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Selecting Soybean Cultivars for Dual Resistance to Soybean Cyst Nematode and Sudden Death Syndrome Using Two DNA Markers.

DURING THE LAST DECADE, DNA-marker studies have identified and mapped quantitative trait loci (QTL) and their underlying genes associated with pest resistance in several plant species including soybean (Staub et al., 1996). The predictive value of a DNA marker depends on linkage to the resistance gene and the phenotypic expression of the gene in other genetic backgrounds and environments.

Soybean cyst nematode and sudden death syndrome (Roy, 1997) cause substantial losses in seed yield (Wrather et al., 1995, 1996). To reduce recurring yield losses, soybean breeders have developed cultivars with field resistance to these pests. Resistance to SDS (Chang et al., 1996, 1997; Njiti et al., 1996) is polygenic and quantitative, but resistance to SCN may be qualitative (Webb et al., 1995; Concibido et al., 1996) and may be under the control of two loci (Chang et al., 1997; Meksem et al., 1999). Further, resistance to SCN is race and cultivar specific, therefore easily overcome by pathogen mutation, whereas resistance to SDS is not race-cultivar specific and therefore not easily overcome by pathogen mutation (Njiti et al., 1997b). Using DNA markers, a gene cluster on molecular Linkage Group G conditioning resistance to SDS was dissected into resistance to root infection conditioned by Rfsl and resistance to leaf scorch by Rft1 (Meksem et al., 1999). Several groups have identified a major gene for resistance to SCN (rhgl) in the same region of Linkage Group G for SCN, (Webb et al., 1995; Concibido et al., 1995; Chang et al., 1997). In addition to the gene on Linkage Group G, the gene Rhg4 on Linkage Group A2 is an important gene for resistance to SCN race 3 in some populations (Weisemann et al., 1992; Webb et al., 1995; Mahalingam and Skorupska, 1995; Chang et al., 1997) but not all (Concibido et al., 1997). Coinheritance of the SDS- and SCN-resistant phenotype in cultivar trials (Gibson et al., 1994) and inheritance studies (Mathews et al., 1991; Njiti et al., 1996) has been explained by the close linkage of rhg1 (for resistance to SCN) to two genes for resistance to SDS on Linkage Group G (Meksem et al., 1999).

Satt038 is a microsatellite-based marker that maps to Linkage Group G (Concibido et al., 1997; Mudge et al., 1997). In the `Evans' X PI209332 population, Satt038 alone was 95% accurate in predicting SCN phenotype (Mudge et al., 1997). Satt038 cosegregates with Satt275, which maps to a position that is 0.2 centimorgans (cM) from the SDS resistance gene (Rfs1) and 2 cM from the SCN resistance gene (rhg1) in Essex X Forrest (Meksem et al., 1999). BLT65, a sequence characterized amplified regions marker was mapped 0.65 cM from the i locus on Linkage Group A2 (Weisemann et al., 1992). The i locus is 0.35 to i cM from the Rhg4 locus (Mahalingam and Skorupska, 1995; Webb et al., 1995). However, in Essex x Forrest, fine mapping showed that BLT65 maps 3 cM from Rhg4 and that it provides half of a bigenic resistance to SCN race 3 (Meksem et al., 1999).

The use of diagnostic DNA markers for resistance to SDS may make the breeding process more efficient. Problems associated with conventional selection for resistance to SDS include the environmental dependence of leaf symptom development, maturity date influences on resistance, nonuniform infestation, and interactions with other diseases and pests (Rupe, 1989; Gibson et al., 1994). Problems with conventional greenhouse selection for SCN include high cost and race instability. The QTL for resistance to SCN are expected to function in many genetic backgrounds (Webb et al., 1995; Concibido et al., 1997; Chang et al., 1997; Mahalingam and Skorupska, 1995), but it is not known whether QTL for resistance to SDS can function in genetic backgrounds other than those in which they are mapped. This study used recombinant inbred lines from Flyer (McBlain et al., 1990) x Hartwig (Anand, 1992). Flyer is a BC3F2 plant selection from the cross [`A3127'.sup.4] x L24 and Hartwig was derived from [`Forrest'.sup.3] x PI437654. Our objective was to evaluate the effectiveness of DNA markers for QTL identified in Essex x Forrest recombinant inbred lines as marker-based selection tools for SDS- and SCN-resistant phenotypes among Flyer x Hartwig recombinant inbred lines.

MATERIALS AND METHODS

Genetic Material

Flyer is a Maturity Group IV cultivar that is susceptible to SDS and SCN (McBlain et al., 1990; Gibson et al., 1994). Hartwig is a Maturity Group V cultivar that is resistant to all known races of SCN and partially resistant to SDS (Anand, 1992; Chang et al., 1996). The cross Flyer x Hartwig was made in Southern Illinois University at Carbondale in 1991. The [F.sub.1] and [F.sub.2] plants were grown in Carbondale in 1992 and 1993 respectively. [F.sub.3] seeds were sent to Puerto Rico for advance to the [F.sub.5] generation by single pod descent (Brim, 1966). Seven hundred and thirty nine individual F, plants were harvested at SIUC in 1994, without intentional selection, and each [F.sub.5] plant was designated as a recombinant inbred line. The seeds were kept in cold storage until 1996, when a random sample of 94 recombinant inbred lines was row planted in the field for seed increase but did not produce enough seed for the 1997 field studies due to deer damage. In the fall of 1996, [F.sub.5:7] seeds (from the summer 1996 seed increase) were sent to Puerto Rico for further increase. The number of recombinant inbred lines increased was intended to fit a field trial design of 96 entries (including parents) and four row plots for evaluation of agronomic traits of importance. The fields used to advance the population and seed increase were not infested with SCN at detrimental concentration and did not have a history of SDS leaf scorch.

Marker Methodology

[F.sub.5:6] seeds of all 739 recombinant inbred lines were planted in the greenhouse and leaf samples harvested for DNA extraction. DNA was extracted according to Gu et al. (1995), with some modifications (Prabhu et al., 1997). About 50 mg of young leaf tissue was homogenized either manually or in a Matrix Mill (Gu et al., 1995) with 50 [micro]L of 0.5 M NaOH. Ten microliters of this NaOH extract was added to 90 [micro]L of 100 mM Tris pH 8, and 5 [micro]L of this DNA was used in the amplification reaction.

BLT65 was amplified according to the following conditions: 200 mM deoxynucleotides, 1 unit AmpliTaq (Perkin Elmer Cetus, Norwalk, CT), ix buffer supplied with the enzyme, 0.4 mM each BLT65 primers, 4 mM Mg[Cl.sub.2], and 5 [micro]L of DNA in a 25-[micro]L reaction volume. Cycling conditions included one cycle of 94 [degrees] C for 2 min, 35 cycles of 94 [degrees] C for 30 s, 57 [degrees] C for 30 s, 72 [degrees] C for 1.5 min, and one cycle of 72 [degrees] C for 6 min. The polymerase chain reaction products were electrophoretically separated on a 20 by 10 cm gel 1.4% (w/v) agarose gel and visualized by ethidium bromide staining. Based on the size of the polymorphic band, recombinant inbred lines were scored as either Hartwig genotype (H) or Flyer genotype (F). The sequences of the BLT65 primers were GCA GAT ATC AAC AGT TGG GAC and GGA ATG GAC AGC TCG TAA AGC C.

Satt038 was amplified according to Mudge et al. (1997) and separated on a 4% (w/v) Metaphor (FMC BioProducts, Rockford, ME) gel. The sequence of Satt038 primers are GGG AAT CTT TTT TTC TTT CTA TTA AGT T and GGG CAT TGA AAT GGT TTT AGT CA (Mudge et al., 1997). The gel was poured according to the manufacturer instructions and DNA was electrophoresed at 80 V for 3 h and visualized by staining with ethidium bromide. Bands in recombinant inbred lines were scored as being descended from Hartwig (H) or Flyer (F). The gels were reused up to ten times by storing it in 1 x Tris-borate-EDTA at 4 [degrees] C between runs. Hartwig and Flyer amplified DNA samples were included as controls with every set of eight lines to facilitate scoring.

The use of Satt038 and BLT65 to genotype the recombinant inbred lines provided four genotype combinations: H/H, H/F, F/H, and F/F. Although all recombinant inbred lines were genotyped by either one or both markers, only the 94 recombinant inbred lines that were previously planted for seed increase had enough seeds for field evaluation. Due to the labor-intensive nature of phenotype evaluation for F. solani infection severity, the sample size for field evaluation was limited to 50 recombinant inbred lines plus the parents.

Field Testing of Marker-Selected Lines

A stratified random sample (randomized within each genotype or stratum) of 50 [F.sub.5:8] recombinant inbred lines encompassing four genotypes (12 H/H, 11 H/F, 9 F/H, 18 F/F), plus Hartwig and Flyer, were planted in F. solani-infested fields and monitored for SDS resistance. Aliquots of the same genotypes were also screened as seedlings in the greenhouse for SCN race 3 resistance.

Recombinant inbred lines were planted in a randomized complete block design at two locations in 1997 in two-row plots with two replications. Two locations, Ridgway and Ullin, in southern Illinois were selected on the basis of a history of uniform SDS leaf symptoms.

The Ullin soil type was Bonnie silt loam, Fine silty, mixed, active, acid, mesic, Typic, Fluvaquents, and the Ridgway soil type was Reesville silt loam, Fine silty, mixed, superactive, mesic, Aerie, Epiaqualfs. Experiments were planted on 11 June 1997 at Ridgway and 19 June 1997 at Ullin. Rows were 0.75 m wide and 3.0 m long with about 17 plants [m.sup.-1].

Disease Scoring for Sudden Death Syndrome and Soybean Cyst Nematode

Tap roots were collected from each location at the R6 (three plants) and at the R8 (five plants). Fusarium solani isolation and quantification were performed as described in Njiti et al. (1997b, 1998). The selective medium was modified by adding 0.08 g [L.sup.-1] of streptomycin (Sigma Chemical Co., St. Louis, MO) for the isolation at R6 and 0.08 g [L.sup.-1] of streptomycin and rifampicin (Sigma Chemical Co.) for the isolation at R8. The infection severity score was calculated as a percentage of root segments yielding blue F. solani f. sp. glycine from sampled plants in each plot.

Soybean cyst nematode race 3 phenotype was determined at SIUC in a randomized complete block design with two five-plant replications. It was scored, according to the number of white female cysts on the roots, on a scale of 0 (complete resistance) to 6 (very susceptible) as follows: 0 = 0, 1 = 1 to 5,2 = 6 to 10, 3 = 11 to 30, 4 = 31 to 50, 5 = 51 to 100, and 6 = [is greater than] 100 white female cysts on the roots of each genotype. Essex was used as the susceptible check in this experiment. The SCN index of parasitism was determined as the ratio of the SCN score of each genotype to the SCN score of Essex times 100. The SCN race of the soil used in this assay was determine by the procedure in Njiti et al. (1996).

Statistical Analysis

The data were subjected to analysis of variance (ANOVA) (SAS Institute, Cary, NC), with mean separation by LSD ([Alpha] = 0.05) (Gomez and Gomez, 1984). Genotype and recombinant inbred lines within genotype were considered as fixed-effect variables, while location and replication were considered as random-effect variables. Location is random within the context of fields in southern Illinois with a history of SDS leaf scorch.

RESULTS AND DISCUSSION

Marker Screening

Amplification profiles with BLT65 showed one (Flyer) band or two (Hartwig) bands (Fig. 1A). For Satt038, the difference between the Hartwig and Flyer bands was small (Fig. 1B). A total of 739 recombinant inbred lines were attempted to be genotyped by one pass agarose gel marker-assisted selection (MAS). About 72%, or 535 lines, were successfully genotyped with both markers (Table 1).

[Figure 1 ILLUSTRATION OMITTED]

Table 1. Segregation of two DNA markers among recombinant inbred lines (RILs) from Flyer (F) x Hartwig (H).
                                Allele   Number     Number
Marker (number)                 from:    observed   expected

Satt038 (613)([dagger])         H        230        306.5
                                F        383        306.5
BLT65 (671)([dagger])           H        281        335.5
                                F        390        335.5
Satt038 & BLT65 (535)([double
  dagger])                      HH       93         133.7
                                HF       112        133.7
                                FH       166        133.7
                                FF       164        133.7

Marker (number)                      [X.sup.2]

Satt038 (613)([dagger])          18.9
                                 19.4
                                          38.3(*)
BLT65 (671)([dagger])            8.9
                                 8.9
                                          17.8(*)
Satt038 & BLT65 (535)([double
  dagger])                      12.4
                                 3.5
                                 7.8
                                 6.9
                                          30.6(*)


(*) Significant at P [is less than or equal to] 0.05.

([dagger]) Chi-square tests the expected genetic ratio of 1 H:1 F.

([double dagger]) Chi-square tests the expected genetic ratio of 1 HH:1 HF:1 FH:1 FF.

A chi-square analysis of segregation ratios indicated that there was a significant (P [is less than or equal to] 0.05) deviation from the expected 1:1 genetic ratio within each marker (Table 1), indicating that segregation within this population was not random at these loci. The skewed segregation ratio for each marker alone was also reflected in the ratio obtained for the four genotypes when both markers were used (Table 1), as the observed ratio of the four genotypes was significantly different (P [is less than or equal to] 0.05) from the expected 1:1:1:1 genetic ratio (Table 1). The Hartwig allele for Satt038 was unintentionally selected against in this population. Errors in scoring, a sampling bias, a nonrandom population, selection against the late maturity of Hartwig, or zygotic selection (Webb et al., 1995) may account for the skewed segregation ratio.

Phenotype Determination

Mean F. solani infection severity among genotypes that were predicted to be resistant to F. solani was stable, from 28 to 29% between R6 and R8 (Table 2). However, there was a large increase in mean infection severity, from 31 to 42%, among genotypes that were predicted to be susceptible to F. solani (Table 2). This difference in infection severity between R6 and R8 may have resulted from increased selectivity of the isolation medium at R8 following the addition of rifampicin or from additional infection between R6 and R8. Genotypes that were predicted to be susceptible to F. solani may also be more susceptible to other microorganisms that grow faster than F. solani on the less selective medium.

Table 2. Fusarium solani infection severity (IS) means among 50 recombinant inbred lines of Flyer (F) x Hartwig (H) by two DNA markers individually and combined.
Marker                         Allele

                                n
Satt 038                       H (84)([sections])
                               F(116)
BLT65                          H (108)
                               F (92)
Satt038 & BLT65                HH (48)
                               HF (44)
                               FH (36)
                               FF (72)
  LSD([paragraph]) P = 0.05

                                   R6 Sampler
                                                   IS
Marker                  P     [R.sup.2]   means [+ or -] SEM

                                 %
Satt 038              0.61      0.6        29.3 [+ or -] 1.9
                                           30.7 [+ or -] 1.8
BLT65                 0.60      0.6        29.5 [+ or -] 2.0
                                           30.7 [+ or -] 1.8
Satt038 & BLT65       0.78      2.3        29.9 [+ or -] 2.3
                                           28.7 [+ or -] 3.3
                                           29.0 [+ or -] 3.3
                                           31.8 [+ or -] 2.1
  LSD([paragraph])
    P = 0.05                                       6.9

                             R8 Sample([double dagger])
                                                   IS
Marker                   P     [R.sup.2]   means [+ or -] SEM

                                   %
Satt 038               0.0001     28       28.1 [+ or -] 1.9
                                           41.6 [+ or -] 1.9
BLT65                  0.4100      1.4     34.4 [+ or -] 2.0
                                           37.2 [+ or -] 2.0
Satt038 & BLT65        0.0016     28       28.6 [+ or -] 2.5
                                           27.7 [+ or -] 2.9
                                           40.8 [+ or -] 2.8
                                           42.1 [+ or -] 3.2
  LSD([paragraph])
   P = 0.05                                        6.4


([dagger]) Isolation medium contained tetracycline, neomycin, and streptomycin.

([double dagger]) Isolation medium contained tetracycline, neomycin, streptomycin, and rifampicin.

([sections]) Number in parentheses represents the number of values going into each mean.

([paragraph]) LSD is only for the four genotypes with both markers.

A combination of late planting and dry conditions during the critical period (R5 to R6) for SDS foliar symptoms (Rupe et al., 1993; Gibson et al., 1994) resulted in very low foliar disease index ([is less than] 1%). Hence, there were no analyses with field disease index. This scenario is an example of the problems encountered when using leaf scorch to select for SDS resistance in the field.

Mean infection severity at R8 was significantly higher (P = 0.0001; [R.sup.2] = 28%) for genotypes carrying the Flyer allele at Satt038 ([Satt038.sub.166]) than for the genotypes carrying the Hartwig allele at Satt038 ([Satt038.sub.172]) (Table 2).

There was significant variation (P [is less than or equal to] 0.05) among recombinant inbred lines within genotype (Table 3), suggesting that Satt038 did not account for all the variation in F. solani infection severity. Effective selection for F. solani resistance with additional makers or by conventional methods is possible within the [Satt038.sub.172] genotype (Chang et al., 1997). BLT65 alone was not effective in selecting for SDS resistance (Tables 2 and 3)

Table 3. Mean square (MS) values from analysis of variance on infection severity among four genotypes of 50 recombinant inbred lines (RILs) from Flyer x Hartwig.
                                  F-test       Mean squares
Source                       df   devisor    R6            R8

Location                     1       10     1809        10 933
Rep (loc.)                   2       10     1290(**)       445
Genotype                     3        7      107         2 932
  Satt038 (contrast)         1        7       87         8 722(*)
  BLT65 (contrast)           1        7       54             6
  Satt038 x BLT65            1        7      180            74
Loc. x genotype              3       10      362           514
RILs (genotype)             46        9      298           466(**)
Loc. x RILs (genotype)      46       10      275           236
Error                       94               226           241


(*), (**) Significant at the 0.05 and 0.01 levels of probability, respectively.

Analysis of infection severity within the Flyer-type and Hartwig-type (Maturity Groups IV and V, respectively) indicated that the [Satt038.sub.172] genotype mean infection severity was significantly (P [is less than or equal to] 0.05) lower than the [Satt038.sub.166] genotype within early maturity (26.8 vs. 32.6) and late maturity (32.8 vs. 38.9) groups. In the Essex x Forrest population (Maturity Group V), Satt275 (0.2 cM from Satt038 in other crosses) has been found to be significantly associated with reduced infection (Njiti et al., 1998; Meksem et al., 1999). Taken together, the infection severity data suggest that Satt038 can select for Rfsl or resistance QTL of similar effect in multiple genetic backgrounds and across maturity groups (Maturity Groups IV-V).

Using infection severity means (pooled across samples and location) for phenotype selection, with a cutoff of infection severity [is less than or equal to] 30% (mean of resistant parent) for resistance to F. solani infection, the correspondence between marker-based selection and selection by phenotype was 78% when the Hartwig allele of Satt038 was present alone, 27% when the Hartwig allele of BLT65 was present alone, 67% when the Hartwig alleles of Satt038 and BLT65 were present together, and 6% when the Flyer allele of Satt038 and BLT65 were present together. Satt038 maps on Linkage Group G close to a region containing a cluster of disease resistance genes including rhg1 and Rfs1 and may explain why MAS for resistance to F. solani with this marker had a high correspondence with phenotype. BLT65 maps to a region on Linkage Group A2 that contains Rhg4 but does not contain a QTL for resistance to F. solani. This may explain the low correspondence between MAS with this marker and infection severity phenotype. There was no evidence of epistatic interaction on infection severity between the two markers. One recombinant inbred line with the Flyer allele from both markers was found to have a resistant phenotype; this may have been a result of phenotype or genotype scoring errors or recombination between markers and genes.

Mean SCN index of parasitism was significantly lower (P = 0.046, [R.sup.2] = 16%) for the genotypes carrying the Hartwig allele for both Satt038 and BLT65 (Table 4). Although each of these markers identified regions associated with quantitative SCN resistance in crosses with plant introductions (Webb et al., 1995; Concibido et al., 1997), in this population both markers were required for effective recovery of SCN resistance. Satt038 alone was slightly effective in recovering SCN resistance, but BLT65 alone was not (Table 4). Satt038 had a significant mean square but BLT65 did not (Table 5). There was a significant interaction between Satt038 and BLT65.

Table 4. Soybean cyst nematode (SCN) race 3 index of parasitism (IP) means among 50 soybean recombinant inbred lines of Flyer (F) x Hartwig (H) within two DNA markers individually and combined.
Marker              Allele                P        [R.sup.2]

                                                   %
Satt038           H (46)([dagger])       0.076     6.4
                  F (54)
BLT65             H (42)                 0.64      0.4
                  F (58)
Satt038 & BLT65   HH (24)                0.046    16
                  HF (22)
                  FH (18)
                  FF (36)
                  LSD P = 0.055
                    ([double dagger])

                      Mean SCN IP
Marker                  [+ or -] SE

Satt038            47.2 [+ or -] 6.4
                   71.0 [+ or -] 8.5
BLT65              57.7 [+ or -] 7.5
                   63.9 [+ or -] 8.5
Satt038 & BLT65    32.0 [+ or -] 8.3
                   67.4 [+ or -] 8.0
                   85.7 [+ or -] 10.0
                   62.1 [+ or -] 12.1
                   26


([dagger]) Number in parentheses represents the number of values going into each mean.

([double dagger]) LSD is only for the four genotypes with both markers.

Table 5. Mean square (MS) values from analysis of variance on soybean cyst nematode race 3 index of parasitism among four genotypes of 50 recombinant inbred lines (RILs) from Flyer x Hartwig.
                               F-test
Source                   df   devisor            MS

Replication              1       7            3 182
Genotype                 3       7           11 428(*)
  Satt038 (contrast)     1       7           13 877(*)
  BLT65 (contrast)       1       7               73
  Satt038 X BLT65        1       7           20 335(**)
RILs (genotype)          46      7            3 963(*)
Error                    49                   2 117


(*), (**) Significant at the 0.05 and 0.01 levels of probability, respectively.

While 60% of the recombinant inbred lines within the genotypes carrying both chromosomal regions containing rhg1 and Rhg4 exhibited strong resistance (index of parasitism [is less than] 10%) to SCN race 3 among all the 10 replicates per recombinant inbred line tested, 25% were susceptible (index of parasitism [is less than] 32%), and 15% had a wide range of index of parasitism (0-157%) among replicates and were considered to be segregating for resistance to SCN race 3. Hence, the mean index of parasitism of the genotype was higher than expected (Table 4). One recombinant inbred line (F x H 35) predicted to be susceptible ([Satt038.sub.166], [BLT659.sub.960]) to SCN race 3 exhibited complete resistance (index of parasitism = 0), either indicating an error in scoring the markers and phenotypes or recombination between markers and genes.

Using an index of parasitism [is less than or equal to] 30% as the cutoff for resistance to SCN (Concibido et al., 1996; Mudge et al., 1997), the efficiency of marker-based selection of SCN race 3 resistance was 11% for Satt038 alone, 0% for BLT65 alone, and 67% when the Hartwig allele of both markers was present. Again, the low efficiency of MAS is largely due to phenotype scoring errors (20-30%) and recombination between markers and genes ([approximately equals] 5%).

Implications for Breeding Programs

Both [Satt038.sub.172] and [BLT65.sub.1160] were required for partial SCN resistance, suggesting bigenic inheritance requiring rhg1 from Linkage Group G and Rhg4 from Linkage Group A2 as detected with PI437654 x BSR101 data (Webb et al., 1995) and Essex x Forrest (Chang et al., 1997; Meksem et al., 1999).

We found Satt038 alone to be effective in selecting recombinant inbred lines with resistance to infection by F. solani. This resistance is likely to be derived from Forrest via the Rfsl gene that was previously identified (Meksem et al., 1999). The use of BLT65 in addition to Satt038 did not improve resistance to infection by F. solani. In the greenhouse, we have shown that recombinant inbred lines carrying [Satt038.sub.172] have significantly lower SDS leaf scorch (data not shown) following seedling infection by F. solani at low inoculum density (Njiti et al., 1997a). The recombinant inbred lines carrying the Hartwig allele at Satt038 and BLT65 will be enriched fourfold for dual resistance across a nonselected population.

These results provide a genetic basis for field data (Gibson et al., 1994) showing that cultivars derived from Hartwig and Forrest selected on the basis of the SCN phenotype reduce F. solani infection severity. Conversely, selection based on the SDS phenotype alone may not provide as high a protection level against SCN.

The DNA marker screening was accomplished in 60 person-hours at a cost of $1.50 per sample for reagents. Currently we need 40 to 50 person-hours per 1000 samples and $1.00 per sample for reagents. For SDS the cost of DNA marker selection ($1.00 per line, 6 person-minutes per line) compares favorably with field screening for disease index in multiple rows ($150.00 per line per row) or infection severity ($300.00 per line per row). Costs of screening for resistance to SCN are intermediate ($5.00 per line, 10 person-minutes per line) but seasonal greenhouse space is often not sufficient for soybean breeders.

Alleles of genes conferring partial resistance to SDS in Forrest appear to be present in Hartwig, as inferred from the closely linked (0-1 cM) microsatellite marker SIUC-SAT122 (Meksem et al., 1999). Flyer, being derived from Essex, is expected to be [approximately equals] 47% identical by descent to Essex. Hartwig, as a BC2 recovery from Forrest (Anand, 1992), is expected to be [approximately equals] 87% identical by descent to Forrest. Therefore, the Flyer x Hartwig population is expected to share [approximately equals] 67% of its genome with the Essex x Forrest population. This may account for the segregation of similar resistant QTL in the two populations. Given that the genomes of the mapping and breeding population differ in descent by [is greater than] 30%, and considering the broad-based nature of the soybean genome in Flyer, this QTL can function in multiple genetic backgrounds. The Flyer x Hartwig population, unlike the Essex x Forrest population, segregates for maturity; however, maturity group did not influence the effectiveness of the F. solani infection severity resistance QTL.

Abbreviations: cM, centimorgans; MAS, marker-assisted selection; SCN, soybean cyst nematode; SDS, sudden death syndrome; SIUC, Southern Illinois University at Carbondale; QTL, quantitative trait loci.

ACKNOWLEDGMENTS

The authors acknowledge Dr. Perry Cregan, USDA, Beltsville for the Satt038 primer sequence; Dr. Ben Matthews for the sequence of the BLT65 primers; and Tracy Doubler, Robert Suttner, Dustie Werner, and Arunima Das for laboratory and field work.

REFERENCES

Anand, S.C. 1992. Registration of `Hartwig' soybean. Crop Sci. 32:1069-1070.

Brim, C.A. 1966. Modified pedigree method of selection in soybeans. Crop Sci. 6:220.

Chang S.J.C., T.W. Doubler, V. Kilo, R.J. Suttner, J.H. Klein, M.E. Schmidt, P.T. Gibson, and D.A. Lightfoot. 1996. Two additional loci underlying durable field resistance to soybean sudden death syndrome (SDS). Crop Sci. 36:1624-1628.

Chang S.J.C., T.W. Doubler, V. Kilo, R.J. Suttner, M.E. Schmidt, P.T. Gibson, and D.A. Lightfoot. 1997. Association of field resistance to soybean sudden death syndrome (SDS) and cyst nematode (SCN). Crop Sci. 37:965-971.

Concibido, V., S. Boutin, R. Denny, R. Hautea, J. Off, and N.D. Young. 1997. Genome mapping of a soybean cyst nematode resistance genes in `Peking', PI 91763, and PI 88788 using DNA markers. Crop Sci. 37:258-264.

Concibido, V., S. Boutin, R. Denny, R. Hautea, J. Off, and N.D. Young. 1995. The soybean cyst nematode resistance gene on Linkage Group G is common among sources of resistance. Soybean Genet. Newsl. 22:269-272.

Concibido, V., N.D. Young, D.A. Lange, R.L. Denny, D. Danesh, and J.H. Off. 1996. Targeted comparative genome analysis and qualitative mapping of a major partial-resistance gene to the soybean nematode. Theor. Appl. Genet. 93:234-241.

Gibson, P.T., M.A. Shenaut, R.J. Suttner, V.N. Njiti, and O. Myers, Jr. 1994. Soybean varietal response to sudden death syndrome, p. 20-40. In D. Wilkinson (ed.) Proc. 24th Soybean Seed Res. Conf. Chicago, IL. 6-7 Dec. 1994. Amer. Seed Trade Assoc., Washington DC.

Gomez, A.K., and A.A. Gomez. 1984. Statistical procedures for agricultural research. 2nd ed. John Wiley & Sons, New York.

Gu, W.K., N.F. Weeden, J. Yu., D.H. Wallace. 1995. Large scale cost-effective screening of PCR products in marker-assisted selection application. Theor. Appl. Genet. 91:465-470.

Mahalingam, R., and H.T. Skorupska. 1995. DNA markers for resistance to Heterodera glycines I. race 3 in soybean cultivar Peking. Breeding Sci. 45:435-443.

Matthews, W.J., V.N. Njiti, P.T. Gibson, and M.A. Shenaut. 1991. Inheritance of soybean SDS response in segregating F5 and F6 derived lines. Soybean Genet. Newsl. 18:102-108.

McBlain, B.A., R.J. Fioritto, S.K. St. Martin, A. Calip-Dubois, A.F. Schmitthenner, R.L. Cooper, and R.J. Martin. 1990. Registration of Flyer soybean. Crop Sci. 30:425.

Meksem, K., T.W. Doubler, K. Meksem, V.N. Njiti, K. Chancharoenchai, P.E. Cregan, and D.A. Lightfoot. 1999. Separation of loci underlying resistance to SDS and SCN in near isogeneic lines. Theor. Appl. Genet. In press.

Mudge, J., P.B. Cregan, J.P. Kenworthy, J.H. Orf, and W.D. Young. 1997. Two microsatellite markers that flank the major soybean cyst nematode resistance locus. Crop Sci. 37:1611-1615.

Njiti, V.N., T.W. Doubler, R.J. Suttner, L.E. Gray, P.T. Gibson, and D.A. Lightfoot. 1998. Resistance to soybean sudden death syndrome and root colonization by Fusarium solani f. sp. glycines in near-isogenic lines. Crop Sci. 38:422-430.

Njiti, V.N., J.E. Johnson, G.A. Torto, L.E. Gray, and D.A. Lightfoot. 1997a. An effective greenhouse assays for field resistance to SDS. Soybean Genet. Newsl. 24:132-135.

Njiti, V.N., M.A. Shenaut, R.J. Suttner, M.E. Schmidt, and P.T. Gibson. 1996. Soybean reponse to soybean sudden death syndrome: Inheritance influenced by cyst nematode resistance in Pyramid x Douglas progenies. Crop Sci. 36:1165-1170.

Njiti, V.N., J.R. Suttner, L.E. Gray, P.T. Gibson, and D.A. Lightfoot. 1997b. Rate reducing resistance to Fusarium solani f. sp phaseoli underlies field resistance to soybean sudden death syndrome. Crop Sci. 37:132-138.

Prabhu, R.R., T.W. Doubler, S.J.C. Chang, and D.A. Lightfoot. 1997. Development and utility of sequence characterized amplified regions (SCARS) from RAPD markers linked to SDS and SCN QTLs. Soybean Genet. Newsl. 24:128-131.

Roy, K.W. 1997. Fusarium solani on soybean roots: Nomenclature of the causal agent of sudden death syndrome and indentity and relevance of F. solani form B. Plant Dis. 81:259-266.

Rupe, J.C. 1989. Frequency and pathogenicity of Fusarium solani recovered from soybeans with sudden death syndrome. Plant Dis. 73:581-584.

Rupe, J.C., W.E. Sabbe, R.T. Robbins, and E.E. Gbur. 1993. Soil and plant factors associated with sudden death syndrome of soybean. J. Prod. Agric. 6:218-221.

Staub, J.E., F.C. Serquen, and M. Gupta. 1996. Genetic markers, map construction, and their application in plant breeding. HortScience 31:729-740.

Webb, D.M., B.M. Baltazar, A.P. Rao-Arelli, J. Schupp, K. Clayton, P. Keim, and W.D. Beavis. 1995. Genetic mapping of soybean cystnematode race-3 resistance loci in soybean PI 437.654. Theor. Appl. Genet. 91:574-581.

Weisemann, J.M., B.F. Mathews, and T.E. Devine. 1992. Molecular markers located proximal to the soybean cyst nematode resistance gene Rhg4. Theor. Appl. Genet. 85:136-138.

Wrather, J.A., T.R. Anderson, D.M. Arsyad, J. Gai, D.L. Ploper, A. Porta-Puglia, H.H. Ram, and J.T. Yorinori. 1996. Soybean disease loss estimates for the top ten producing countries during 1994. Plant Dis. 81:107-110

Wrather, J.A., A.Y. Chambers, J.A. Fox, W.F. Moore, and G.L. Sciumbato. 1995. Soybean disease loss estimates for southern United States, 1974 to 1994. Plant Dis. 79:1076-1079.

R. R. Prabhu, V. N. Njiti, B. Bell-Johnson, J. E. Johnson, M. E. Schmidt, J. H. Klein, and D. A. Lightfoot(*)

Dep. of Plant Soil and General Agriculture, Center for Excellence in Soybean Research, Teaching and Outreach, Southern Illinois University, Carbondale, IL62901. Received22 June 1998. (*) Corresponding author (ga4082@siu.edu).

Published in Crop Sci. 39:982-987 (1999).
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Author:Prabhu, R.R.; Njiti, V.N.; Bell-Johnson, B.; Johnson, J.E.; Schmidt, M.E.; Klein, J.H.; Lightfoot, D
Publication:Crop Science
Article Type:Statistical Data Included
Geographic Code:1USA
Date:Jul 1, 1999
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