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Crop Science 43:850-857 (2003)
© 2003 Crop Science Society of America

CROP BREEDING, GENETICS & CYTOLOGY

Quantitative Trait Loci Conditioning Resistance to Fusarium Head Blight in Wheat Line F201R

Xiaorong Shena, Mariana Ittub and Herbert W. Ohm*,a

a Department of Agronomy, 1150 Lilly Hall, Purdue University, West Lafayette, IN 47907-1150, USA
b Institute for Cereals and Industrial Crops-Fundulea, Academy of Agricultural and Forestry Science, Romania

* Corresponding author (hohm{at}purdue.edu)


   ABSTRACT
TOP
 NOTES
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Fusarium head blight (FHB) of wheat (Triticum aestivum L.) is a devastating disease in wheat production worldwide. Identifying resistance genes and understanding the genetic basis of resistance to FHB are prerequisites to developing cultivars that can avoid losses from FHB. This investigation of quantitative trait loci (QTL) was performed in a recombinant inbred (RI) population derived from a cross between the FHB-moderately susceptible cv. Patterson and the FHB-resistant line Fundulea 201R (F201R). Bulk DNAs from the 11 most resistant and 12 most susceptible lines of the phenotypic distribution of the RI population, together with the parental lines, were screened with simple sequence repeat (SSR) markers. Regional QTL mapping identified four interval regions, located on chromosomes 1B, 3A, 3D, and 5A, that conferred resistance to FHB. The QTLs located on chromosomes 1B and 3A, contributed by F201R, had large effects and were consistently expressed in three environments. The four QTLs together accounted for 32.7% of the phenotypic variation, or 43.0% of the genotypic variation. The QTL on chromosome 3A is located in the same region as a QTL that was detected in wild tetraploid wheat T. dicoccoides (Koern. ex Asch. & Graebner) Aarons. The possibility that the FHB resistance QTLs of F201R and that of T. dicoccoides on chromosome 3A have the same origin is discussed.

Abbreviations: FHB, Fusarium head blight • QTL, quantitative trait loci • SSR, simple sequence repeat • PCR, polymerase chain reaction • MAS, marker-assisted selection • LOD, logarithm of the odds


   INTRODUCTION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
WHEAT IS A STAPLE FOOD CROP in the USA and worldwide. In the past decade, there have been epidemics of FHB in many areas where the flowering period coincides with warm and wet weather. FHB is caused by several fungi in the genus Fusarium. In North America and Asia, F. graminearum Schwabe (telemorph Gibberella zeae) is the predominant causal agent. The primary loss from FHB is reduced yield. In addition, FHB damage is manifested as lowered grain quality, such as shriveled kernels, contamination with mycotoxins, and reduction in seed quality (McMullen et al., 1997). One approach to reduce severity of FHB in the field is the use of fungicides, but the effectiveness of fungicides has been variable (McMullen et al., 1997). Considering cost and environmental concerns, it is important to minimize application of chemicals; and resistant wheat cultivars will be an essential component of a disease management strategy.

Resistance to FHB in wheat has been identified, mainly from three gene pools: winter wheats from Eastern Europe; spring wheats from China and Japan; and Brazil (Miedaner, 1997). Exotic resistant sources are also identified in T. dicoccoides (Stack et al., 2002; Otto et al., 2002), Roegneria kamoji (Ohwi) Ohwi ex Keng (Liu et al., 2000), R. ciliaris (Trin.) Nevski, Leymus racemosus (Lam.) Tzvel (Chen and Liu, 2000). Studies of the inheritance of FHB resistance have shown that it is a complex trait conditioned by oligo- or multiple genes (Bai and Shaner, 1994; Van Ginkel et al., 1996; Singh et al., 1995; Ban and Suenage, 2000). Complete resistance in wheat has not been reported to date. The goal of conventional breeding for FHB resistance is to pyramid resistance genes from various gene pools to increase the resistance level. However, frequently one is not certain which FHB resistance gene(s) have been integrated into breeding lines. In addition, disease evaluation is problematic because of large effects of environment on disease establishment and development after infection. In the field, some lines may escape infection if they flower during a dry or cool period, whereas lines that flower during wet and warm weather may be severely infected. Molecular markers offer the opportunity to select specific genotypes to increase selection efficiency.

Mapping efforts to date have identified a major gene on chromosome 3BS in the Chinese wheat line Sumai 3 and its derivatives (Waldron et al., 1999; Anderson et al., 2001; Buerstmayr et al., 2002; Zhou et al., 2002). This QTL can explain up to 60% of the phenotypic variation (Buerstmayr et al., 2002). Wild tetraploid wheat T. dicoccoides is also identified to possess a major resistance QTL on chromosome 3A (Otto et al., 2002), which accounted for 37% of the phenotypic variation or 55% of the genotypic variation. Reports on gene mapping aimed at FHB resistance in European wheat germplasm are few, though they are thought to be important resistance sources (Miedaner, 1997). Here we report our mapping results from a Romanian winter wheat cultivar Fundulea 201R (F201R) which was reported as having FHB resistance genes derived from cultivars NS 732 and Amigo and having no relation to any of the previously described sources of resistance (Ittu et al., 2001b). The mapping of QTLs involved in the FHB resistance in F201R would enable us to discover new genes. The objective of this study is to determine the chromosomal location of the QTLs and to identify useful molecular markers to complement phenotypic selection.


   MATERIALS AND METHODS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Plant Materials
A population consisting of 318 recombinant inbred lines (RILs) derived from the cross of cv. Patterson x Fundulea 201R was developed by single-seed descent. Patterson (Ohm et al., 1998) is moderately susceptible to FHB. The FHB resistant wheat line F201R was developed by the wheat breeding team from the Research Institute for Cereals and Industrial Crops- Fundulea (Romania). This line is a result of a special program aimed to accumulate resistance genes of various origins from the cross F156I5-2112 x F2076W12-11, with no parental relationship with Chinese lines (Ittu et al., 1998, 2001a).

Disease evaluations of the 318 RILs were performed in F4:5 and F5:6 generations in a greenhouse at Purdue University in fall 2000 and spring 2001. A subset of 118 random RILs (F6:7) was tested for a third time in the greenhouse in fall 2001. The two parental lines were included in each experiment as checks. The F1 hybrid was included in the third experiment. In each of the three experiments, 10 to 12 plants per line were inoculated and evaluated for type II resistance, which is the resistance to fungal spread after inoculation (Schroeder and Christensen, 1963).

Disease Evaluation Procedure
The point inoculation technique was used in our study. Inoculum was produced in a mung bean soup culture of a local isolate of F. graminearum that was provided by Dr. Gregory Shaner, Department of Botany and Plant Pathology, Purdue University. Ten microliters of inoculum, containing 500 to 1000 conidia spores, were placed into a basal floret of the third or fourth spikelet from the tip of primary spikes at anthesis. The inoculated plants were immediately placed under a fine mist environment for 4 d, during which plants were misted for 3 min every 30 min. Then they were transferred to an area of the greenhouse away from the mist but with high humidity and at 22 to 27°C. All plants were randomly placed on the greenhouse benches. The number of discolored spikelets and the total number of spikelets below and including the inoculation point was recorded at 20 d after inoculation. Disease severity was defined as (number of diseased spikelets/number of total spikelets) x 100%.

SSR Assay
DNA samples were prepared from F7 seedlings of each RIL according to previously described protocols (Saghai-Maroof et al., 1984). Bulked segregant analysis (Michelmore et al., 1991) was used in this study. Equal amounts of DNA from the 11 most stably resistant lines and the 12 most susceptible lines were pooled, respectively, to construct the resistant and susceptible bulks. Sequence information of the SSR primers was made available from Röder et al. (1998), Pestsova et al. (2000), and by P. Cregan, USDA-ARS, Beltsville, MD (by request). A total of 293 SSR primer pairs were screened on the parents and the bulks. PCR conditions were as follows: 1x buffer, 1.5 mM MgCl2, 2.0 mM dNTPs, 250 µM oligonucleotide primers, 40 ng DNA, and 1 u Taq polymerase in a 25-µL reaction volume. The reaction mixtures were denatured at 94°C for 2 min, followed by 35 cycles consisting of 94°C for 30 s, 55°C (or 60°C) for 40 s, 72°C for 1 min, and a final extension at 72°C for 7 min. DNA products were resolved on 3% (w/v) Metaphor agarose gels (Cambrex Corporation, East Rutherford, NJ).

Polymorphic markers between the bulks were confirmed by genotyping the individuals from each bulk. If significant marker-trait association was inferred with a F test (P < 0.01), the whole population was genotyped.

Gliadin Analysis
The 1B·1R translocation of F201R was identified with gliadin analysis. To detect the gliadin spectrum of F201R, a starch-gel electrophoresis was performed by the method described by Sozinov and Poperelya (1980).

Statistical Analysis
The disease evaluation experiments were arranged in a completely randomized design. Analysis of variance (GLM program, SAS Institute, 1999) was performed to calculate the mean disease severity for each RIL and mean square of each variable. Both RIL and Experiment were random effects. Since data were not balanced (some plants died after transplanting), "proc varcomp" was used to estimate variance components. Broad sense heritability based on entry mean was calculated by the following formula:

where {sigma}2g is the genetic variance component among the RILs, {sigma}2g is the environment (among experiments) variance component, {sigma}2gxe is the environment x genetic variance component, r is the number of experiments, and n is the average number of plants tested per line per experiment. Marker-trait association was initially tested by one-way analysis of variance. If the P value was smaller than 0.05, additional markers in that region were tested. A regional genetic map was constructed by Mapmaker/Exp 3.0b. The Kosambi map function was used to estimate the distance between markers. Composite interval mapping (Zeng, 1993, 1994) was performed to locate the position of QTLs by means of QTL Cartographer. Significance threshold was determined by a 1000-permutation test (Doerge and Churchill, 1996) in the software. Percentage of diseased spikelets was the basic measurement for QTL mapping. To compare the effect of different disease measurements on the detection of QTL, the number of diseased spikelets, instead of the percentage, was also used for QTL mapping. The SAS program "PROC GLM" and "PROC REG" were used to test the interaction of multiple loci and estimate the joint effects of these loci. Genetic variance explained by the markers was calculated as R2markers/H2 x 100%.


   RESULTS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Response of Two Parental Lines and Their F1 Hybrid
The two parents, Patterson and F201R, consistently displayed significant difference in response to F. graminearum infection in the three evaluations in the greenhouse. F201R had a high level of resistance. In most cases, only the inoculated spikelet became diseased, though two plants in the spring of 2001 had 50% disease severity. Averaged over the three tests, mean disease severity of F201R and Patterson was 15.3 and 63.5%, respectively (P < 0.001). Mean disease severity of the F1 hybrid in experiment three was 38.4%, and was not significantly different from the midparent value. This indicated that the overall effect of gene action is additive.

Segregation of RI Lines
The 318 RILs showed significant variation for disease severity in Fall 2000 and Spring 2001. Likewise, the random 118 lines displayed significant variation in Fall 2001. The population mean did not significantly deviate from the midparent value and F1 mean. The frequency distribution of mean disease severity of the RILs was nearly normal in all experiments. Mean disease severity across the first two experiments ranged from 11.0 to 84.1% with an overall population mean of 41.8% (Fig. 1). No line was more resistant than F201R on the basis of the least significant difference (LSD0.05 = 20.1%). However, there were four lines with higher mean disease severity than Patterson.



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  		Fig. 1. Frequency distribution of FHB severity in wheat RI population PattersonxF201R. Data averaged over two tests.

 
An analysis of variance showed that variation among RILs was significant (F = 2.73, P < 0.0001). Variation due to different environment (experiments) and RIL x environment interaction was also significant. Broad sense heritability was estimated to be 0.76 on the basis of entry means.

Consistency of Disease Evaluation
Environment had a significant impact on disease progress, as revealed by analysis of variance. Ranks of lines varied between the first two experiments, in which the entire RI population was evaluated. However, the correlation coefficients among three experiments were significantly different from zero, as follows: 0.41 between Exp.1 and Exp.2, P < 0.001; 0.46 between Exp. 1 and Exp. 3, P < 0.001; 0.52 between Exp. 2 and Exp. 3, P < 0.001. Among the top 60 resistant lines whose disease severity was less than 20% in Exp. 1, 11 lines had consistent low disease severity in Exp. 2. At the susceptible tail, 12 lines were identified to be consistently more susceptible than Patterson in the two experiments. These lines were used to construct the resistant and susceptible bulks for DNA analysis.

Bulked Segregant Analysis
DNA was pooled from the 11 resistant and 12 susceptible RILs described above. Of the 293 SSR primer pairs screened, 14 pairs amplified polymorphic DNA bands between the two bulks (Fig. 2). Significant marker-trait association was suggested for each of these 14 markers by genotyping individuals in the two bulks, analyzed by one-way analysis of variance. However, after genotyping the whole population, only 13 markers retained significance at the {alpha} = 0.05 (Table 1).



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  		Fig. 2. Gel electrophoresis showing the polymorphisms between the wheat parents Patterson and F201R and R and S bulks from an RI population derived from a cross between these parents. M is the 20-base pair ladder.

 

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  		Table 1. One-way ANOVA for markers that are potentially linked to FHB resistance in a recombinant inbred wheat population derived from Patterson x F201R.

 
QTL Mapping
On the basis of the published wheat SSR map (Röder et al., 1998; Pestsova et al., 2000) and an unpublished map provided by R. Ward (personal communication), all available polymorphic markers surrounding the chromosomal regions that had potential QTLs were genotyped in the RILs. A total of 19 markers were grouped and ordered by Mapmaker/Exp 3.0b. There were nine, three, three, and four SSR markers in each linkage group (Fig. 3), belonging to 1B, 3A, 3D, and 5A chromosomes. Six markers, five of which were dominantly inherited, were closely linked in a 3.2-centimorgan (cM) region in chromosome 1B. All six markers showed segregation distortion ({chi}2 values ranged from 25.0 to 36.1, P < 0.0001). Gliadin analysis showed that F201R is a carrier of the Sec-1 (Gli-R1) allele (McIntosh et al.,1993, 1998) that replaces the wheat Gli-B1 allele, indicating presence of the 1BL·1RS translocation. This translocation was also detected in its direct seed parent, F156-I5-2112. Pedigree analysis suggests that 201R inherited this translocation from the line Aura, which in its genealogy has the Russian cultivar Aurora, carrier of 1BL·1RS. The presence of the translocation may explain the segregation distortion in this chromosome region.



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  		Fig. 3. Linkage map for Fusarium head blight resistance QTL in the wheat cross Patterson x F201R.

 
Since the six SSR markers in chromosome 1B are closely linked, only the codominant marker Xbarc8 was used in QTL mapping to avoid colinearity, which has the potential to inflate the effect of the QTL. Composite interval mapping, with the complete data set of 318 RI lines averaged over the two experiments, and the subset of 118 lines averaged over the three experiments, generated two major peaks that exceeded the logarithm of odds (LOD) threshold, suggesting linkage of the markers with FHB resistance. They were located on chromosomes 1B and 3A (Table 2). The QTL near the centromere of 1B was located between the interval of Xbarc8 (1BS) and Xgwm131 (1BL). It accounted for 18.7% of the phenotypic variation for FHB resistance (LOD score 12.4). The QTL is about 4.0 cM from Xbarc8, and 10.6 cM from Xgwm131. The second QTL was located on the short arm of chromosome 3A, also near the centromere. It was tightly linked to markers Xgwm674 and Xbarc67, which are 2.8 cM apart. This QTL explains 13.0% of the phenotypic variation, with a LOD score of 10.6. RILs with favorable alleles on 1B and 3A had a mean disease severity of 26.8%, while RILs with both unfavorable alleles had a mean disease severity of 50.6%. The effects of the 1B and 3A QTLs were similar as RILs with only one of the two favorable alleles had the same disease severity (Fig. 4).


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  		Table 2. Summary of QTLs for FHB resistance detected by composite interval mapping in the wheat population Patterson x F201R.

 


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  		Fig. 4. Fusarium head blight severity for genotypes with the two major resistance QTLs in the wheat cross Patterson x F201R. AA: F201R allele at Xbarc8 (1B); aa: Patterson allele at Xbarc8 (1B); BB: F201R allele at Xgwm674 (3A); bb: Patterson allele at Xgwm674 (3A).

 
Two additional minor QTLs were detected with the 318-line data set (Table 2). One is located near the centromere of 3D, the other one is near the end of the short arm of 5A. The QTL on 3D, represented by the marker Xgwm341, was contributed by the moderately susceptible parent Patterson. The LOD score of the two minor QTLs were 2.06 and 1.91. They explained 2.2% and 2.1% of phenotypic variation, respectively.

The QTLs on 1B and 3A were consistently detected in all three experiments, while the two minor QTLs were only detected in one or two of the experiments (data not shown). The effects of the two major QTLs, on 1B and 3A, were sufficiently large that they were detected with the subset of 118 random RILs in each of the three experiments and when data were combined across all three tests. Neither of the minor QTLs was detected with the subset data (Table 2). These results emphasize the importance of large population size for detection of QTLs with small effects.

QTL mapping results based on number of diseased spikelets produced results similar to those obtained from percentage of diseased spikelets (data not shown). This is expected because in this study, the correlation coefficient was 0.95 between number of diseased spikelets and percentage of diseased spikelets.

Multiple Regression of the Four Loci on FHB Resistance
Four-way ANOVA, based on the four closest markers revealed by composite interval mapping in each chromosome region, was performed to evaluate the interaction among the four QTLs. There was no indication of interaction between any of the two loci (P-values ranged from 0.25 to 0.73). Thus, these four loci acted independently from each other. Multiple regression of the four loci on FHB severity showed that the favorable alleles on 1B, 3A, 3D, and 5A decreased disease severity by 11.2, 10.6, 5.2, and 4.9%, respectively (Table 3). The QTL on 3D was in cv. Patterson's allele, explaining the transgressive segregation at the susceptible tail of the phenotypic distribution. The four loci collectively explain 32.7% of the phenotypic variation. Given the broad sense heritability 0.76, they account for 43% of the genotypic variation.


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  		Table 3. Multiple regression of four marker loci on FHB disease severity (R2 = 0.327) in the wheat cross Patterson x F201R.

 

   DISCUSSION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Expression of resistance to Fusarium head blight of wheat is complex. It has been proposed that there are at least five components of FHB resistance (Mesterhazy, 1995). Several traits were used to evaluate FHB resistance in some studies, including incidence, visual rating, deoxynivalenol (DON) content, relative yield, and diseased kernels. Correlation among these traits is high in some studies (Buerstmayr et al., 1999; Bai et al., 2001; Miedaner et al., 2001). Molecular mapping has shown that a QTL conditioning low DON accumulation is located at the same region as a gene controlling disease spread, measured as percentage of diseased spikelets or area under the disease progress curve (Bai et al., 2000). It is not known if they are pleiotropic or linked. However, other research showed that the association among these FHB-resistant traits is low, especially in the field conditions (Mesterhazy et al., 1999). This is probably due to the environmental variation or different mechanisms underlying different FHB-resistant expression. Looking at traits other than disease severity may facilitate identifying additional QTLs involved in the FHB resistance.

The phenotypic survey of the 318 RILs, derived from the cross of Patterson x F201R, did not display a bimodal distribution which indicates a major QTL controlling FHB resistance, as reported by Bai et al. (1999), Waldron et al. (1999), and Buerstmayr et al. (2002). In our study, the distribution of the mean disease severity of the RILs was normal with transgressive segregation toward the susceptible tail, suggesting polygenic inheritance. The mode of inheritance appeared additive on the basis of the performance of F1 hybrid. Bulked segregant analysis, coupled with QTL mapping with SSR markers at known chromosomal locations, suggested four QTLs in this population. The QTLs on 1B and 3A had larger effects and were consistently expressed in all environments and in a small population, while QTLs on 3D and 5A had minor effects and were detected in only certain environments and on large population size.

The six markers that are associated with the FHB resistance QTL on 1B were closely linked. All of them are distal to the 1B QTL. Severe segregation distortion was observed with these markers. Segregation distortion has been proposed to be associated with the gametophyte gene (ga) conferring reduced pollen competitiveness (Nakagahra et al., 1972), or as a result of a cross between distantly related species. Considering that the 1BL·1RS translocation is common in European wheat germplasm, and F201R was developed from a complex cross, we conducted starch-gel electrophoresis to examine the spectrum of gliadin proteins and found that F201R carries the rye secalin (sec-1 locus) indicative of the 1BL·1RS translocation. However, recombination was observed between these six markers, indicating that the break-point of the translocation is distal to the markers. The distance between the FHB resistance QTL and Xbarc8 was estimated to be 4.0 cM, on the basis of the distance between the peak LOD score position and Xbarc8. Marker Xgwm131, which is on 1BL, is 10.6 cM on the other side of the QTL. We were not able to determine if the FHB resistance gene is on 1BS or 1BL. The centromere region of 1B is a gene-rich region, containing Yr15, YrH52 (Peng et al., 1999), and GliB. In an association study of FHB resistance with protein markers, Ittu et al. (2000) found that a significant increase in FHB resistance was associated with the allele sec-1 in cv. Sincron. However, they also found overlapping distribution of FHB resistance for RILs with alternative alleles at the Gli-B1 locus, suggesting that the QTL for FHB resistance may not be on the translocated rye chromosome arm 1RS, but linked to it; i.e., in the 1B region of the 1BL·1RS chromosome. In our experience, the 1B·1R translocation is not associated with FHB resistance because a high percentage of susceptibility is found in those translocation lines. Our molecular evidence in this study also suggests that the resistance QTL is outside of the translocated 1R chromosome segment. In another QTL mapping study with the CIMMYT line CM-82036 as resistance source, Buerstmayr et al. (2002) detected a minor FHB resistance QTL on 1B, tagged by a protein marker from Glu-B1. In their research, the major gene, which was derived from Sumai 3, accounted for a large proportion of the phenotypic variation. These results together with ours provide some evidence that there is probably a common locus on 1B for FHB resistance. However, the effect of this FHB resistance QTL may vary in different genetic backgrounds.

It is interesting to note that the second QTL in the resistant parent F201R is near the centromere of 3AS, similar to the location of the FHB resistance QTL derived from the wild tetraploid wheat T. dicoccoides (Otto et al., 2002). That QTL, designated as Qfhs.ndsu-3AS, was mapped near Xgwm2. The distance between Xgwm2 and Xgwm674 is 19.0 cM on their map. In our population, the QTL was closer to Xgwm674 than to Xgwm2, and the distance between the two markers was 8.3 cM (Fig. 3). Although we have no evidence that the 3A QTL in F201R is allelic to Qfhs.ndsu-3AS, we cannot exclude the possibility that they have the same origin. In tomato, the resistance gene to Pseudomonas syringae pv. tomato in two wild species, Lycopersicon pimpinellifolium (Jusl.) Mill. and L. hirsutum var. glabratum Mill., were mapped at the same locus. Subsequent gene cloning and sequence characterization showed that the resistance gene Pto in the two species shared 97% nucleotide identity, indicating that the specificity of the Pto gene for the Pseudomonas AvrPto protein evolved before the divergence of L. hirsutum and L. pimpinellifolium (Riely and Martin, 2001). Comparative mapping often reveals synteny across related species. Thus, the 3A QTL in F201R and in T. dicoccoides could be derived from an ancient gene for FHB resistance.

Chromosomes 3D and 5A are statistically significant for potential QTLs, although the effects are small. Wheat chromosome 5A has been reported to carry a type II resistance gene (Buerstmayr et al., 1999, 2002) as well as a type I resistance gene (Xu et al., 2001), but they were in different chromosomal regions based on corresponding marker positions. The 3D QTL is located near the centromere of 3D, a homeologous region of the 3A QTL. One can postulate that they may be orthologous, after millions of years of evolution the 3A QTL still has a large effect, while the 3D QTL lost some of its effect. This is also a possible interpretation for the relationship between the 3A QTL in F201R and in T. dicoccoides.

The four QTLs in this study accounted for 32.7% of the total phenotypic variation in this population. Given the heritability of 0.76, they explain 43.0% of the genotypic variation. Other QTLs probably remain undetected. There could be two factors attributable to undetected QTLs: (i) low coverage of chromosomes with the currently available SSR markers; and (ii) the lack of power to detect epistasis with our methodology. To explore epistasis between two loci, a comprehensive mapping study is needed.

Several quantitative trait loci for FHB resistance have been mapped in different wheat populations (reviewed by Kolb et al., 2001). The resistance QTL with the largest effect is located in the distal region of 3BS, and its effect appears to be consistant in different genetic backgrounds. The SSR markers associated with 3BS QTL in Sumai 3 are also polymorphic between the two parents in this population, but no linkage relationship with FHB resistance is suggested by one-way analysis of variance. The band patterns in F201R are also different from those in Sumai 3 (data not shown). This excludes the existence of the 3BS QTL in F201R. Our study indicates that genetic diversity for FHB resistance exists in wheat. The genetic basis of FHB resistance in F201R is different from that in Chinese lines. Therefore, it should be possible to pyramid different genes to elevate the effectiveness of the FHB resistance. SSR markers closely linked to those QTLs enable wheat breeders to pyramid different resistance genes with marker-assisted selection (MAS), to possibly achieve more effective FHB resistance. Increased effectiveness of FHB resistance by pyramiding more than one FHB resistance genes is already amply demonstrated in wheat cultivar Sumai 3 compared with levels of FHB resistance of its parental lines (Bai and Shaner, 1994). Also, we have developed lines from Ning 7840, each with one or another FHB resistance gene (unpublished). All of these lines with only one of the FHB resistance genes of Ning 7840 have FHB resistance that is less effective than that of Ning 7840.


   ACKNOWLEDGMENTS
 
Partial support for this research was provided by the U.S. Wheat and Barley Scab Initiative, USDA/ARS, Award No. 59-0790-9-057 to H. Ohm. We thank Marion S. Röder (Institut für Pflanzengenetik und Kulturpflanzenforschung (IPK), 06466 Gatersleben, Germany) and Perry Cregan (Soybean Genomics and Improvement Laboratory, USDA, ARS, Beltsville Agriculture Research Center, Beltsville, MD 20705) for making SSR primer sequences available; and Richard Ward (Department of Crop and Soil Science, Michigan State University, East Lansing, MI 48824) for mapping information for the BARC SSR markers.


   NOTES
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 NOTES
ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Contribution from Purdue Univ., Agric. Res. Programs as Journal Article No. 16838.

Received for publication July 15, 2002.


   REFERENCES
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 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
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 DISCUSSION
 REFERENCES
 




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The SCI Journals Agronomy Journal Vadose Zone Journal
Journal of Plant Registrations Soil Science Society of America Journal
Journal of Natural Resources
and Life Sciences Education		 Journal of
Environmental Quality