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Published online 2 December 2005
Published in Crop Sci 46:168-173 (2006)
© 2005 Crop Science Society of America
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CROP BREEDING, GENETICS & CYTOLOGY

Rps8 Maps to a Resistance Gene Rich Region on Soybean Molecular Linkage Group F

Stuart G. Gordona, Steven K. St. Martinb and Anne E. Dorrancea,*

a Dep. of Plant Pathology, The Ohio State University, Wooster, OH 44691-4096
b Dep. of Horticulture and Crop Science. The Ohio State University, Columbus, OH 43210-1086

* Corresponding author (dorrance.1{at}osu.edu)


   ABSTRACT
TOP
 NOTES
 ABSTRACT
INTRODUCTION
 METHODS AND MATERIALS
 RESULTS
 DISCUSSION
 REFERENCES
 
Phytophthora root and stem rot caused by Phytophthora sojae M.J. Kaufmann & J.W. Gerdemann is a serious disease of soybean [Glycine max (L.) Merr.] worldwide. Recently, a new locus for resistance to P. sojae, Rps8, was identified and mapped in two small soybean populations. The objective of this study was to verify the genomic location of Rps8 in a larger population. One hundred thirty-eight F2:3 families from a cross between ‘Williams’ (rps8/rps8) x PI 399073 (Rps8/Rps8) were genotyped by simple sequence repeat (SSR) and restriction fragment length polymorphism (RFLP) markers. From this set of families, 138 and 69 were phenotyped with P. sojae races 1 and 25, respectively. The segregation ratio for each race fit a 3:1 resistant:susceptible, confirming that Rps8 segregated as a single dominant gene. On the basis of linkage analysis with SSR and RFLP markers, Rps8 was located on molecular linkage group F in this population. This region of the soybean genome contains numerous other resistance gene loci as well as pathogen and pest resistance QTL.

Abbreviations: LOD, log-likelihood • MLG, molecular linkage group • PCR, polymerase chain reaction • PI, plant introduction • QTL, quantitative trait loci • RGA, resistance gene analog • RFLP, restriction fragment length polymorphism • SSR, simple sequence repeat


   INTRODUCTION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
METHODS AND MATERIALS
 RESULTS
 DISCUSSION
 REFERENCES
 
PHYTOPHTHORA root and stem rot is a serious disease of soybean caused by Phytophthora sojae. Single dominant resistance genes, named Rps genes, mediate resistance to P. sojae via the hypersensitive response in a gene-for-gene manner (Grau et al., 2004). Rps genes have been favored to manage this disease largely because of their effectiveness and ease of manipulation by plant breeders (Grau et al., 2004). Seven loci for resistance to P. sojae (Rps1 to Rps7) have been described and mapped to four molecular linkage groups in soybean: F, G, J, and N (Diers et al., 1992; Demirbas et al., 2001; Grau et al., 2004). The location of the Rps loci on molecular linkage groups is as follows: Rps1 and Rps7 are located on molecular linkage group (MLG) N (Weng et al., 2001), Rps2 on MLG J (Polzin et al., 1994), Rps3 on MLG F (Diers et al., 1992, Demirbas et al., 2001), and Rps4 and Rps6 on MLG G (Demirbas et al., 2001; Sandhu et al., 2004). Evidence suggests that Rps5 is also located on MLG G, linked to Rps4 (Diers et al., 1992), but conclusive assignment of this locus is presently lacking (Demirbas et al., 2001). A recent study suggests that Rps4 and Rps6 are actually alleles of the same locus (Sandhu et al., 2004). Rps1 and Rps3 have multiple alleles (Grau et al., 2004).

Single-gene-mediated resistance to plant pathogens is usually of a gene-for-gene nature, and as such is typically nondurable (Parlevliet, 2002). Individual Rps genes have remained effective for 8 to 15 yr of deployment in cultivars (Schmitthenner, 1985). Schmitthenner et al. (1994) identified races of P. sojae in 1994 that elicited susceptible interactions with Rps1k, which has been widely deployed beginning in 1982. In addition, races of P. sojae elicit susceptible responses with Rps genes that have not been widely deployed on a commercial basis (Abney et al., 1997; Dorrance et al., 2003). Several reports suggest that P. sojae populations can shift rapidly in response to selection pressure (Tooley and Grau, 1982; Kaitany et al., 2001). New Rps alleles must be identified and evaluated against sufficient numbers of P. sojae isolates to verify their effectiveness for a given geographic region. These alleles can then be incorporated into soybean cultivars to keep pace with P. sojae populations that continually adapt to overcome currently deployed Rps genes (Schmitthenner et al., 1994).

Dorrance and Schmitthenner (2000) evaluated soybean plant introductions (PIs) from the USDA soybean germplasm collection and found several South Korean accessions with potentially new Rps alleles using P. sojae isolates which had combined virulence to all known Rps genes, two-gene and most three-gene combinations. Thirty-two PIs were resistant to all isolates used in the study. The resistance gene from one of these, PI 399073, segregated as a single Rps locus in an earlier study (Burnham et al., 2003) and is the resistant parent in the present study.

Rps8, identified in PI 399073, was previously mapped to MLG A2 in two small populations of 39 and 55 F2:3 families, respectively (Burnham et al., 2003). The primary focus for this study was to confirm the location of Rps8 in a much larger population. Evidence is presented which demonstrates that Rps8 maps to MLG F above the SSR locus, Satt114. Efforts are underway to identify markers more tightly linked to Rps8 and to characterize its relationship to other resistance loci in this region. Rps3 is also located on MLG F (Diers et al., 1992; Demirbas et al., 2001), and the potential relationship between Rps8 and Rps3 is discussed.


   METHODS AND MATERIALS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 METHODS AND MATERIALS
RESULTS
 DISCUSSION
 REFERENCES
 
Plant Material
The mapping population for this study consisted of 138 F2:3 families from a cross of PI 399073 (Rps8/Rps8) and Williams (rps/rps). Eight F1 plants from this cross were allowed to self pollinate to produce F2 seeds. The F2 plants were self-pollinated and each plant was threshed individually to yield F2:3 seed for both genotyping and disease evaluations. For SSR marker loci on MLG A2 and F, both Williams and PI 399073 are homozygous (data not shown), suggesting that they are both pure lines.

Disease Evaluations
Two P. sojae isolates with the pathotypes race 1 (vir 7) and race 25 (vir 1a, 1b, 1c, 1k, 7) were used to evaluate resistance response. These P. sojae isolates were maintained at the Department of Plant Pathology, OARDC and were collected in Ohio. These isolates were shared with all of the Land Grant Universities in the North Central Region in September 2002 as well as deposited in the National Soybean Pathogen Collection Center at the University of Illinois (http://nspcc.cropsci.uiuc.edu/; verified 22 August 2005). Differential checks were included in all inoculation experiments to ensure that the P. sojae isolate elicited the appropriate response. These differential checks are as follows: Williams (rps/rps); ‘Harlon’ (Rps1a/Rps1a), ‘Harosoy 13XX’ (Rps1b/Rps1b), ‘Williams 79’ (Rps1c/Rps1c); PI 103091 (Rps1d/Rps1d); ‘Williams 82’ (Rps1k/Rps1k); L76–1988 (Rps2/Rps2); L83–570 (Rps3/Rps3); PRX 146–36 (Rps3b/Rps3b); PRX 145–48 (Rps3c/Rps3c); L85–2352 (Rps4/Rps4); L85–3059 (Rps5/Rps5); ‘Harosoy 62XX’ (Rps6/Rps6), ‘Harosoy’ (Rps7/Rps7), and PI 399073 (Rps8/Rps8). These differential checks were also used to evaluate the consistency and aggressiveness of the isolates as indicated by the total number of susceptible differential check seedlings that died out of the total inoculated.

Ten to 30 individual F3 seedlings per F2:3 family were inoculated with P. sojae race 1 in the laboratory by means of a modified hypocotyl inoculation technique as previously described (Burnham et al., 2003). For each F2:3 family between 10 and 30 seedlings were scored. Thirty seedlings were placed on paper towels for inoculation, but fewer than 30 seedlings were actually inoculated because of variability in germination and growth of the seedlings. Families that had fewer than 10 seedlings scored were omitted from the analysis, for a final population size of 138 F2:3 families. Reactions were recorded as a percentage of dead seedlings in each F2:3 family, 0 to 100%, after 7 d. These percentages were used to develop two Rps8 genotypic classifications, resistant (R_), a combination of homozygous R (0–20%) and segregating (RS) (21–79%) and susceptible (S), 80 to 100% for each F2 plant from which an F2:3 family was derived. This classification is often used in race characterization of P. sojae on the differentials (pure lines) (Abney et al., 1997; Dorrance et al., 2003; Kaitany et al., 2001). In addition a subset of F2:3 families was inoculated with P. sojae isolate race 25 to confirm single-gene segregation and consistency of response of each family to the various isolates. These inoculations provided data on 69 F2:3 families for race 25.

Genotypic Analysis
Between 10 and 15 seedlings from each F2:3 family were bulked for genotyping. The bulked tissue was placed in liquid nitrogen, lyophilized, and ground for DNA extraction. DNA was extracted by a modified CTAB method (Saghai-Maroof et al., 1984) and yielded 500 µL of sample ranging 100 to 125 ng/µL.

A total of 379 SSR markers were screened for polymorphism between Williams and PI 399073. SSRs were chosen to provide thorough genome coverage (Cregan et al., 1999; Song et al., 2004). Reactions were run as previously described (Cregan et al., 1999), and PCR products (20 µL) were resolved on 4.5% (w/v) high resolution agarose gels (Amresco, Solon, OH), stained with ethidium bromide and visualized on a UV light box.

For RFLP analysis (including RGA probe EP-42I18r), 3 µg DNA samples were digested with restriction enzymes HhaI and DraI (Promega, Madison, WI) according to the manufacturer's instructions, electrophoresed on 0.8% (w/v) agarose gels, and transferred to nylon membranes. Probes were amplified from genomic DNA. Briefly, probe sequences were downloaded from GenBank via the map link at Soybase http://soybase.org/ssr.html; verified 22 August 2005). Primers specific to the probe sequences were designed by means of the Primer 3 program (http://frodo.wi.mit.edu/cgi-bin/primer3/primer3_www.cgi; verified 22 August 2005) and PCR was run under standard conditions. Southern hybridizations were performed by standard procedures (Gardiner, 1998). After washing, membranes were wrapped in cellophane and placed on molecular imaging screens for 24 to 48 h. Hybridization signals were detected with a Storm 840 PhosphorImager (Molecular Dynamics, Sunnyvale, CA).

Data Analysis
The molecular marker and Rps8 data were tested for segregation distortion by chi-square analysis. Any marker that deviated significantly (P < 0.01) from the expected 1:2:1 segregation ratio was not included in the final analysis. The phenotypic Rps8 data were tested for goodness-of-fit to a 3:1 ratio.

Single factor analyses and genetic map construction were performed with the marker data. Analyses were performed using SAS PROC GLM, and the model was yij = µ + {alpha}i + Eij, where yij is the phenotypic classification of the jth genotype of the ith marker class, µ is the population mean, {alpha}i is the effect of the ith marker class and Eij is the experimental error (SAS Institute, 2000). As a supplement to analysis of resistance as a Mendelian trait, P. sojae resistance was also analyzed as a quantitative trait locus (QTL) by composite interval analysis. The percentage of the seedlings resistant to P. sojae was used in the single factor analysis with the marker data. MLG F was scanned for QTLs at 5 cM in the QTL analysis program MapQTL 4.0 (Van Ooijen et al., 2002). Marker cofactors were selected by the Automatic Cofactor Selection option in MapQTL and then modified according to the program instructions (Van Ooijen et al., 2002) to finish with a set of cofactor loci closest to the significant maxima in the QTL likelihood map.

Rps8 was placed on the genetic linkage map on the basis of the combination of homozygous resistant with the segregating class and the homozygous susceptible (3:1) with the molecular markers (Fig. 1 ). Genetic linkage maps of MLG F were constructed with Joinmap 3.0 linkage analysis software (Van Ooijen and Voorrips, 2001). Linkage groups were determined using a log-likelihood (LOD) threshold of 3.0. The calculation of linkage maps was performed using all pairwise recombination estimates smaller than 0.45 and a LOD score larger than 2.0. Kosambi's mapping function was used. Two markers, Sat_120 and Satt510, were excluded from the analysis because they displayed significant (P > 0.01) segregation distortion. The final map positions of markers were compared with the published soybean integrated map (Cregan et al., 1999, Song et al., 2004).



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  		Fig. 1. Location of Rps8 on MLG F in F2 population of Williams (susceptible), crossed to PI 399073 (resistant). The map on the right is the integrated soybean map (Cregan et al., 1999) available at the soybase website (Grant et al., 2002). Markers are to the right and centimorgan distances to the left. Maps were generated in Joinmap using Kosambi's mapping function.

 

   RESULTS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 METHODS AND MATERIALS
 RESULTS
DISCUSSION
 REFERENCES
 
The phenotypes for the parents in this population reacted to the P. sojae races as expected. Williams was susceptible to P. sojae races 1 (8 of 8 seedlings dead) and 25 (10 of 13 seedlings dead) and PI 399073 was completely resistant (0 of 6 and 0 of 12 seedlings dead for races 1 and 25, respectively). The differential checks also reacted as expected (data not shown). Rps8 segregated 109:29 resistant:susceptible for response to P. sojae race 1 (Table 1 and Fig. 2 ). A subset of the population was inoculated with P. sojae race 25. A total of 69 families segregated 54:15 resistant:susceptible, which is also consistent with a single gene (Table 1). The individual families were consistent in their response to both P. sojae races 1 and 25.


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  		Table 1. Segregation of resistance to Phytophthora sojae Races 1 and 25 in the F2 soybean population of Williams x PI 399073.

 


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  		Fig. 2. Number of F2:3 families in a cross of PI 399073 x Williams broken down by (1A) proportion of dead seedling in each F2:3 family, in 10% increments, and (1B) the combination of resistant and segregating (R__) and homozygous susceptible (SS) classes, following inoculation with Phytophthora sojae.

 
A total of 379 SSR primers were screened. Particular attention was given to assure that linkage groups harboring previously reported Rps loci, F, G, J N, as well as A2 were covered (Table 2). Of the 379 SSR loci, 104 were polymorphic between the two parents (Table 2). Additionally, nine RFLP and two RGA loci previously mapped near Rps3 (Ashfield et al., 2003) on MLG F were screened with 15 different restriction endonucleases. Three RFLP loci, K644, R45, and php2265, and one RGA, EP-42I18r (Ashfield et al., 2003), provided useful polymorphisms. The remaining RFLP loci were either monomorphic or gave undecipherable banding patterns. These polymorphic SSR and RFLP marker data were analyzed by single factor ANOVA to detect association between marker genotype and response to P. sojae. Several markers on MLG F were highly significant for reaction to P. sojae on the basis of ANOVA (P < 0.0001). No other linkage groups contained significant markers (P = 0.01). Using a significance threshold of P = 0.01 for the F test, one would expect one marker to randomly give a false positive for every 100 markers assayed.


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  		Table 2. Association of resistance to Phytophthora sojae with SSR markers used for genome scan of a cross of PI 399073 and Williams and construction of MLG F map.

 
The linkage analysis program Joinmap was used to calculate genetic distance between Rps8 and SSR and RFLP molecular markers on MLG F. The position of Rps8 on MLG F relative to these markers is shown in Fig. 1. The positions of marker loci used in this population and Rps3, taken from the soybean integrated map (Cregan et al., 1999), are also shown. The order of the molecular markers is consistent with their order in the integrated map (Cregan et al., 1999, Song et al., 2004). The cM distance of our map, 111 cM from Satt516 to Satt522, is also in close agreement with the integrated map, 116 cM (Fig. 1) (Cregan et al., 1999). The recombination values and linkage LOD scores for Rps8 and linked markers are shown in Table 3. Using the race 25 phenotypic data, Rps8 mapped to the same location (data not shown). We also mapped Rps8 as a quantitative trait locus. The QTL peak centered over Satt114 with a maximum LOD score over 20.


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  		Table 3. Recombination between Rps8 and linked markers on MLG F in a cross of PI 399073 and Williams.

 

   DISCUSSION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 METHODS AND MATERIALS
 RESULTS
 DISCUSSION
REFERENCES
 
Rps8 was previously mapped to MLG A2 (Burnham et al., 2003) using two small mapping populations of 38 and 54 individuals, respectively. In that study, the initial association of markers on A2 with the resistance phenotype utilized the smaller population, and ANOVA resulted in a marginally significant P value (P = 0.0527) for a single marker on A2, Satt228 (Burnham et al., 2003). With the 31 SSR markers used in the prior study (Burnham et al., 2003), and a significance threshold of P = 0.05, one can expect one marker to give a false positive association with the resistance phenotype. Selection of a more stringent P value would have prevented the false positive association (Lewers et al., 1999). In the present study, the mapping population is much larger and 11 SSR markers on MLG F are associated with the resistance phenotype at highly significant P values. In addition, for each F2:3 family the data-set consisted of 10 to 30 seedlings compared with 10 in the previous study, thus minimizing misclassification as a potential pitfall.

Utilizing a larger soybean population in this study, we report the placement of Rps8 on MLG F of the soybean genetic map in a 31-cM interval between the SSR markers Satt425 and Satt114 (Fig. 1). Rps8 is above the cluster of resistance gene loci and resistance QTL on MLG F. The map of MLG F derived by means of SSR, RFLP and RGA markers in this population is consistent with the integrated map and previously reported results (Diers et al., 1992; Tamulonis et al., 1997; Ashfield et al., 1998). This is as expected since SSR markers in particular have displayed consistent positions across multiple soybean mapping populations (Shoemaker et al., 2004).

Rps3 has also been placed on MLG F, but that study was performed using RFLPs (Diers et al., 1992). Rps3 has not been ordered in relation to the SSR markers on MLG F, although bulked segregant analysis and recombination estimates have associated this locus with several SSRs on MLG F (Demirbas et al., 2001). On the basis of the current map position for Rps3, these studies suggest that it is a distinct Rps locus rather than an allele of Rps8. However, to be certain that Rps8 is distinct from Rps3, allelism tests must be performed or the genes must be mapped in the same segregating population as was done recently for Rps1 and Rps7 (Weng et al., 2001). Mapping Rps8 and Rps3 in separate populations with a common susceptible host would also provide solid corroborating evidence.

There are two possible approaches to allelism tests between Rps8 and Rps3. First, a large population (1000 + F2:3 families) of an Rps8/Rps8 line crossed with an Rps3/Rps3 line could be used to detect homozygous susceptible individuals. If Rps8 and Rps3 are allelic, no such individuals would be expected. The departure from a 15:1 segregation ratio for two Rps alleles at closely linked loci, which both confer resistance to a given race, would be indicative of their genetic linkage. If the linkage is close, a very large population is necessary to have a high likelihood of recovering even a single homozygous susceptible individual. For example, if Rps3 and Rps8 are linked at a genetic distance of 10 cM, to have a 95% probability of recovering at least one homozygous susceptible individual, a population of 1197 F2 individuals is necessary. If the genetic distance is 30 cM, then 200 individuals is sufficient to recover two individuals at 95% probability.

Second, to perform allelism tests between Rps3 and Rps8 in a much smaller population (100–200 F2:3 families), two P. sojae isolates that are either virulent to Rps8, but not Rps3 or virulent to Rps3 but not to Rps8 are required. Thus, both genes could be mapped in the same population. Rps8-derived resistance conferred a resistant response to all but one of 216 P. sojae isolates tested (Dorrance, 2004). Unfortunately, this isolate also elicits a susceptible interaction with Rps3a. Efforts are in progress to identify either an isolate which differentiates between Rps8 and Rps3. Approaches such as mapping Rps3 and Rps8 in different populations, but with a common susceptible parent as an alternate to allelism tests are also in progress. However, a map position for Rps8 that is above Satt114 suggests that Rps8 is not an allele of Rps3.

Molecular markers are useful for crop improvement because they allow indirect selection of desirable genotypes without costly, time-consuming phenotypic analysis (Young, 1999). The hypocotyl inoculation technique employed in this study is relatively fast and inexpensive. Since PI 399073 is an unimproved genotype with poor agronomic characteristics, markers tightly linked to Rps8 will be as useful in avoiding linkage drag as for selecting the Rps8 locus per se. Furthermore, molecular markers will allow the genetic architecture of resistance loci to be characterized, thereby laying the foundation for cloning and other endeavors. An advanced population (~400 families) is in development to construct a fine-scale genetic and physical map of Rps8 and the surrounding region.

Linkage group F of the soybean genome harbors many single-gene resistance loci and QTL. In addition to Rps loci, genes for resistance to bacteria, Rpg1 (Ashfield et al., 1998), and virus, Rsv1 (Yu et al., 1994), pathogens and QTL for resistance to insects (Rector et al., 1999) and a nematode (Tamulonis et al., 1997) previously have been mapped to MLG F. In addition this region is a hotspot for resistance-gene like sequences of as yet undefined function or specificity (Jeong et al., 2001). Rpg1-b confers resistance to Pseudomonas syringae pv. glycinea (Coerper 1919) Young, Dye & Wilkie 1978 and is tightly linked to Rps3, but the two are not allelic (Ashfield et al., 1998). The Rsv1 locus was shown to be made up of tightly linked NBS-LRR genes, and not alleles at a single locus (Hayes et al., 2004). Furthermore, many uncharacterized NBS-LRR genes and gene candidates map to this region of MLG F (Jeong et al., 2001; Ashfield et al., 2003; Hayes et al., 2004), providing grist for the evolutionary mill of pathogen resistance.


   ACKNOWLEDGMENTS
 
We thank Sue Ann Berry and Krissana Kowitwanich for technical assistance they provided.


   NOTES
TOP
 NOTES
ABSTRACT
 INTRODUCTION
 METHODS AND MATERIALS
 RESULTS
 DISCUSSION
 REFERENCES
 
Salaries and research support provided by State and Federal Funds appropriated to the Ohio Agricultural Research and Development Center (OARDC), The Ohio State University. This research project was supported by Ohio's Soybean Producers' check-off dollars through the Ohio Soybean Council

Received for publication April 21, 2005.


   REFERENCES
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 METHODS AND MATERIALS
 RESULTS
 DISCUSSION
 REFERENCES
 





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