles (N and S). In addition, the mixed NM phenotype appeared to be transitional and SMV-strain dependent. The mosaic symptom becomes predominant at a later stage when a virulent stain is used. The existence of a mixed NM phenotype and its shifting over time as observed in this research are two unique phenomena for future study of SMV x soybean interactions.
In summary, LN in PI 507389 has unique features: (1) N symptoms develop in a very short time after inoculation and are very severe compared to other types of N, (2) PI 507389 is the only soybean line with an allele at the Rsv1 locus that confers N to G1 but no R to any other strains of SMV, (3) the allele for LN response is recessive to the allele for R and codominant with the allele for S, and (4) the S allele may become dominant over the LN allele at a later stage in response to more virulent SMV strains. With the approval of the Soybean Genetics Committee, the gene symbol Rsv1-n is assigned for the allele conferring LN in PI 507389.
|
Footnotes |
|---|
Corresponding Editor: William F. Tracy
Received July 18, 2002
Accepted January 15, 2003
|
References |
|---|
|
TopAbstractMaterials and MethodsResults and DiscussionReferences |
|---|
-
Bowers GR, Jr, Paschal EH, II, Bernard RL, Goodman RM, 1992. Inheritance of resistance to soybean mosaic virus in "Buffalo" and "HLS" soybean. Crop Sci. 32:67-72.
Buss GR, Chen P, Tolin SA, Roane CW, 1989. Breeding soybeans for resistance to soybean mosaic virus. In: Proc World Soybean Res Conf IV (Pascale AJ, ed). Buenos Aires: Argentina Soybean Association; 1144–1154.
Buss GR, Ma G, Chen P, Tolin SA, 1997. Registration of V94-5152 soybean germplasm line resistant to soybean mosaic potyvirus. Crop Sci. 37:1987-1988.
Buss GR, Ma G, Kristipati S, Chen P, Tolin SA, 1999. A new allele at the Rsv3 locus for resistance to soybean mosaic virus. In: World Soybean Res Conf VI. Chicago: Proceedings; 490.
Buzzell RI, Tu JC, 1984. Inheritance of soybean resistance to soybean mosaic virus. J Hered. 75:82.
Buzzell RI, Tu JC, 1989. Inheritance of a soybean stem-tip N reaction to soybean mosaic virus. J Hered. 80:400-401.
Chen P, Buss GR, Roane CW, Tolin SA, 1991. Allelism among genes for resistance to soybean mosaic virus in strain-differential soybean cultivars. Crop Sci. 31:305-309.
Chen P, Buss GR, Roane CW, Tolin SA, 1994. Inheritance in soybean of resistant and necrotic reactions to soybean mosaic virus strains. Crop Sci. 34:414-422.
Chen P, Buss GR, Tolin SA, Gunduz I, Cicek M, 2002. A valuable gene in Suweon 97 soybean for resistance to soybean mosaic virus. Crop Sci. 42:333-337.
Chen P, Ma G, Buss GR, Gunduz I, Roane CW, Tolin SA, 2001. Inheritance and allelism of Raiden soybean for resistance to soybean mosaic virus. J Hered. 92:51-55.
Cho EK, Chung BJ, 1976. Studies on identification of soybean virus diseases in Korea, I. Preliminary studies on a soybean virus disease. Korean J Plant Prot. 15:61-68.
Cho EK, Chung BJ, Lee SH, 1977. Studies on identification and classification of soybean virus diseases in Korea, II. Etiology of a necrotic disease of Glycine max. Plant Dis Rep. 61:313-317.
Cho EK, Goodman RM, 1979. Strains of soybean mosaic virus: classification based on virulence in resistant soybean cultivars. Phytopathology. 69:467-470.[ISI]
Cho EK, Goodman RM, 1982. Evaluation of resistance in soybeans to soybean mosaic virus strains. Crop Sci. 22:1133-1136.
Chung BJ, Lee SH, Sung JM, 1973. An investigation on soybean mosaic virus: varietal resistance and seed transmission. Symp Plant Environ Res and Summ:73–77.
Dunleavy JM, 1973. Viral diseases. In: Soybeans: Improvement, production and uses (Caldwell BE, ed). Madison, WI: American Society of Agronomy; 505–523.
Hill JH, 1999. Soybean mosaic. In: Compendium of soybean diseases, 4th ed (Hartman GL, Sinclair JB, and Rupe JC, eds). St. Paul, MN: American Phytopathology Society Press; 70–71.
Hill JH, Bailey TB, Benner HI, Tachibana H, Durand DP, 1987. Soybean mosaic virus: Effects of primary disease incidence on yield and quality. Plant Dis. 71:237-239.
Hunst PL, Tolin SA, 1982. Isolation and comparison of two strains of soybean mosaic virus. Phytopathology. 72:710-713.
Kiihl RAS, Hartwig EE, 1979. Inheritance of reaction to soybean mosaic virus in soybeans. Crop Sci. 19:372-375.
Kwon SH, Oh JH, 1980. Resistance to a necrotic strain of soybean mosaic virus in soybeans. Crop Sci. 20:403-404.
Ma G, Chen P, Buss GR, Tolin SA, 1995. Genetic characteristics of two genes for resistance to soybean mosaic virus in PI486355 soybean. Theor Appl Genet. 91:907-914.[ISI]
Pietersen G, Garnett HM, 1992. Properties and strain identity of soybean mosaic virus isolates from the Transvaal, South Africa. Phytophylactica. 24:279-283.
Ross JP, 1983. Effect of soybean mosaic on component yields from blends of mosaic resistant and susceptible soybeans. Crop Sci. 23:343-346.
Tu JC, Buzzell RI, 1987. Stem-tip necrosis: a hypersensitive, temperature dependent, dominant gene reaction of soybean to infection by soybean mosaic virus. Can J Plant Sci. 67:661-665.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  A. Shi, P. Chen, D. X. Li, C. Zheng, A. Hou, and B. Zhang Genetic Confirmation of 2 Independent Genes for Resistance to Soybean Mosaic Virus in J05 Soybean Using SSR Markers J. Hered., May 19, 2008; (2008) esn035v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Ma, P. Chen, G. R. Buss, and S. A. Tolin Genetics of Resistance to Two Strains of Soybean Mosaic Virus in Differential Soybean Genotypes J. Hered., July 1, 2004; 95(4): 322 - 326. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||