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Published online 24 February 2006
Published in Crop Sci 46:910-916 (2006)
© 2006 Crop Science Society of America
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GENOMICS, MOLECULAR GENETICS & BIOTECHNOLOGY

Potential Application of TRAP (Targeted Region Amplified Polymorphism) Markers for Mapping and Tagging Disease Resistance Traits in Common Bean

Phillip N. Miklasa,*, Jinguo Hub, Niklaus J. Grünwaldc and Karen M. Larsena

a USDA-ARS, Vegetable and Forage Crops Research Unit, Prosser, WA 99350
b USDA-ARS, Sunflower Research Unit, Northern Crop Science Laboratory, Fargo, ND, 58105
c USDA-ARS, Horticultural Crops Research Lab., Corvallis, OR 97330

* Corresponding author (pmiklas{at}pars.ars.usda.gov)


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Genetic resistance is an important component of integrated strategies used to control problematic diseases in common bean (Phaseolus vulgaris L.). Molecular linkage maps have been used to identify, tag, and map disease resistance genes and QTL in common bean, leading to improved breeding strategies and implementation of marker-assisted selection. Most widely used marker types, random amplified polymorphic DNA (RAPD) and amplified fragment length polymorphisms (AFLP), for linkage mapping in bean are located randomly throughout the genome and associate with particular traits by chance. We sought to determine the potential application of a new marker system, TRAP, which uses expressed sequence information and a bioinformatics approach to generate polymorphic markers around targeted candidate gene sequences. TRAP markers were amplified by fixed primers designed against sequenced expressed sequence tag (EST) associated with disease resistance in the Compositae Genomics database or against sequenced resistance gene analog (RGA) from common bean. Seventeen of 85 TRAP markers located in the BAT 93/Jalo EEP558 core mapping population mapped in the vicinity of R genes. Six of 21 TRAP markers generated in the Dorado/XAN 176 mapping population were linked with newly identified QTL, two conditioning resistance to ashy stem blight (14% and 16% of the phenotypic variation explained, R2), and one each conferring resistance to Bean golden yellow mosaic virus (BGYMV) (15%) and common bacterial blight (30%). The TRAP marker system has potential for mapping regions of the common bean genome linked with disease resistance.

Abbreviations: EST, expressed sequence tag • QTL, quantitative trait locus (loci) • RGA, resistance gene analog • TRAP, targeted region amplified polymorphism


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
A GOAL of many crop-breeding programs is to incorporate marker-assisted selection (MAS) for disease resistance with traditional approaches to expedite germplasm enhancement and cultivar development (Miklas et al., 2006). For example, pyramiding genes for durable disease resistance against a hypervariable plant pathogen is facilitated by a combination of traditional greenhouse inoculation tests for detection of the epistatic gene followed by MAS of hypostatic genes (Miklas and Kelly, 2002; Kelly et al., 2003). Marker-assisted selection is also extremely useful for detection of individual resistance genes difficult to assay with the pathogen, such as bgm-1 in common bean conditioning resistance to BGYMV (Urrea et al., 1996) and Bct for resistance to Beet curly top virus (Larsen and Miklas, 2004). Resistances to those and other diseases are difficult to assess by means of the pathogen because natural epidemics are unpredictable and the pathogen–vector is not amenable to ex situ disease screening methods.

RAPD has been the predominant marker system used to identify markers tightly linked with disease resistance traits in bean (Kelly and Miklas, 1998). Informative RAPD markers with utility for MAS are often converted to sequence-characterized amplified polymorphism (SCAR) markers to facilitate utilization across laboratories. RAPDs are arbitrary sequences of amplified DNA that are uniformly distributed across the genome. For this reason thousands of PCR reactions may be necessary to identify a single RAPD marker that is located in the specific genomic region of a targeted gene or trait. AFLP, also considered a random marker, generates more polymorphisms per PCR reaction for higher throughput; therefore, is replacing RAPD as the marker of choice for tagging traits and constructing genetic linkage maps. However, because the AFLP method also amplifies random sequences, the efficiency of both RAPD and AFLP for tagging specific traits can be low. Another shortcoming of both RAPDs and AFLPs is that they are primarily dominant markers systems that are unable to distinguish heterozygotes. Although microsatellite markers, also referred to as simple sequence repeats (SSR), are available in common bean only a few (<70) have been developed (Blair et al., 2003; Gómez et al., 2004). Thus, for common bean, SSRs are most applicable for map integration and genetic diversity studies. Generation and detection of RFLP markers is cumbersome and as with SSRs too few have been developed in common bean to be useful for gene tagging studies. A new random marker system called sequence related amplified polymorphism (SRAP) uses primers with AT- or GC-rich cores to amplify intragenic polymorphisms (Li and Quiros, 2001). SRAP has potential for candidate gene analysis of QTL (quantitative trait loci), and has been used to measure genetic diversity in pumpkin (Cucurbita pepo L.) germplasm (Ferriol et al., 2003) and to distinguish buffalograss [Buchlöe dactyloides (Nutt.) Engelm.] biotypes (Budak et al., 2004). The potential of SRAP for tagging specific traits in common bean has not been investigated.

Resistance gene analogs (RGAs) are PCR-generated markers designed from conserved sequence motifs of cloned resistance (R) genes. Generally, RGAs occur in clusters and map close to resistance genes in bean (Creusot et al., 1999; Ferrier-Cana et al., 2003; Geffroy et al., 1999; Lopez et al., 2003; Rivkin et al., 1999) and other crops (Kanazin et al., 1996; Leister et al., 1996; Shen et al., 1998). RGAs have been found associated with R genes in bean conditioning resistance to anthracnose caused by Colletotrichum lindemuthianum (Sacc. & Magn.) Scrib. (Creusot et al., 1999; Ferrier-Cana et al., 2003; Geffroy et al., 1999) and QTL conditioning partial resistance to anthracnose, angular leaf spot [Phaeoisariopsis griseola (Sacc.) Ferraris], and BGYMV (Lopez et al., 2003). Geffroy et al. (1999 and 2000) employed RGAs in the discovery, genomic characterization and evolutionary understanding of the R gene clusters conditioning resistance to bean anthracnose. RGAs provide a marker system that could be used to specifically tag disease resistance traits. However, RGAs are not yet amenable for high throughput gene tagging and marker-assisted selection in bean because too few have been developed for such purposes.

A simple and rapid PCR-based marker system, TRAP, was recently developed which uses EST information and a bioinformatics approach to generate polymorphic markers around targeted candidate gene sequences (Hu and Vick, 2003). TRAPs are amplified by one fixed primer designed from a target EST sequence in the database and a second primer of arbitrary sequence except for AT- or GC-rich cores that anneal with introns and exons, respectively. TRAPs were effectively used in assessing genetic diversity among wild sunflower (Helianthus annuus L.) accessions (Hu et al., 2003), in fingerprinting lettuce (Lactuca sativa L.) cultivars (Hu et al., 2005), in tagging a recessive branching gene in sunflower (Rojas-Barros et al., 2005), and in mapping QTL in a wheat (Triticum aestivum L.) intervarietal recombinant inbred population (Liu et al., 2005). Our objective was to determine potential application of the TRAP marker system for mapping and tagging disease resistance traits in common bean. Thus, the fixed primers used to generate TRAPs in this study were based on resistance gene sequences obtained from Compositae EST and Phaseolus sequence databases.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Plant Materials
The recombinant inbred line (RIL) mapping population BAT 93/Jalo EEP 558 (BJ) was obtained from P. Gepts (University of California-Davis). The BJ population has been widely used to integrate common bean linkage maps (Freyre et al., 1998) and has become the core map for genomic placement of economically important traits (Kelly et al., 2003; Miklas et al., 2006). Only 70 of the BJ RILs were available for use in this study. The Dorado (syn. DOR 364)/XAN 176 (DX) population consisting of 79 RILs was obtained from J. Beaver (University of Puerto Rico-Mayaguez) and has been used previously to map loci conditioning resistance to diseases caused by bacterial, fungal, and viral pathogens in common bean (Miklas et al., 2000).

DNA Isolation and TRAP Primer Design
A composite leaf tissue sample (approximately 50 mg) was collected from the first emerging trifoliolate leaves from four plants of each RIL and the parents for both mapping populations. Genomic DNA was extracted with the FastDNA Kit (Bio 101, Vista, CA) according to manufacturer instructions. The purified DNA was adjusted to 10 ng µL–1 with a fluorometer before all PCR reactions.

Fixed primers were either designed against the sequenced EST associated with disease resistance in the Compositae Genomics database: http://cgpdb.ucdavis.edu/database/php_my_admin/php_my_admin.php; verified 21 November 2005 (Michelmore, personal communication, 2002) or against sequenced RGAs from common bean in the National Center for Biotechnology Information database: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=nucleotide&cmd=search&term=phaseolus+resistance+gene ; verified 6 December 2005. The fixed primers were selected by using the web-based PCR primer designing program "Primer 3" http://www-genome.wi.mit.edu/cgi-bin/primer/primer3.cgi; verified 21 November (Rozen and Skaletsky, 2000) with the following parameters: primer optimum, maximum, and minimum sizes set at 18 nt; and primer optimum, maximum, and minimum Tm at 53, 55, and 50°C, respectively.

Fixed primers were derived from sunflower ESTs (Compositae Genetics database) that were selected for homology to disease resistance genes of different plant species. For example, EST contig A20101, has homology to: (i) LRR receptor-like protein kinase of Nicotiana tabacum, (ii) receptor-like protein kinase (EC 2.7.1.) of Oryza sativa, (iii) receptor protein kinase (TMK1), putative; protein id: At1 g66150.1 of Arabidopsis thaliana, and (iv) receptor-like kinase RHG4 of Glycine max. Fixed primers derived from sunflower ESTs were also readily available for exploring the use of TRAP in bean, since the TRAP technique was originally developed with sunflower (Hu and Vick, 2003).

For development of arbitrary primers, the general principles of PCR primer design were upheld so as to avoid self-complementarity and improper GC content (40–60%). In addition, the following three parts were incorporated in each arbitrary primer: (i) the selective nucleotides were 3 to 4 nucleotides at the 3' end, (ii) the "core," consisted of 4 to 6 nucleotides with AT or GC rich regions, and (iii) a filler sequence makes up the 5' end (Li and Quiros 2001). The arbitrary primers used in the current study were selected from the SRAP primer list published by Li et al. (2003). The arbitrary primers were 5' end-labeled with IR dye 700 or IR dye 800 for autodetection by the Li-Cor Global DNA Sequencer (Li-Cor Biosciences, Lincoln, NE), or 5' end-labeled with 5-FAM dye for autodetection by the ABI Avant 3100 DNA sequencer (Applied Biosystems, Foster City, CA). The fixed and labeled primers were made by Qiagen-Operon (Alameda, CA). Table 1 lists primers used in this study.


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  		Table 1. Four multiplex and three single-plex PCR used to generate TRAP markers for candidate disease resistance sequences in common bean mapping population BAT 93/Jalo EEP 558.

 
PCR Protocols
For the Li-Cor Genotyper system PCR was conducted with a final reaction volume of 15 µL in 96-well microtiter plates in a GenAmp 9700 thermal cycler (Applied Biosystems, Foster City, CA) with the following components: 2 µL of the 10 to 30 ng µL–1 DNA sample, 1.5 µL of 10x reaction buffer (Qiagen, Valencia, CA), 1.0 µL of 25 mM MgCl2, 1 µL of 5 mM dNTPs, 0.3 pmol each of 700- and 800-IR dye labeled arbitrary primers, 10 pmol of the fixed primer, and 1.5 units of Taq DNA polymerase (Qiagen, Valencia, CA). The PCR was performed by initially denaturing template DNA at 94°C for 2 min; then 5 cycles at 94°C for 45 s, 35°C for 45 s and 72°C for 1 min; followed by 35 cycles at 94°C for 45 s, 50°C for 45 s, and 72°C for 1 min; then a final extension step at 72°C for 7 min. Note that a lower annealing temperature was used the first five cycles to ensure amplification of multiple fragments, followed by the minimum annealing temperature of 50°C for the last 35 cycles. For the ABI DNA sequencer detection system PCR was conducted in a 15-µL reaction mixture consisting of 20 ng DNA sample, 1.5 µL 10x reaction buffer, 2.5 mM MgCl2, 15 mM dNTPs, 0.75 pmol 5' (5-FAM) labeled arbitrary primer, 37.5 pmol fixed primer, 0.25 units of AmpliTaq DNA polymerase Stoffel Fragment (Applied Biosystems, Foster City, CA). Upon completing the PCR cycles, 7 µL of 5x loading dye [containing 0.313 M Tris-HCl pH 6.8 at 25°C, 10% (w/v) SDS, 0.05% (w/v) bromophenol blue, and 50% (v/v) glycerol] were added to the reaction mixture. A 1-µL aliquot was loaded onto a 6.5% (w/v) polyacrylamide sequencing gel in a Li-Cor Global DNA Sequencer using protocols recommended by the manufacturer. Electrophoresis was conducted at 1500 V for 3.5 h with polymorphic fragments visually scored from the printed images collected by the SAGA software. The sizes of the amplified fragments detected ranged from 40 to 1000 bp.

A total of 0.5 µL of PCR product was added to 9.3 µL deionized formamide and 0.2 µL Rox labeled 500-bp size standard to resolve labeled amplified PCR product using the 3100 Avant Genetic Analyzer. Sequence analysis was conducted with a 36-cm capillary filled with POP4 at a constant temperature of 60°C. The injection protocol was 12 s at 15 A and the run protocol was 34 min at 13 A. Sequences were analyzed by the software package GeneScan and Genotyper (Applied Biosystems) and images were visually inspected for presence of polymorphic fragments. The sizes of the amplified fragments detected ranged from 40 to 600 bp.

Linkage Mapping and QTL Analysis
TRAP markers were integrated in the BJ and DX genetic linkage maps by MAPMAKER/EXP 3.0 (Lander et al., 1987). First TRAP markers were assigned to a linkage group by the GROUP command (LOD 3.0). Once grouped, the position of a TRAP within a linkage group relative to other framework markers was determined by the TRY command. Molecular marker data for the BJ population was kindly provided by P. Gepts (University of California-Davis, CA).

Association of TRAP markers with resistance to common bacterial blight (Xanthomonas campestris pv. phaseoli (Smith) Dye = X. axonopodis pv. phaseoli (Smith) Vauterin et al.), ashy stem blight [Macrophomina phaseolina (Tassi) Goid.], and BGYMV segregating in the DX population (Miklas et al., 2000) was determined by linear regression of disease score means on individual marker genotypes using PROC GLM (SAS Institute, 1987). F tests significant at P < 0.01 were used to indicate linkage between a TRAP and QTL.


   RESULTS AND DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
CONCLUSIONS
 REFERENCES
 
BJ Mapping Population
Eighty-five of 107 TRAP markers found segregating in the BJ population were placed on the core map (Table 1 and Fig. 1 ). Note that the linkage groups in Fig. 1 closely resemble the maps presented by Kelly et al. (2003) and Miklas et al. (2006), which correspond to the core map version of Freyre et al. (1998). The four multiplex PCR utilizing fixed primers from the Compositae Genomics database and visualized by the Li-Cor system detected 47 TRAP markers, 41 of which were mapped. Generally, one arbitrary primer reaction in the multiplex PCR had clearer band visualization than the partner arbitrary primer reaction, suggesting further optimization of the multiplex reaction is warranted for this particular common bean population. The three single-plex PCR visualized by the ABI 3100 DNA capillary sequencer generated 60 TRAP markers, of which 44 were placed on the BJ core map.


Figure 1
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  		Fig. 1. Comprehensive genomic map of disease resistance genes and QTL in common bean. A few genes and QTL involved in resistance to insect pests are included. The linkage groups correspond to the core map version of Freyre et al. (1998), and resemble the maps presented by Kelly et al. (2003) and Miklas et al. (2006). TRAP markers have PM and NG prefixes and are located on the right or left of the linkage group. Directly to the left of each linkage group are the framework molecular markers (smaller font), the monogenic disease resistance genes (shaded boxes), defense related genes (underlined), and arcelin genes (clear box). The Co are anthracnose resistance loci, Ur rust resistance loci, Pse halo blight resistance loci, I and bc are dominant and recessive genes respectively for resistance to BCMV, Phg angular leaf spot resistance locus, and Bct is a locus for resistance to BCTV. To the right of each linkage group are QTL mapped in different populations: ALS, resistance to angular leaf spot; ANT, anthracnose; ASB, ashy stem blight; BGYMV, Bean golden yellow mosaic virus; BBS, bacterial brown spot; CBB, common bacterial blight; FRR, Fusarium root rot; HB, halo blight; LH, leaf hopper; TP, thrips; WB, web blight; and WM, white mold resistance. Symbols in subscript represent the source population of the QTL (refer to Miklas et al., 2005). Gene and QTL locations are approximate because most were not directly mapped in the BAT 93/Jalo EEP558 population. The total distance of each linkage group is expressed in Kosambi cM (bottom-right).

 
The fixed primers from sunflower ESTs were as efficient as fixed primers derived from common bean RGAs for generating TRAP markers, which is indicative of the conservative nature of resistance genes across species. The Ga5 primer was the most efficient arbitrary primer tested in the multiplex reactions for generating TRAPs and is the reason why it was used exclusively in this study with the single-plex reactions run on the ABI 3100 DNA capillary sequencer. Results indicate that both DNA sequence detection systems effectively generated TRAPs, but the capillary system which detected 20 TRAPs per single-plex PCR on average was more efficient than the polyacrylamide system which detected 12 TRAPs per multiplex PCR. The high level of polymorphism detected per fixed–arbitrary primer pair reaction is attributable to the core mapping population being derived from a wide cross between parents of diverse Middle American (BAT 93) and Andean (Jalo EEP558) origin.

All the primer pairs amplified TRAPs of different sizes that mapped to the exact same locations (e.g., PM1.479 and PM1. 825 on B6; NG1.161 and NG1.342 on B7), which is characteristic of amplified template DNA possessing repeated sequences. Repeated DNA sequences are commonly found in R-gene clusters (Hulbert et al., 2001). A few TRAPs derived from different fixed primers also mapped to the same location (e.g., PM3a.406 and NG1.385 on B1; NG3.368 and PM4.603 on B5), which supports the conservative nature of R-gene sequences in general. Of the TRAP markers detected in this study, 10% were codominant, which is twice the frequency observed for RAPD (Miklas et al., 2000).

Eighty-five TRAP markers were positioned across all 11 linkage groups (Fig. 1). Many of the remaining unmapped TRAP markers were linked with one another (data not shown). Only eight TRAPs were completely unlinked with another marker. Linkage group B8 had the most TRAPs with 11 and B10 the least with three. TRAP markers tended to cluster with one another, with clusters of TRAPs most pronounced on B1, B4, B6, B8, and B11. It will be interesting to see if the TRAP makers not associated with disease resistance traits on the current core map, such as those clustered toward the end of B6, are tagging nonfunctional R genes or resistance genes yet to be mapped.

Seventeen TRAP markers mapped to 11 genomic regions containing major R genes that primarily controlled resistance to specific pathotypes of the hypervariable pathogens causing anthracnose and rust diseases (Table 2). Most of the 17 R-gene-associated TRAPs (PM3b.475, NG.122, NG1.391, PM2b.396, PM1.522, NG3.325, PM2b.570, PM3a.366, PM2b.852, NG1.514, and PM4.719) mapped near or within R-gene clusters on B4, B7, B8, and B11 (Fig. 1). There were also many TRAP markers that mapped near QTL conditioning disease resistance. The colocation of QTL with R-gene clusters and TRAP markers on B4, B7, B8, and B11, provide further support for the assumption that certain quantitative resistance is under similar mechanisms of control as R genes (Lefebvre and Chèvre, 1995). Associations of RGA and/or R genes with QTL conditioning disease resistance have been observed in common bean (Geffroy et al., 2000; Lopez et al., 2003), pepper (Capsicum annuum L.) (Pflieger et al., 1999) and potato (Solanum tuberosum L.) (Gebhardt and Valkonen, 2001).


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  		Table 2. Genomic association of 17 TRAP markers with major disease resistance R genes in the BAT 93/Jalo EEP 558 mapping population (see Fig. 1 for explanation of gene symbols).

 
Two TRAP markers, NG3.81 and NG3.325, generated by a fixed primer designed from the published DNA sequence for RGA1 in bean were linked with R genes conditioning resistance to bean rust on linkage group B11 in the BJ core map (Fig. 1). Lopez et al. (2003) previously mapped RGA1 (A and B variants) to B11 but in the vicinity of anthracnose resistance gene Co-2. Molecular characterization of the genomic region possessing Co-2 revealed the presence of conserved sequence motifs belonging to the NBS-LRR disease resistance gene family (Creusot et al., 1999). It is not surprising that TRAP markers generated from a fixed primer (RGA1) associated with anthracnose resistance would map in the vicinity of rust resistance because R genes for anthracnose and rust colocate (Miklas et al., 2002; Kelly and Vallejo, 2004) on linkage groups B1, B4, and B11. Colocation of R genes, as in this example for anthracnose and rust, suggests they may derive from a common ancestral R gene that underwent duplication and divergence (Geffroy et al., 1999; Hulbert et al., 2001; Michelmore and Myers, 1998).

DX Mapping Population
There were only 21 TRAP markers generated by eight multiplex PCR in the DX population. The low frequency of 1.3 TRAPs generated per primer pair is attributable to derivation of the DX population from a narrow cross between parents (Dorado and XAN 176) of similar Race Mesoamerican origin within the Middle American gene pool. Similarly, Haley et al. (1994) using RAPDs observed less polymorphism among bean genotypes compared within a race or gene pool and more polymorphism among genotypes compared across gene pools and races.

Eight of the 21 TRAPs were unlinked, four integrated into existing linkage groups, and nine formed new partial linkage groups consisting of 2, 3, and 4 TRAP markers. None of the 21 TRAP markers were associated with any of the existing eight QTL or two R genes for rust resistance previously detected and mapped in the population (Miklas et al., 2000). However, four new putative QTL (P < 0.01) for resistance to ashy stem blight (2), BGYMV, and common bacterial blight in the greenhouse leaf-inoculation assay, were detected by TRAP markers (Table 3).


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  		Table 3. TRAP markers in the Dorado/XAN 176 RIL population associated with QTL conditioning resistance to common bacterial blight (CBB), Bean golden yellow mosaic virus (BGYMV), and ashy stem blight (ASB).

 
The TRAP H64.245, forming a partial linkage group consisting of three TRAP markers, was linked with QTL conditioning resistance to common bacterial blight expressed in greenhouse leaf inoculation assays (19 and 30% of phenotypic variation explained, R2) (Table 3). The G64.680 marker, also a component of a partial linkage group comprised of three TRAPs, detected a QTL conferring resistance to ashy stem blight in the field (14%). The unlinked TRAP G64.345 detected a QTL for resistance to ashy stem blight (15.8%) in a different field environment. G64.700 detected a QTL for BGYMV (13.4%) in one of three test environments. These putative QTL expressed in individual environments require further proof of expression in additional environments and populations to confirm their existence.

The same genomic regions possessing H64.245, G64.680, and G64.345 also detected QTL of minor effect (P < 0.03) against different pathogens BGYMV (8.2%), CBB (14.5%), and BGYMV (9.8%), respectively (data not shown). The genomic regions in common bean that possess QTL conferring resistance to multiple pathogens (see review by Miklas et al., 2006) was observed by Miklas et al. (2000) in the same Dorado/XAN 176 population and in a different population by Lopez et al. (2003). Whether the TRAP markers are detecting individual QTL with pleiotropic effect against multiple pathogens or a cluster of linked QTL each with specificity for resistance to a different pathogen could not be determined in this study.


   CONCLUSIONS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
REFERENCES
 
As observed in earlier studies, the TRAP technique detected numerous polymorphic markers that were reproducible and heritable as either dominant or codominant markers. TRAP markers in the BJ core mapping population mapped to 11 genomic regions with known R genes and to regions possessing QTL controlling disease resistance. TRAP markers newly identified four putative QTL conditioning resistance to bacterial, fungal, and viral diseases in the Dorado/XAN 176 population. TRAP markers, with fixed primers designed against sequences associated with disease resistance show promise for mapping regions of the P. vulgaris genome linked to resistance.

Received for publication August 8, 2005.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 




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