HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Figures Only Full Text (PDF) Free Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (56) Citing Articles via Google Scholar Google Scholar Articles by Kolb, F.L. Articles by Fedak, G. Search for Related Content PubMed Articles by Kolb, F.L. Articles by Fedak, G. Agricola Articles by Kolb, F.L. Articles by Fedak, G. Related Collections Crop Genetics Plant Disease

SYMPOSIUM ON GENETIC SOLUTIONS TO FUSARIUM HEAD BLIGHT IN WHEAT AND BARLEY

Host Plant Resistance Genes for Fusarium Head Blight

Mapping and Manipulation with Molecular Markers

^a Dep. of Crop Sciences, Univ. of Illinois, 1102 S. Goodwin Ave., Urbana, IL 61801
^b Oklahoma State Univ., Dep. of Plant and Soil Sciences, Stillwater, OK 74078
^c Dep. of Agronomy and Plant Genetics, Borlaug Hall, Univ. of Minnesota, St. Paul, MN 55108
^d Agriculture and Agri-Food Canada, Bldg. 50, Central Experimental Farm, Ottawa ON, Canada K1A OC6

* Corresponding author (f-kolb{at}uiuc.edu)

	ABSTRACT

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 
Fusarium head blight (FHB), caused by Fusarium graminearum Schwabe [teleomorph Gibberella zeae (Schwein.)], or scab, causes severe reductions in yield and quality of wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.). Evaluation of FHB resistance is laborious and subject to environmental influence; therefore, molecular markers for FHB resistance genes will greatly enhance selection for FHB resistance. This review seeks to summarize information on molecular markers associated with quantitative trait loci (QTL) for resistance to FHB in wheat and barley and the use of those markers for marker assisted selection. Our goal is to summarize the current state of knowledge on the genetics of FHB resistance, the map locations of QTL for FHB resistance, and the future directions and potential applications of this research. In wheat, five types of resistance have been described, and Type II resistance (expressed in Chinese wheat cultivar Sumai 3) is the easiest type to assess. Several research groups are developing molecular markers associated with genes for FHB resistance from Sumai 3, a widely used source of Type II resistance in wheat breeding programs worldwide. In four different populations, each having Sumai 3 or a derivative as one parent, one to four QTL have been identified that explain up to 63% of the variation in resistance. QTL were identified on chromosomes 3BS and 6BL in three or more populations. Recently, in barley, restriction fragment length polymorphism (RFLP) markers associated with genes for FHB resistance, deoxynivalenol (DON) accumulation, and kernel discoloration were identified on all seven chromosomes. Three regions, located on chromosomes 2, 3, and 5 were identified in several mapping populations. Comparing the QTL locations between wheat and barley shows that the barley chromosome 3 QTL is located in a syntenous region in wheat. The following areas of research on molecular markers associated with FHB resistance should be emphasized: (i) identifying and mapping better resistance sources in wheat and barley; (ii) validating QTL in additional populations; and (iii) developing markers that can be easily used in breeding programs and across populations.

Abbreviations: AFLP, amplified fragment length polymorphism • cM, centimorgan • FHB, Fusarium head blight • QTL, quantitative trait locus (or loci) • RAPD, random amplified polymorphic DNA • RFLP, restriction fragment length polymorphism • RIL, recombinant inbred line • SNP, single nucleotide polymorphism • SSR, single sequence repeat (or microsatellite) • STS, sequence tagged site

	INTRODUCTION

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 
FUSARIUM HEAD BLIGHT, a widespread and destructive disease of wheat and barley, significantly reduces yield and quality. FHB is caused by several Fusarium species, but in the USA, FHB is caused primarily by Fusarium graminearum Schwabe [teleomorph = Gibberella zeae (Schwein.) Petch; synonym = G. saubinatti]. FHB causes significant economic losses in many wheat and barley producing regions throughout the world, and host-plant resistance is important in reducing losses due to FHB (Bai and Shaner, 1994; McMullen et al., 1997; Steffenson, 1998). Schroeder and Christensen (1963) reviewed early research on FHB resistance, and differences in cultivar resistance to FHB were identified many years ago (Bai and Shaner, 1994; Immer and Christensen, 1943). Bai and Shaner (1994) stated that Arthur first described differences in susceptibility to FHB among wheat cultivars in 1891. Phenotypic evaluation of FHB resistance requires significant time and resources (Bai and Shaner, 1994; Rudd et al., 2001; Campbell and Lipps, 1998), and the environment greatly influences expression of FHB resistance. Genotype x environment interaction further complicates the phenotypic evaluation of FHB resistance (Bai and Shaner, 1994; Groth et al., 1999). An important research objective is development of the capability to use molecular markers routinely to screen experimental breeding lines for FHB resistance. To be most effective for marker assisted selection, the markers should provide a rapid means of determining which breeding lines in a population carry alleles for FHB resistance.

To reach this major objective, several steps need to be accomplished. The first step is to identify the major QTL for FHB resistance and locate them to chromosomes. The second step is to confirm the magnitude and map position of the QTL. Markers can be used for selection without knowing their locations; however, to enhance our understanding of the genetics of resistance and to aid in finding better markers than those currently available, the locations of the QTL should be determined. The third step is to identify markers that are closely linked and flanking the QTL. While flanking markers require breeders to work with more markers, they are helpful in minimizing selection of lines in which recombination has occurred between the marker and the QTL. In addition, flanking markers greatly improve the efficiency of a backcrossing procedure (Young and Tanksley, 1989). Finally, to be most efficient, "user-friendly" markers should be developed.

This review seeks to describe the current literature and research on the use of molecular markers for QTL associated with resistance to FHB in wheat and barley. Our goal is to provide the current state of knowledge on the genetics of FHB resistance, the map locations of QTL for FHB resistance, the future directions of this research, and the potential applications.

	Nature of the Inheritance of Resistance to FHB

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 
The expression of resistance to FHB in wheat and barley is complex. Five types of resistance have been proposed in wheat (Mesterhäzy, 1995). Type II resistance in wheat (resistance to spread of the fungus in the head) has been investigated more extensively than other types of resistance. In barley, two of the fives types have been described: Type I (resistance to initial infection) and Type II (resistance to spread of disease in the head). Most wheat breeding efforts have concentrated on Type II resistance, whereas in barley the emphasis has been on Type I resistance derived from diverse sources (Buerstmayr et al., 1999; Rudd et al. 2001). Many resistant sources being used in wheat trace back to the Chinese cultivar, Sumai 3. The expression of the disease, as well as the consequences of infection, also differ in wheat and barley. In barley, particularly malting barley, the primary concern is the accumulation of the mycotoxin deoxynivalenol (DON). Accumulation of mycotoxin is also a concern in wheat, but reductions in yield and test weight are also major concerns. Resistance to accumulation of DON would be very desirable, particularly in barley, but to date there is little evidence for it. Type II resistance has been identified in barley (Zhu et al, 1999), but its value is not clear (Capettini, 1999).

A critical factor that has confounded the attempts to quantify resistance and select for resistant genotypes is the correlation of resistance to other traits associated with inflorescence morphology. This has been particularly true in barley. By means of near-isogenic lines, traits such as late heading, tall plant height, lax spike, hulless kernel, and two-row spike have been associated with resistance (Steffenson et al., 1996). One concern is that the expression of these other traits can interfere with the accurate measurement of resistance. In addition, these traits may result in apparent resistance by increasing the probability that the host escapes infection by the pathogen rather than reducing disease by a physiological defense response in the host. Furthermore, if the trait correlated with resistance is undesirable (e.g., tall, lodging-susceptible plants), then it will be necessary to determine if the correlation is due to pleiotropy or tight linkage.

The complex expression of resistance to FHB is further reflected in its mode of inheritance. Different studies of FHB resistance in wheat have shown from two to six genes to be involved in FHB resistance. As early as 1955, Nakagawa (1955) suggested that at least three loci controlled FHB resistance. FHB resistance in Sumai 3 has been reported to be conditioned by three genes (Yao et al., 1997), but in populations used in some studies only two genes were segregating (Van Ginkel et al., 1996). In other studies, more than three genes were thought to be associated with FHB resistance (Yu, 1982). Frontana, a FHB resistant spring wheat cultivar, has either Type I, or Type I and Type II, resistance. In one study, FHB resistance in Frontana was reported to be controlled by three or more genes (Singh et al. 1995), but in another study it was shown that Frontana and Ning 7840 (derived from Sumai 3) each possess two unique dominant genes for FHB resistance (Van Ginkel et al. 1996).

Genes for FHB resistance in wheat have been reported to be located on many different chromosomes (Buerstmayr et al., 1999; Yao et al., 1997); 18 of the 21 wheat chromosomes have been reported to be involved in FHB resistance (Fedak et al., 1998). Only chromosomes 1A, 6A, and possibly 1D have not been reported to be associated with FHB resistance. Because there are many contradictory reports, many questions remain regarding the location of genes for FHB resistance. There are at least seven reasons for the differences in the literature on the location of FHB resistance genes. First, because FHB resistance is a quantitative trait we expect that several genes will be segregating in many crosses. Second, the number of genes segregating in these populations may vary depending upon genetic backgrounds and the magnitude of the difference in resistance between the two parents in each cross. Furthermore, the more susceptible parent in a cross can influence the number of genes detected because even fairly susceptible parents can contribute FHB resistance alleles (Buerstmayr et al., 1998; Waldron et al., 1999). Third, different research groups have studied different sources of resistance. Many groups have studied resistance derived from Sumai 3; however, Sumai 3 has been reported to be heterogenous (Waldron et al., 1999), and the Sumai 3 source used by different groups may differ. Some researchers have studied crosses made directly with Sumai 3, while others have studied populations in which a line derived from Sumai 3 (such as the "Ning" series of lines) was used as the resistant parent. Fourth, whereas most research groups have studied resistance to Fusarium graminearum, some studies have also been conducted on resistance to F. culmorum (Wm. G. Sm.) Sacc. (Buerstmayr et al., 1998; Snijders and Perkowski, 1989; Mesterhäzy, 1988). When genotypes have been evaluated for FHB resistance with more than one Fusarium species, the correlation between resistance ratings using different Fusarium species has been high (Miedaner, 1997),but use of different Fusarium species or different isolates of F. graminearum could contribute to differences among results from different studies. Fifth, whereas most genetic studies and molecular marker studies of FHB resistance in wheat have assessed primarily Type II resistance, genes for other types of FHB resistance may have been segregating in these populations and may confound the determination of the number of genes involved in FHB resistance. Sixth, variation in techniques employed for phenotypic evaluation and the environments in which evaluations were conducted can also contribute to differences in results. For example, studies conducted in a greenhouse with needle inoculation and assessing only Type II resistance may show different results from a field experiment. This is especially important for FHB evaluation in wheat because there are different types of resistance and spore germination, initiation of infection, and symptom spread within the head are all influenced by temperature and relative humidity. Low temperatures or lack of moisture may lead to low disease levels even in susceptible cultivars. For genetic studies and molecular mapping, accurate phenotypic evaluations are critical. Seventh, genotype x environment interactions are frequently large, and field nursery results can also differ over years (Groth et al., 1999). If there is a large amount of environmental variation in the phenotypic data, the estimated number of genes involved in resistance and the amount of variation explained by the detected QTL may not be accurate. Thus, repeated evaluation of a mapping population for FHB resistance is essential.

	Molecular Markers and Maps

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 
Available Barley and Wheat Molecular Markers and Genetic Maps
. Well-developed barley genetic maps exist as the result of the efforts of numerous groups worldwide. These maps include: RFLP (about 3000 probes); amplified fragment length polymorphism (AFLP) (about 1000 markers); single sequence repeat, or microsatellite (SSR) (about 250 primer pairs); isozyme protein markers; and morphological markers (about 200 markers) [GRAINGENES database (http://wheat.pw.usda.gov/; verified December 1, 2000); Becker et al., 1995; Ellis et al., 1997; Graner et al., 1991; Heun et al., 1991; Kleinhofs, 1997; Kleinhofs et al., 1993; Waugh et al., 1997)]. In addition, these markers have been incorporated into bin maps (Kleinhofs and Graner, 1999) (http://barleygenomics.wsu.edu/; verified December 1, 2000). Numerous studies identifying QTL for malting quality, agronomic performance, and disease resistance have been conducted in barley (see Hayes et al., 1993; Tinker et al., 1996; Qi et al., 1998).

RFLP and SSR maps have been developed for wheat (Nelson et al., 1995a, b,c; Van Deynze et al., 1995; Dubcovsky et al., 1996; Marino et al., 1996; Boyko et al., 1999; Röder et al., 1998). The close relatedness of barley and wheat allow mapping RFLPs from either species in the other. Combining markers from barley, rye (Secale cereale L.), and other relatives of wheat provides more than 5000 RFLP markers, in addition to AFLP, SSR, morphological, and isozyme markers [McGuire and Qualset, 1997; GRAINGENES database (http://wheat.pw.usda.gov/)]. Almost 100 QTL controlling agronomic performance and disease resistance have been identified in different maps (see Campbell et al., 1999; Faris et al., 1997; Nelson et al., 1997; Waldron et al., 1999).

	Wheat FHB QTL Mapping

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 
The number of published reports on molecular markers associated with FHB resistance is fairly small, but the number is expected to increase dramatically in the next few years. In wheat, random amplified polymorphic DNA (RAPDs), RFLPs, AFLPs, and SSRs associated with genes for FHB resistance have all been reported (Table 1). Bai (1995) reported RAPD markers associated with two loci for FHB resistance in a population of 133 recombinant inbred lines from the cross Ning 7840/Clark. Ning 7840 is derived from Sumai 3 and Clark is a susceptible soft red winter wheat cultivar. Ban (1997) reported on RAPD markers associated with two FHB resistance loci in 110 doubled haploid lines derived from Fukuhokomugi/Oligo Culm. Three of the markers were in one linkage group, and the fourth occurred in a separate group. Ban and Suenaga (1997)(1998) reported RAPD markers associated with a FHB resistance locus on 5AL. They reported that the FHB resistance locus on 5AL was linked to B1 (awn suppressor locus) in repulsion with a recombination value of 15.1 ± 3.3% in a Sumai 3/Gamenya doubled haploid population of 137 lines and 21.4 ± 4.3% in a Sumai 3/Emblem doubled haploid population of 73 lines.

Bai et al. (1999a) identified 11 linked AFLPs associated with a major QTL for FHB resistance in a Ning 7840/Clark recombinant inbred line population (133 lines). This population was evaluated for FHB resistance by the needle inoculation technique in the greenhouse on F₅, F₆, F₇, F₈, and F₁₀ plants. One QTL with a major effect explained from 23 to 53% of the variation in FHB resistance depending upon the generation. In further research with this population, two additional QTL associated with FHB resistance were identified (Bai et al. 1999b). Averaged over five generations evaluated in the greenhouse, the three QTL collectively explained about 63% of the variation in FHB resistance. Because this research was conducted in the greenhouse with inoculation, the variation assessed was associated only with Type II resistance. Also, because the evaluations were conducted in the greenhouse, environmental variation was smaller than would be expected in the field. If evaluations had been conducted in the field, the percentage of the variation associated with a QTL might have been lower. Research is in progress to assign these AFLP markers to linkage groups on the W7984/Opata M85 ITMI map.

SSR markers have been developed for wheat, and several research groups (Procunier et al., 1998; Anderson et al., 1999; Chen et al., 2000; Gupta et al., 2000; Zhou et al., 2000) have used SSRs (microsatellites) in conjunction with FHB resistance. Procunier et al. (1998) used SSRs in research with F₁ pentaploids from a cross of Sumai 3 / DT486 (susceptible tetraploid) and tetraploid D chromosome addition lines. They used SSRs that were previously mapped to known D genome chromosomes and reported that the Sumai 3 FHB resistance genes are not located in the D genome. Otto et al. (1999) used a population of 83 recombinant inbred chromosome lines derived from a cross between Langdon and a disomic substitution line for chromosome 3A from Triticum dicoccoides (Koern. ex Asch. & Graebner) Aarons. They identified a QTL for FHB resistance on chromosome 3A. The SSR marker Xgwm2 was closely associated with FHB resistance and explained 38% of the phenotypic variation.

In summary, on the basis of published molecular marker information and genetic studies, chromosomes 5A, 3BS, and 6BS seem to be likely locations for FHB resistance genes from Sumai 3. In addition, 2AL, 3A, and 7A also appear to be involved in FHB resistance in wheat. Several groups are currently working on molecular markers for FHB resistance in wheat using a variety of populations. Information on location of QTL for FHB resistance should improve dramatically in the near future.

	Barley FHB QTL Mapping

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 
Two recent studies in barley have identified QTL for FHB resistance on all seven chromosomes. Using a six-rowed barley population of 110 F₄ derived lines, de la Peña et al. (1999) identified QTL on all chromosomes except chromosome 6, whereas Zhu et al. (1999) identified QTL on all chromosomes except chromosome 7 using a two-rowed population of 144 doubled haploid lines. In both studies, some of the FHB QTL mapped to the same location as QTL for other traits that were phenotypically correlated with FHB. The traits that were both phenotypically and genetically correlated with FHB resistance included: DON concentration, heading date, plant height, seeds/inflorescence, and lateral floret size. Further research will be necessary to determine if these coincident QTL are due to close linkage or pleiotropy. More recent work on a doubled haploid population derived from a cross between Chevron and the cultivar Stander has also identified QTL associated with FHB resistance (Ma et al., 2000). In addition to the traits mentioned above, this group found FHB QTL coincident with spike angle and kernel plumpness. They concluded that QTL on chromosomes 1H, 2H, and 4H may be the most useful for marker assisted selection. These three QTL are not associated with late heading or plant height.

Several QTL for FHB resistance in barley were identified in independent mapping efforts. On chromosome 2, Ksuf15 and MWG503 were associated with resistance in Chevron/M69 (110 F₄ derived lines) and Gobernadora/CMB643 populations (144 doubled haploid lines), respectively. Both markers were not evaluated in both populations, but are 3 centimorgans (cM) apart on a consensus barley map (Qi et al., 1996). In the Chevron population, this QTL was only associated with FHB resistance, while in the Gobernadora/CMB643 population it was associated with resistance, lateral floret size, and seeds per inflorescence. The latter two traits were not measured in the Chevron/M69 population, so it is not possible to determine if the Chevron-derived resistance is associated with inflorescence morphology at this locus. Also on chromosome 2, the Chevron allele of the marker ABC306 was associated with resistance to DON accumulation, FHB resistance, and late heading in both the Chevron/M69 and Chevron/Stander populations. On chromosome 3, ABG713A and ABC261B were both associated with FHB resistance in the Chevron/M69 and Gobernadora/CMB643 populations, respectively. These markers are 7 cM apart on the consensus barley map (Qi et al., 1996). CDO395 (also on chromosome 3) was associated with FHB resistance in both the Chevron/M69 and Chevron/Stander populations. On chromosome 5, the marker ABG452 was associated with resistance to FHB and accumulation of DON in both the Chevron/M69 and Chevron/Stander populations. The identification of these QTL in independent mapping studies indicates that they are robust and may be useful in marker assisted breeding programs.

Several other mapping efforts to identify new or verify previously identified FHB QTL are in progress (Table 2). Several of the QTL regions identified in the Chevron/M69 population are being followed in populations created with Chevron/M69 progeny. These populations have less variability for traits correlated with FHB and may provide more unbiased estimates of the effects of alleles at FHB QTL. The barley FHB QTL studies published to date have involved only crosses within either the six-rowed or two-rowed barley gene pools. Two-rowed barley generally appears to have more resistance than six-rowed barley, and many of the sources of FHB resistance are two-rowed. Efforts to introgress resistance from two-rowed barley into six-rowed barley have met with limited success. The mapping population derived from the cross between Frederickson, a two-rowed resistance source, and Stander should help clarify the role of two-rowed/six-rowed spike morphology in FHB resistance.

	Do Wheat and Barley FHB Resistance QTL Reside in Syntenous Chromosomal Locations?

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

To determine if the FHB resistance QTL are located in syntenous locations, we focused our attention on the two major QTL that map to chromosomes 2 and 3 in wheat and barley. Examining the potential syntenous relationships between these two major FHB resistance QTL revealed that the chromosome 2 and 3BS QTL appear to lie in nonsyntenous and syntenous locations, respectively (Fig. 1; de la Peña et al., 1999; Waldron et al., 1999; Ma et al., 2000). The QTL on chromosome 3 is located in a region flanked by the RFLP markers bcd907 and abg471 in both wheat and barley, indicating that it lies in a syntenous location. In barley, this QTL has been identified in two independent mapping studies (de la Peña et al., 1999; Ma et al., 2000). In wheat, the chromosome 3 BS QTL is the major QTL identified to date, and it has been identified in mapping studies conducted by a number of research groups (Anderson et al., 1999; Chen et al., 2000; Gupta et al., 2000; Zhou et al., 2000). Whether or not these are orthologous genes contributing to resistance is not known. The QTL located on chromosome 2 in wheat and barley does not appear to exhibit synteny.

View larger version (22K): [in this window] [in a new window]   Fig. 1. The barley and wheat chromosome 3 FHB resistance QTL are located in a syntenous region. This figure combines the results of four different mapping studies. The marker locations for the wheat chromosome 3BS map are based on the Sumai3/Stoa mapping population (Waldron et al., 1999). The marker locations for the barley chromosome 3HS map are based on the barley consensus map (Qi et al., 1996). The bars indicate the regions on chromosome 3 that are associated with FHB resistance. The key indicates the mapping studies conducted to identify the QTL and the LOD score associated with that QTL.

	Future Research

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

In both wheat and barley, better sources of resistance need to be identified and mapped. In barley, the resistance identified so far seems to be largely associated with morphological attributes of the plants. In wheat, most molecular marker research has focused on Type II resistance (especially Sumai 3-derived genes). The current sources of resistance are desirable initially, but other types of resistance and other sources of resistance also need to be identified. This is particularly important since we would like to combine FHB resistance genes from different sources to produce transgressive segregants with a higher level of FHB resistance. In wheat, identifying molecular markers associated with genes for resistance to FHB in addition to Type II resistance is the goal. However, this may be difficult because of the greater environmental variation which may be associated with the phenotypic evaluation of resistance other than Type II resistance. In barley, identifying sources of resistance that are not associated with deleterious phenotypic traits is the goal. As these new sources of FHB resistance in wheat and barley are identified, they need to be mapped to identify potentially new QTL for resistance.

Confirming resistance QTL is important because many loci have been identified from similar sources of resistance, and many have not been consistent across environments. Independent confirmation of each QTL is extremely important before breeders use the markers to conduct marker assisted selection. The University of Minnesota barley breeding program is simultaneously confirming FHB QTL and breeding for resistance. In other words, lines from the mapping populations that contain putative QTL regions are used for the next round of crosses. The subsequent population that is derived from the cross is used to validate the QTL of interest. In this fashion, it is possible to conduct phenotypic selection for resistance while confirming QTL of interest.

As molecular markers associated with FHB are identified, how should chromosome regions to be employed in marker assisted selection programs be chosen? Several criteria should be considered in choosing chromosome regions to emphasize (de la Peña et al., 1999). Markers associated with QTL with the largest effects should be chosen. These markers will be closely linked to a genomic region with a gene or genes with large effect(s). Regions carrying QTL that are significant in multiple environments and/or in several mapping populations should be emphasized. Genes for FHB resistance linked to genes for correlated traits should be avoided, because genes for correlated traits can confound selection for FHB resistance genes. In addition, it is necessary to determine if coincident QTL are the result of tight linkage or pleiotropy. In the case of tight linkage, screening large numbers of recombinants may be necessary to break up the linkage. If pleiotropy is observed, the gene may be undesirable if both resistance and an undesirable trait are conditioned by the same allele.

Breeders would like to be able to use the same markers on different populations. At a minimum, breeders need markers that can be used for selection in populations carrying the same source of resistance (e.g., Sumai 3). The problems encountered in using markers across different populations should be addressed. Characterizing the parents in a cross addresses some of these issues, but the situation becomes more complex when three-way or four-way crosses are involved. Dudley (1993) described several factors that should be considered in determining if a marker can be used for selection in two populations: (i) the marker must be polymorphic in both populations, and the QTL must be segregating; (ii) the linkage phase of the marker and the QTL must be known in the two populations; and (iii) genotypes of other QTL can have an effect (background effect) on the magnitude of the effect of the QTL for which markers are being used.

The use of molecular markers for FHB resistance breeding provides another tool for the plant breeder. To make marker assisted selection feasible on a large scale for evaluation of many breeding lines from many populations, markers need to be developed that can be readily used by breeders, including markers such as SSRs, sequence tagged sites (STSs), and single nucleotide polymorphisms (SNPs). In addition, breeding programs will have to develop the capacity to evaluate molecular markers in large numbers of breeding lines. As breeding programs become more automated and markers associated with FHB resistance are identified, breeding schemes to employ these markers will need to be developed. In this issue, Van Sanford et al. (2001) discuss proposed integrated systems for the development and utilization of molecular markers in marker assisted selection for FHB resistance.

	ACKNOWLEDGMENTS

 
We thank Carla Otto and Shahryar Kianian for providing information on the research with Triticum dicoccoides derived resistance and Nora Lapitan for providing information on mapping FHB resistance in barley.

Received for publication April 15, 2000.

	REFERENCES

TOP ABSTRACT INTRODUCTION Nature of the Inheritance... Molecular Markers and Maps Wheat FHB QTL Mapping Barley FHB QTL Mapping Do Wheat and Barley... Future Research REFERENCES

 

• Anderson, J.A., B.L. Waldron, B. Moreno-Sevilla, R.W. Stack, and R.C. Frohberg. 1998. DNA markers for Fusarium head blight resistance QTL in two wheat populations. p. 57–59. In P. Hart et al. (ed.) Proc. 1998 National FHB Forum. University Printing, East Lansing, MI.
• Anderson, J.A., B.L. Waldron, R.W. Stack, and R.C. Frohberg. 1999. Update on DNA markers for Fusarium head blight resistance QTL in two wheat populations. p. 19–21. In J. Wagester et al. (ed.) Proc. 1999 National FHB Forum. University Printing, East Lansing, MI.
• Bai, G-H., and G. Shaner. 1994. Scab of wheat: Prospects for control. Plant Dis. 78:760–766.
• Bai, G-H. 1995. Scab of wheat: Epidemiology, inheritance of resistance and molecular markers linked to cultivar resistance. Ph.D. thesis (AAI9622661, Dissertation Abstracts International, Volume: 57-03, Section B, p. 1537). Purdue University, West Lafayette, IN.
• Bai, G-H., F.L. Kolb, G. Shaner, and L.L. Domier. 1999a. Amplified fragment length polymorphism markers linked to a major quantitative trait locus controlling scab resistance in wheat. Phytopathology 89:343–348.[ISI]
• Bai, G-H., F.L. Kolb, G.E. Shaner, and L.L. Domier. 1999b. Using an AFLP map to identify scab resistance QTL in wheat. p. 22–24. In J. Wagester et al. (ed.) Proc. 1999 National FHB Forum. University Printing, East Lansing, MI.
• Ban, T. 1997. Genetic analysis of fusarium head blight resistance using wheat doubled haploids. p. 71–78. In H.J. Dubin et al. (ed.) Proc. Fusarium Head Scab: Global Status and Future Prospects. CIMMYT, Mexico, D.F., Mexico.
• Ban, T., and K. Suenaga. 1997. Inheritance of resistance to Fusarium head blight caused by F. graminearum in wheat. Cereal Res. Comm. 25:727–728.
• Ban, T., and K. Suenaga. 1998. Genetic analysis of resistance to Fusarium head blight caused by Fusarium graminearum in wheat. p. 192–196. In A.E. Slinkard (ed.) Proc. 9th International Wheat Genetics Symposium, Saskatoon. 2–7 Aug. 1998. Univ. Extension Press, Saskatoon, SK, Canada.
• Becker, J., P. Vos, M. Kuiper, F. Salamini and M. Heun. 1995. Combined mapping of AFLP and RFLP markers in barley. Mol. Gen. Genet. 249:65–73.[ISI][Medline]
• Bennetzen, J.L., and M. Freeling. 1993. Grasses as a single genetic system: Genome composition, collinearity and compatibility. Trends Genet. 9:259.[ISI][Medline]
• Bennetzen, J.L., P. SanMiguel, M. Chen, A. Tikhonov, M. Fracki, and Z. Avramova. 1998. Grass genomes. Proc. Natl. Acad. Sci. (USA) 95:1975–1978.[Abstract/Free Full Text]
• Boyko, E.V., K.S. Gill, L. Mickelson-Young, S. Nasuda, W.J. Raupp, J.N. Ziegle, S. Singh, D.S. Hassawi, A.K. Fritz, D. Namuth, N.L.V. Lapitan, and B.S. Gill. 1999. A high-density genetic linkage map of Aegilops tauschii, the D-genome progenitor of bread wheat. Theor. Appl. Genet. 99:16–26.
• Buerstmayr, H., L. Doldi, M. Lemmens, B. Steiner, S. Berlakovich, and P. Ruckenbauer. 1998. Analysis of Fusarium head blight (scab) resistance in wheat by classical, cytogenetical, and molecular tools. p. 197–199. In A.E. Slinkard (ed.) Proc. 9th International Wheat Genetics Symposium, Saskatoon. 2–7 Aug. 1998. Univ. Extension Press, Saskatoon, SK, Canada.
• Buerstmayr, H., M. Lemmens, G. Fedak, and P. Ruckenbauer. 1999. Back-cross reciprocal monosomic analysis of Fusarium head blight resistance in wheat (Triticum aestivum L.). Theor. Appl. Genet. 98:76–85.
• Campbell, K.G., C.J. Bergman, D.G. Gualberto, J.A. Anderson, M.J. Giroux, G. Hareland, R.G. Fulcher, M.E. Sorrells, and P.L. Finney. 1999. Quantitative trait loci associated with kernel traits in a soft x hard wheat cross. Crop Sci. 39:1184–1195.[Abstract/Free Full Text]
• Campbell, K.A.G., and P.E. Lipps. 1998. Allocation of resources: Sources of variation in Fusarium head blight screening nurseries. Phytopathology 88:1078–1086.[ISI]
• Capettini, F. 1999. Inheritance of Resistance to Fusarium Head Blight in Barley. Ph.D. thesis (ADG9941711, Dissertation Abstracts International, Volume: 60-08, Section B, p. 3628). University of Minnesota, St. Paul, MN.
• Chen, M., P. SanMiguel, A.C. de Oliveira, S-S. Woo, H. Zhang, R.A. Wing, and J.L. Bennetzen. 1997. Microlinearity in sh2-homologous regions of the maize, rice, and sorghum genomes. Proc. Natl. Acad. Sci. (USA) 94:3431–3435.[Abstract/Free Full Text]
• Chen, J., C.A. Griffey, M.A. Saghai Maroof, W. Zhao, W. Xie, and T. Pridgen. 2000. Genetic analysis of resistance to Fusarium head blight in common wheat. p. 19–24. In R.W. Ward et al. (ed.) Proc. of the 2000 National Fusarium Head Blight Forum, Erlanger, KY. 10–12 Dec. 2000. Michigan State University, East Lansing, MI.
• Collins, N.C., C.A. Webb, S. Seah, J.G. Ellis, S.H. Hulbert, and A. Pryor. 1998. The isolation and mapping of disease resistance gene analogs in maize. Mol. Plant-Microbe Interactions 11:968–978.
• de la Peña, R.C., K.P. Smith, F. Capettini, G.J. Muehlbauer, M. Gallo-Meagher, R. Dill-Macky, D A. Somers. and D.C. Rasmusson. 1999. Quantitative trait loci associated with resistance to Fusarium head blight and kernel discoloration in barley. Theor. Appl. Genet. 99:561–569.[ISI]
• Devos, K.M. and M.D. Gale. 1997. Comparative genetics in grasses. Plant Mol. Biol. 35:3–15.[ISI][Medline]
• Dubcovsky, J., M.-C. Luo, G-Y. Zhong, R. Bransteitter, A. Desai, A. Kilian, A. Kleinhofs, and J. Dvorak. 1996. Genetic map of diploid wheat, Triticum monococcum L., and its comparison with maps of Hordeum vulgare L. Genetics 143:983–999.[Abstract]
• Dudley, J.W. 1993. Molecular markers in plant improvement: Manipulation of genes affecting quantitative traits. Crop Sci. 33:362–374.[Free Full Text]
• Ellis, R.P., B.P. Forster, R. Waugh, and N. Bonar. 1997. Mapping physiological traits in barley. New Phytologist 137:149.
• Faris, J.D., J.A. Anderson, L.J. Francl, and J.G. Jordahl. 1997. RFLP mapping of resistance to chlorosis induction by Pyrenophora tritici-repentis in wheat. Theor. Appl. Genet. 94:98–103.[ISI]
• Fedak, G., J. Gilbert, K.C. Armstrong, J.D. Procunier, N. Tinker, G. Butler, and R. Pandeya. 1998. Studies of inheritance of Fusarium head blight resistance in wheat. p. 25–27. In P. Hart et al. (ed.) Proc. 1998 National FHB Forum. University Printing, East Lansing, MI.
• Gale, M.D., and K.M. Devos. 1998. Plant comparative genetics after 10 years. Science 282:656–659.[Abstract/Free Full Text]
• Gallego, F., C. Feuillet, M. Messmer, A. Penger, A. Graner, M. Yano, T. Sasaki, and B. Keller. 1998. Comparative mapping of the two wheat leaf rust resistance loci Lr1 and Lr10 in rice and barley. Genome 41:328–336.[Medline]
• Graner, A., A. Jahoor, J. Schondelmaier, H. Siedler, K. Pillen, G. Fischbeck, G. Wenzel, and R.G. Herrmann. 1991. Construction of an RFLP map of barley. Theor. Appl. Genet. 83:250–256.[ISI]
• Groth, J.V., E.A. Ozmon, and R.H. Busch. 1999. Repeatability and relationship of incidence and severity measures of scab of wheat caused by Fusarium graminearum in inoculated nurseries. Plant Dis. 83:1033–1038.
• Gupta, A., P.E. Lipps, and K.G. Campbell. 2000. Finding quantitative trait locus associated with Fusarium head blight of wheat using simple sequence repeat markers. p. 28–32. In R.W. Ward et al. (ed.) Proc. of the 2000 National Fusarium Head Blight Forum, Erlanger, KY. 10–12 Dec. 2000. Michigan State University, East Lansing, MI.
• Hayes, P.M., B.H. Liu, S.J. Knapp, F. Chen, B. Jones, T. Blake, J. Franckowiak, D. Rasmusson, M. Sorrells, S.E. Ullrich, D. Wesenberg, and A. Kleinhofs. 1993. Quantitative trait locus effects and environmental interaction in a sample of North American barley germplasm. Theor. Appl. Genet. 87:392–401.[ISI]
• Heun, M., A.E. Kennedy, J.A. Anderson, N.L.V. Lapitan, M.E. Sorrells, and S.D. Tanksley. 1991. Construction of a restriction fragment length polymorphism map for barley (Hordeum vulgare). Genome 34:437–447.
• Immer, F.R., and J.J. Christensen. 1943. Studies on susceptibility of varieties and strains of barley to Fusarium and Helminthosporium kernel blight when tested under muslin tents or in nurseries. J. Am. Soc. Agron. 35:515–522.
• Kleinhofs A., A. Kilian, M.A.S. Maroof, R.M. Biyashev, P. Hayes, F.Q. Chen, N. Lapitan, A. Fenwick, T.K. Blake, V. Kanazin, E. Ananiev, L. Dahleen, D. Kudrna, J. Bollinger, S.J. Knapp, B. Liu, M. Sorrells, M. Heun, J.D. Franckowiak, D. Hoffman, R. Skadsen, and B.J. Steffenson. 1993. A molecular, isozyme and morphological map of the barley (Hordeum vulgare) genome. Theor. Appl. Genet. 86:705–712.[ISI]
• Kleinhofs A. 1997. Online data set for the Steptoe x Morex barley mapping population. (see http://genome.cornell.edu/cgi-bin/WebAce/webace?db=graingenes&grep=Steptoe x Morex&longgrep=1; verified January 12, 2001).
• Korzun, V., S. Mayshev, V. Voylokov, and A. Borner. 1997. RFLP-based mapping of three mutant loci in rye (Secale cereale L.) and their relation to homoeologous loci within the Gramineae. Theor. Appl. Genet. 95:468–473.
• Leister, D., J. Kurth, D.A. Laurie, M. Yano, T. Sasaki, K. Devos, A. Graner, and P. Schulze-Lefert. 1998. Rapid reorganization of resistance gene homologues in cereal genomes. Proc. Natl. Acad. Sci. (USA) 95:370–375.[Abstract/Free Full Text]
• Ma, Z., B.J. Steffenson, L.K. Prom, and N.L.V. Lapitan. 2000. Mapping of quantitative trait loci for Fusarium head blight resistance in barley. Phytopathology 90:1079–1088.
• Marino, C.L., J.C. Nelson, Y.H. Lu, M.E. Sorrells, P. Leroy, N.A. Tuleen, C.R. Lopes, and G.E. Hart. 1996. Molecular genetic maps of the group 6 chromosomes of hexaploid wheat (Triticum aestivum L. em Thell.). Genome 39:359–366.[Medline]
• McGuire, P.E., and C.O. Qualset (ed.). 1997. Progress in genome mapping of wheat and related species: Joint proceedings of the 5th and 6th public workshops of the International Triticeae Mapping Initiative, 1–3 Sep. 1995, Norwich UK and 30–31 Aug. 1996, Sydney Australia. Report No. 18. University of California Genetic Resources Conservation Program, Davis CA.
• McMullen, M., R. Jones, and D. Gallenberg. 1997. Scab of wheat and barley: A re-emerging disease of devastating impact. Plant Dis. 81:1340–1348.
• Mesterhäzy, A. 1988. Expression of resistance of wheat to Fusarium graminearum and F. culmorum under various experimental conditions. J. Phytopathol. 123:304–310.
• Mesterhäzy, A. 1995. Types and components of resistance to Fusarium head blight of wheat. Plant Breed. 114:377–386.
• Miedaner, T. 1997. Breeding wheat and rye for resistance to Fusarium diseases. Plant Breed. 116:201–220.
• Moore, G. 1995. Cereal genome evolution: Pastoral pursuits with ‘Lego’ genomes. Curr. Opinions Genet. Dev. 5:717–724.
• Nakagawa, M. 1955. Studies on ear scab resistance of wheat plants: Genetical factors affecting the inheritance of ear-scab disease of wheat plants. Japan J. Breed. 5:15–22 (cited in Schroeder and Christensen).
• Nelson, J.C., M.E. Sorrels, A.E. Van Deynze, Y.H. Lu, M. Atkinson, M. Bernard, P. Leroy, J.D. Faris, and J.A. Anderson. 1995a. Molecular mapping of wheat: Major genes and rearrangements in homoeologous groups 4, 5, and 7. Genetics 141:721–731.[Abstract]
• Nelson, J.C., A.E. Van Deynze, E. Autrique, M.E. Sorrells, Y.H. Lu, M. Merlino, M. Atkinson, and P. Leroy. 1995b. Molecular mapping of wheat: Homoeologous group 2. Genome 38:516–524.[Medline]
• Nelson, J.C., A.E. Van Deynze, E. Autrique, M.E. Sorrells, Y.H. Lu, W. Negre, M. Bernard, and P. Leroy. 1995c. Molecular mapping of wheat homoeologous group 3. Genome 38:525–533.[Medline]
• Nelson, J.C., R.P. Singh, J.E. Autrique, and M.E. Sorrells. 1997. Mapping genes conferring and suppressing leaf rust resistance in wheat. Crop Sci. 37:1928–1935.[Abstract/Free Full Text]
• Otto, C.D., S.F. Kianian, E.M. Elias, R.W. Stack, and L.R. Joppa. 1999. Molecular mapping for FHB resistance in a RICL population of tetraploid wheat. p. 159. Agron. Abstr. ASA, Madison, WI.
• Paterson, A.H., Y-R. Lin, Z. Li, K.F. Shertz, J.F. Doebley, S.R.M Pinson, S-C. Liu, J.W. Satnsel, and J.E. Irvine. 1995. Convergent domestication of cereal crops by independent mutations at corresponding genetic loci. Science 269:1714–1718.[Abstract/Free Full Text]
• Procunier, J.D., J. Gilbert, T. Aung, M. Gray, and S. Prashar. 1998. Microsatellite identification of specific D chromosomes for fusarium head blight resistance in hexaploid wheat. p. 143–144. In A.E. Slinkard (ed.) Proc. 9th International Wheat Genetics Symposium, Saskatoon. 2–7 Aug. 1998. Univ. Extension Press, Saskatoon, SK, Canada.
• Qi, X., P. Stam, and P. Lindhout. 1996. Comparison and integration of four barley genetic maps. Genome 39:379–394.[Medline]
• Qi, X., R.E. Niks, P. Stam, and P. Lindhout. 1998. Identification of QTLs for partial resistance to leaf rust (Puccinia hordei) in barley. Theor. Appl. Genet. 96:1205–1215.
• Röder, M.S., V. Korzyn, K. Wendehake, J. Plaschke, H. Tixier, P. Leroy, and M.W. Ganal. 1998. A microsatellite map of wheat. Genetics 149:2007–2023.[Abstract/Free Full Text]
• Rudd, J.C., R.D. Horsley, A.L. McKendry, and E.M. Elias. 2001. Host plant resistance genes for Fusarium head blight: I. Sources, mechanisms, and utility in conventional breeding systems. Crop Sci. 41:620–627.[Abstract/Free Full Text]
• Saghai-Maroof, M.A., G.P. Yang, R.M. Biyashev, P.J. Maughan, and Q. Zhang. 1996. Analysis of the barley and rice genomes by comparative RFLP linkage mapping. Theor. Appl. Genet. 92:541–551.
• Schroeder, H.W., and J.J. Christensen. 1963. Factors effecting resistance of wheat to scab caused by Gibberella zeae. Phytopathology 53:831–838.[ISI]
• Sherman, J.D., A.L. Fenwick, D.G. Namuth, and N.L.V. Lapitan. 1995. A barley RFLP map: Alignment of three barley maps and comparisons to Gramineae species. Theor. Appl. Genet. 91:681–690.
• Singh, R.P., H. Ma, and S. Rajaram. 1995. Genetic Analysis of resistance to scab in spring wheat cultivar Frontana. Plant Dis. 79:238–240.
• Snijders, C.H.A., and J. Perkowski. 1989. Effect of head blight caused by F. culmorum on toxin content and weight of wheat kernels. Phytopathology 80:133–140.
• Steffenson, B.J., L.K. Prom, B. Salas, T.G. Fetch, D.G. Wesenberg, and H.E. Bockelman. 1996. Severity of Fusarium head blight and concentrations of deoxynivalenol in near-isogenic lines of barley differing for several agronomic characters. p. 774–776. In G. Scoles and B. Rossnagel (ed.) Proceedings of the 5th International Oat Conference and the 7th International Barley Genetics Symposium. University Extension Press University of Saskatchewan, Saskatoon, SK, Canada.
• Steffenson, B.J. 1998. Fusarium head blight of barley: Epidemics, impact and breeding for resistance. Malting Barley Assoc. Am. Tech Quart. 35:177–183.
• Tinker, M.N., D.E. Mather, B.G. Rossnagel, K.J. Kasha, A. Kleinhofs, P.M. Hayes, D.E. Falk, T. Ferguson, L.P. Shugar, W.G. Legge, R.B. Irvine, T.M. Choo, K.G. Briggs, S.E. Ullrich, J.D. Franckowiak, T.K. Blake, R.J. Graf, S.M. Dofing, M.A. Saghai-Maroof, G.J. Scoles, D. Hoffman, L.S. Dahleen, A. Kilian, F. Chen, R.M. Biyashev, D.A. Kudrna, and B.J. Steffenson. 1996. Regions of the genome that affect agronomic performance in two-row barley. Crop Sci 36:1053–1062.[Abstract/Free Full Text]
• Van Ginkel, M., W. Van Der Schaar, Y. Zhuping, and S. Rajaram. 1996. Inheritance of resistance to scab in two wheat cultivars from Brazil and China. Plant Dis. 80:863–867.
• Van Deynze, A.E., J. Dubcovsky, K.S. Gill, J.C. Nelson, and M.E. Sorrells. 1995. Molecular-genetic maps for chromosome 1 in Triticeae species and their relation to chromosomes in rice and oats. Genome 38:47–59.
• Van Sanford, D., J.A. Anderson, K. Campbell, J. Costa, P. Cregan, C. Griffey, P. Hayes, and R. Ward. 2001. Discovery and deployment of molecular markers linked to FHB resistance: An integrated system for wheat and barley. Crop Sci. 41:638–644.[Abstract/Free Full Text]
• Waldron, B.L., B. Moreno-Sevilla, J.A. Anderson, R.W. Stack, and R.C. Frohberg. 1999. RFLP mapping of QTL for Fusarium head blight resistance in wheat. Crop Sci. 39:805–811.[Abstract/Free Full Text]
• Waugh R., N. Bonar, E. Baird, B. Thomas, A. Graner, P. Hayes, and W. Powell. 1997. Homology of AFLP products in three mapping populations of barley. Mol. Gen. Genet. 255:311–321.[ISI][Medline]
• Yao, J., Y. Ge, S. Wang, G. Yao, C. Zhou, and C. Qian. 1997. Chromosomal location of genes for scab resistance in wheat cultivar Sumai 3. Acta Agronomica Sinica 23:450–453.
• Young, N.D., and S.D. Tanksley. 1989. RFLP analysis of the size of chromosome segments retained around the Tm-2 locus of tomato during backcross breeding. Theor. Appl. Genet. 77:353–359.[ISI]
• Yu, Y-J. 1982. Monosomic analysis for scab resistance and yield components in the wheat cultivar Soo-mo 3. Cereal Res. Comm. 10: 185–189.
• Zhou, W.C., F.L. Kolb, G-H. Bai, G. Shaner, and L.L. Domier, 2000. SSR mapping and sub-arm physical location of a major scab resistance QTL in wheat. p. 69–73. In R.W. Ward et al. (ed.) Proc. of the 2000 National Fusarium Head Blight Forum, Erlanger, KY. 10–12 Dec. 2000. Michigan State University, East Lansing, MI.
• Zhu, H., L. Gilchrist, P. Hayes, A. Kleinhofs, D. Kudrna, Z. Liu, L. Prom, B. Steffenson, T. Trojinda, and H. Vivar. 1999. Does function follow form? Principal QTLs for Fusarium head blight (FHB) resistance are coincident with QTLs for inflorescence traits and plant height in a doubled haploid population of barley. Theor. Appl. Genet. 99:1221–1232[ISI]

This article has been cited by other articles:

				N. S. Hill, S. M. Neate, B. Cooper, R. Horsley, P. Schwarz, L. S. Dahleen, K. P. Smith, K. O'Donnell, and J. Reeves Comparison of ELISA for Fusarium, Visual Screening, and Deoxynivalenol Analysis of Fusarium Head Blight for Barley Field Nurseries Crop Sci., July 1, 2008; 48(4): 1389 - 1398. [Abstract] [Full Text] [PDF]

				J.-B. Yu, G.-H. Bai, S.-B. Cai, Y.-H. Dong, and T. Ban New Fusarium Head Blight-Resistant Sources from Asian Wheat Germplasm Crop Sci., May 1, 2008; 48(3): 1090 - 1097. [Abstract] [Full Text] [PDF]

				J. A. Anderson, S. Chao, and S. Liu Molecular Breeding Using a Major QTL for Fusarium Head Blight Resistance in Wheat Crop Sci., December 18, 2007; 47(Supplement_3): S-112 - S-119. [Abstract] [Full Text] [PDF]

				K. Semagn, H. Skinnes, A. Bjornstad, A. G. Maroy, and Y. Tarkegne Quantitative Trait Loci Controlling Fusarium Head Blight Resistance and Low Deoxynivalenol Content in Hexaploid Wheat Population from 'Arina' and NK93604 Crop Sci., February 6, 2007; 47(1): 294 - 303. [Abstract] [Full Text] [PDF]

				G.-L. Jiang, Y. Dong, J. M. Lewis, L. Siler, and R. W. Ward Characterization of Resistance to Fusarium graminearum in a Recombinant Inbred Line Population of Wheat: Resistance to Fungal Spread, Mycotoxin Accumulation, and Grain Yield Loss, and Trait Relationships Crop Sci., November 21, 2006; 46(6): 2590 - 2597. [Abstract] [Full Text] [PDF]

				X. Shen, M. Ittu, and H. W. Ohm Quantitative Trait Loci Conditioning Resistance to Fusarium Head Blight in Wheat Line F201R Crop Sci., May 1, 2003; 43(3): 850 - 857. [Abstract] [Full Text] [PDF]

				T. Miedaner, B. Schneider, and H. H. Geiger Deoxynivalenol (DON) Content and Fusarium Head Blight Resistance in Segregating Populations of Winter Rye and Winter Wheat Crop Sci., March 1, 2003; 43(2): 519 - 526. [Abstract] [Full Text] [PDF]

				J.C. Rudd, R.D. Horsley, A.L. McKendry, and E.M. Elias Host Plant Resistance Genes for Fusarium Head Blight: Sources, Mechanisms, and Utility in Conventional Breeding Systems Crop Sci., May 1, 2001; 41(3): 620 - 627. [Abstract] [Full Text] [PDF]

				D. Van Sanford, J. Anderson, K. Campbell, J. Costa, P. Cregan, C. Griffey, P. Hayes, and R. Ward Discovery and Deployment of Molecular Markers Linked to Fusarium Head Blight Resistance: An Integrated System for Wheat and Barley Crop Sci., May 1, 2001; 41(3): 638 - 644. [Abstract] [Full Text] [PDF]

This Article Abstract Figures Only Full Text (PDF) Free