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a Black Sea Agric. Res. Inst., P.K. 39, Samsun, Turkey
b Usda, Ars, Saa, Cgbru, P.o. Box 748, Tifton, Ga 31793
c Dep. of Hort. & Crop Sci., Ohio Agric. Res. & Development Center, Ohio State Univ., 1680 Madison, Ave., Wooster, OH
d USDA, ARS, Bldg. 006, Room 100, BARC-West, 10300 Baltimore Ave., Beltsville, MD
e USDA, ARS, Corn Insect and Crop Genetics Research Unit, Dep. of Agronomy, Iowa State Univ., Ames, IA 50011
f Dep. of Agronomy, Univ. of Nebraska, Lincoln, NE 68583-0915
* Corresponding author (jspecht1{at}unl.edu)
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ABSTRACT |
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 TOPNOTES ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Abbreviations: MAS, marker-assisted selection • SSR, simple sequence repeat • NIL, near-isogenic line • BSA, bulked-segregant analysis • LG, linkage group • RFLP, restriction fragment length polymorphism
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INTRODUCTION |
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TOPNOTESABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Naturally occurring resistance to Phytophthora root rot exists in soybean. Monogenic race-specific resistance to the causal organism is known to be controlled by 13 dominant alleles at seven soybean loci, designated Rps1 (Bernard et al., 1957), Rps2 (Kilen et al., 1974), Rps3 (Mueller et al., 1978), Rps4 (Athow et al., 1980), Rps5 (Buzzell and Anderson, 1981), Rps6 (Athow and Laviolette, 1982), and Rps7 (Anderson and Buzzell, 1992). The Rps1 and Rps7 loci are linked (Lohnes and Schmitthenner, 1997), as are the Rps4 and Rps5 loci (Diers et al., 1992).
By means of DNA marker technology (Botstein et al., 1980; Williams et al., 1990; Akkaya et al., 1992; Vos et al., 1995), marker-dense genetic linkage maps have been constructed in many crop species (O'Brien, 1993), including soybean (Shoemaker and Specht, 1995; Keim et al., 1997; Cregan et al., 1999). Plant breeders can use molecular markers to select indirectly individuals in segregating populations that carry a gene for a favorable trait if a tight linkage exists between a marker locus and the genetic locus controlling that trait (Tanksley et al., 1989). Marker-assisted selection (MAS) allows the breeder to bypass laborious and/or costly phenotypic screens. Moreover, if two closely linked marker loci are present on either side of the desired locus, the retention of donor DNA in NILs of cultivars with the introgressed gene could be minimized (Young and Tanksley, 1989).
Bulked segregant analysis is an effective strategy for identifying linkages between genetic markers and qualitative traits (Michelmore et al., 1991). A population of F2 individuals segregating for two alleles of a single gene (or marker) can be sorted into two classes comprised of the contrasting homozygous genotypes. If the DNA bulks corresponding to those two classes display a polymorphism for a genetic marker, linkage between the marker and the segregating locus can be inferred. The number of F2 individuals that should be composited in each bulk is dependent upon the number of false inferences of linkage that the investigator is willing to tolerate. In any event, putative linkages must eventually be verified by a genetic marker analysis of F2 individuals. However, verification of a putative linkage does not necessarily require a complete F2 data set. Allard (1956) published maximum likelihood equations for estimating linkage (i.e., a recombination value and its standard error) from incomplete F2 data. One common example of an incomplete F2 data set is the segregation of a codominant marker within a homozygous genotypic class produced by another marker.
For MAS applications, the most desirable markers would map to a single genomic position but each marker would have many alleles, which would increase the probability of marker polymorphism. SSR markers are single-locus markers for which the variation in the number of tandem two or three base pair repeats offers great potential for multiple allelism (Cregan et al., 1999). SSR technology is also based on the polymerase chain reaction (PCR), which makes it accessible to most plant breeders. Moreover, the DNA amplicons of SSR markers are often resolvable on high-resolution agarose gels stained with ethidium bromide; offering the breeder using MAS a convenient alternative to polyacrylamide gels and radio isotopes.
The objective of this research was to use bulked-segregant analysis to identify soybean SSR markers tightly linked to each of the six known Phytophthora resistance genes: Rps1 to Rps6. SSR linkages have already been identified for the other known resistance gene, Rps7, on the basis of its in situ segregation in one of the mapping populations used in the construction of the soybean SSR map (Lohnes and Schmitthenner, 1997; Cregan et al., 1999).
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MATERIALS AND METHODS |
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TOPNOTESABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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) of observing only rpsrps F3 progeny from a Rpsrps F2 progenitor is qn = 10-6, based on n = 10 F3 seedlings and a q = 0.25 probability of a rpsrps from a heterozygous F2 (Hanson, 1959). If the 10 F3 seedlings segregated for resistance and susceptibility, the F2 progenitor was classified as Rpsrps. However, if all 10 F3 seedlings were deemed resistant, then another 10 F3 seedlings were planted and inoculated, and if all 20 F3 seedlings proved to be resistant, then the F2 progenitor was classified as RpsRps. The probability () of observing only Rps—F3 progeny from a Rpsrps F2 progenitor, is qn = 0.0032, based on n = 20 F3 seedlings and a q = 0.75 probability of RpsRps or Rpsrps from a heterozygous F2. Inoculation of the resistant parents and checks provided periodic assessment of RpsRps seedling death arising from mechanical inoculation injury. The frequency of these was near zero in all screenings. Inoculation of the susceptible parents and checks provided periodic assessment of rpsrps seedling survival (i.e., disease escape) arising from variation in inoculation efficacy or inoculum pathogenicity. Any screening run in which the frequency of disease escapes was in excess of 5% was repeated using remnant F3 seed.
DNA Isolation
Leaf tissue was collected in the field from each parent and from approximately 20 to 25 random F3 plants from the F2:3 progeny rows that had been classified as homozygous dominant RpsRps or recessive rpsrps in the greenhouse screening bioassay described above. No tissue was collected from the F2:3 rows classified as heterozygous. The leaf tissue was transported to the laboratory on dry ice, frozen, and stored at -20°C. The frozen leaf tissue was eventually lyophilized and ground to a fine powder that was also stored at -20°C until DNA extraction could be performed. DNA was extracted using a protocol modified from that of Saghai-Maroof et al. (1984). After DNA extraction and its resuspension in TE, the DNA samples were diluted to 20 ng/mL for SSR analysis.
Bulked Segregant Analysis (BSA) and SSR Marker Electrophoresis/Staining
Paired primers specific for the amplification of each SSR were used. This study was initiated prior to the integration of the soybean SSR and restriction fragment length polymorphism (RFLP) maps (Cregan et al., 1999), when the final map positions of the SSR markers were not yet known, so parental screening for SSR polymorphism was commenced using all available SSRs. After SSR/RFLP map integration, parental SSR assays were limited mainly to those SSRs that were in the same linkage groups as the RFLP markers that Diers et al. (1992) had earlier reported were linked to Rps1 thru Rps5. Because of the multi-locus nature of the RFLP markers linked to Rps4 and Rps5, SSRs linked to each locus of those RFLP markers were used to assay the Rps4 and Rps5 populations. Parental SSR assays of the Rps6 locus, whose map position was unknown, continued until an SSR linkage was found, but thereafter parental assays were limited to SSRs in the same linkage group.
Polymorphism at any given SSR locus was detected according to the procedures of Akkaya et al. (1992) and Rongwen et al. (1995), except that the DNA amplicons were resolved on high resolution agarose gels instead of polyacrylamide gels, and were visualized with ethidium bromide staining instead of 32P labeling. A 10-µL PCR reaction contained 50 ng of genomic DNA (parental, F2 bulk, or F2 individual), 0.1 µM of each primer, 5x Reaction Buffer (250 mM Tris), 0.6 units of AmpliTaq DNA Polymerase (Perkin-Elmer Corporation, Norwlak, CT), 2.5 µM dNTPs. Each sample was covered with 10 to15 µL of light mineral oil and subjected to 31 cycles of denaturing (25 s at 94°C); annealing (25 s at 47°C); and extension (25 s at 68°C) in a DNA thermo-cycler, followed by a final extension step (3 min at 72°C) and incubation at 4°C. After PCR amplification, products were separated by electrophoresis by means of 5% (w/v) agarose gels stained with ethidium bromide and photographed under ultraviolet light. The contrasting DNA bulks were constructed by combining equal amounts of DNA collected from about 15 F2:3 progenies of the 15 to 40 available within each population as either homozygous RpsRps, or homozygous rpsrps. Although 15 individuals per bulk is larger than the recommendation of eight by Michelmore et al. (1991), a lower experimentwise rate of false inferences of putative linkage was preferred for the present study.
The SSR marker assays were conducted in three stages. First, the parents of each cross were screened for polymorphism with SSR markers. Second, the informative (i.e., parentally polymorphic) SSRs were used to screen the contrasting F2 bulks to determine if the parental polymorphism was fully or partially maintained in those bulks. If so, that finding was considered presumptive evidence of linkage. Third, individuals within the F2 homozygous resistant (RpsRps) class, and within the F2 homozygous susceptible (rpsrps) class, were evaluated with any SSR that displayed a polymorphism between the bulks.
Linkage Analysis
Chi-square analyses were conducted to determine if the observed segregation at each givenRps locus fit the expected F2 segregation ratio of 1RpsRps:2Rpsrps:1rpsrps (Table 1) or, if that ratio was not evident, whether the observed segregation fit an expected 3Rps—:1rpsrps ratio. EachRps x rps mating was treated as an AA x BB mating with respect to the coding of the SSR marker alleles (i.e., the Harosoy–E2 (rps) parent was designated as the source of the SSR ‘B’ allele). Chi-square analyses were also performed to determine if the genotypic segregation of an SSR marker within a given F2 homozygous class (either RpsRps or rpsrps) differed significantly from the 1AA:2AB:1BB ratio which would be expected for an SSR locus not linked to the Rps/rps locus (Table 2). In addition, the ratio of AA to BB marker genotypes, when their numbers were summed over the contrasting homozygous classes (i.e., RpsRps and rpsrps), was evaluated to determine if it fit the 1:1 ratio expected if the SSR andRps loci were independent. Because of limited seed amounts, the number of homozygous F2:3 progenies for which DNA was available for SSR genotyping (Table 2) was sometimes slightly less than the number of homozygous F2:3 progenies that were identified in the phenotypic bioassay (Table 1).
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In rare cases, an SSR behaved as a dominant marker (i.e., absence of the Harosoy amplicon), perhaps because one of the primers did not anneal completely with the Harosoy parent locus. To estimate linkage when only the dominant (amplicon present) and recessive (amplicon absent) genotypes of the SSR marker were observable within the homozygous recessive class of a repulsion phase parental mating, Eq. [7] (Allard, 1956) was used:
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In this study, a putative SSR–Rps linkage was considered likely if the calculated p value, plus its standard error, totaled to less than 0.40, and quite likely if more than one SSR in a localized region of a particular linkage group was linked to a given Rps locus. For each SSR–Rps linkage, we report a p value and standard error computed from each homozygous class, as well as a mean p value and standard error computed from the SSR segregation data pooled over both homozygous classes.
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RESULTS |
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TOPNOTESABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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2 = 0.07; P = 0.79), Rps2 (2 = 0.003; P = 0.96), and Rps3 (2 = 1.35; P = 0.24) populations. Although the classification of the resistant F2:3 progenies in these three populations into homozygous (RpsRps) and heterozygous (Rpsrps) classes was apparently not error-free, the Chi-square tests suggested that the observed fraction of susceptible F2:3 progenies was close to that expected for homozygous recessive (rpsrps) progenies, and thus it would be suitable for use in linkage analysis. Relative to the remaining populations, a significant deviation from a 3:1 ratio was observed for Rps1d (2 = 5.17, P = 0.02), Rps1k (2 = 7.21, P = 0.007), and Rps5 (2 = 56.66, P < 0.0001). The segregational skewing in these three populations did not appear to be due to a reversal of dominant and recessive alleles, since significant non-fits to a 1RpsRps:3 (2Rpsrps:1rpsrps) ratio were also evident for Rps1d, Rps1k and Rps5 (2 = 9.21, 12.68, and 11.90, respectively). Because monogenic segregation was not verifiable, these three populations were not suitable for linkage analyses. This was unfortunate with respect to identifying SSRs linked to the Rps5 locus. However, Rps1d and Rps1k are by definition allelic with Rps1, Rps1b, and Rps1c, so any SSR linked to the latter three should also be linked to the first two. The percentage of SSR markers that were polymorphic between the Harosoy–E2 parent and the Clark (Rps1 to Rps2 loci) or Williams (Rps3, Rps4, and Rps6 loci) parents ranged from 16.7 to 30.7%, averaging about 25.5% (Table 2). SSR polymorphism was generally lower in the Williams x Harosoy matings probably because the cultivar A.K. (Harrow), a parent of Harosoy, is nearly identical to the cultivar Illini, a great-grandparent of Williams.
Resistance Locus Rps1
Of the 228 SSRs tested on the Harosoy–E2 and Clark–Rps1 parents, 70 (30.7%) were polymorphic (Table 2). These SSRs were distributed mostly at random over the soybean genetic map. Of the 70 parentally polymorphic SSRs, seven (10%) map to Linkage Group (LG) N. In a prior linkage study involving RFLP markers, Diers et al. (1992) had positioned Rps1 in an RFLP linkage group then known as LG-K. In the recently published soybean SSR map (Cregan et al., 1999), that RFLP linkage group is now part of LG-N.
Putative linkages between the Rps1 locus and the LG-N markers Satt159 and Satt152 were observed in the bulked segregant analysis. To confirm these putative linkages, SSR genotyping was performed on each of 27 homozygous resistant (Rps1Rps1) and 18 homozygous susceptible (rps1rps1) F2 individuals (Table 2). The mean recombination (p) between Satt159 and Satt152 and Rps1 was 0.16 and 0.13, respectively (Table 3). However, the linkage estimates based on the homozygous susceptible rps1rps1 individuals were much lower (for both SSRs, only one progeny was recombinant) when compared to those based on the homozygous resistant Rps1Rps1 individuals. The Rps1 population had satisfactory fits to the expected 1RpsRps:2Rpsrps:1rpsrps ratio (Table 1), and to the expected 3Rps-:1rpsrps ratio; however, the homozygous resistant and heterozygous classes did not fit the expected 1:2 ratio, suggesting that some heterozygous progenies were probably mis-scored as homozygous resistant progenies. If so, then the linkage computed from the homozygous susceptible class in Table 3 may be more reliable. Identical p = 0.03 estimates were derived from that class for the linkage of Rps1 to both Satt152 and Satt159, which is consistent with the tight linkage of the two SSR markers with each other (i.e., 0.5 cM in the map presented by Cregan et al., 1999).
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Tests of F2 individuals for linkage to SSR markers Satt530 and Satt584, which are located 3.2 and 4.8 cM, respectively, below Satt152 (Cregan et al., 1999) revealed that these two markers were tightly linked to Rps1 (Table 3). In fact, within the homozygous susceptible rps1rps1 class, no recombinants were observed for either SSR, suggesting tight linkage. Within the homozygous resistant Rps1Rps1 class, many recombinants were observed but, as was noted before, this class may have been contaminated with heterozygous Rps1rps1 individuals.
Segregation data were also obtained for the polymorphic SSRs Satt257 and Satt022, located 61.5 and 70.5 cM, respectively, below Satt584 (Cregan et al., 1999). As expected, these two SSR markers segregated independently of the Rps1 locus (Table 3).
Segregation of the Rps1b allele fit the expected 1:2:1 ratio, but segregation of the Rps1c allele did not (Table 1). Rps1c segregation did fit a 3:1 ratio (2 = 0.0737, P = 0.7860), so the homozygous recessive class was considered suitable for linkage analysis. The same 228 SSRs tested on the Rps1 population were used to screen the Rps1b and Rps1c populations. Seventy SSRs (30.7%) in the Rps1b population and 65 SSRs (28.5%) in the Rps1c population were polymorphic between the respective parents (Table 2). Several LG-N SSRs segregating in the Rps1 population were not segregating in the Rps1b and Rps1c populations, although Satt152, Satt530, and Satt584 did segregate in all three populations. Satt152 was linked to Rps1, Rps1b, and Rps1c with respective mean p values of 0.13 (Table 3), 0.16 (Table 4), and 0.24 (Table 5). Considering only the SSR genotypes in the homozygous recessive classes, the respective p values were 0.03 (Table 3), 0.09 (Table 4), and 0.15 (Table 5). Satt530 and Satt584 were also linked to Rps1b and Rps1c, but not as tightly as those two SSRs were linked with Rps1. For the homozygous recessive classes, the respective Satt530 and Satt584 linkages to Rps1, Rps1b, and Rps1c were 0.00 and 0.00 (Table 3), 0.12 and 0.20 (Table 4), and 0.14 and 0.21 (Table 5).
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Resistance Locus Rps6
The map position of Rps6 was unknown prior to this investigation. Genotypic segregation in the Rps6 x rps6 population did not deviate significantly from the 1Rps6Rps6:2Rps6rps6:1rps6rps6 ratio expected for a monogenic trait (Table 1). A total of 420 SSRs were tested on Harosoy–E2 and Williams–Rps6, and 81 (19.2%) were polymorphic (Table 2). Of these 81, just two, Satt472 and Satt191 on LG-G, displayed a noticeable difference in the intensities of the parental amplicons in the DNA bulks. SSR segregation data for 19 homozygous resistant and 32 homozygous susceptible classes generated linkage estimates of 0.23 and 0.22 between Rps6 and either Satt472 or Satt191, respectively (Table 9). Satt472 was more tightly linked to Rps4 (Table 8) than it was to Rps6 (Table 9). Satt012, Satt288, and Sct_187, which flank Satt191 or Satt472, were not polymorphic in this Rps6 population. Satt199, located farther above these markers, was parentally polymorphic, but was not linked to Rps6 (Table 9).
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DISCUSSION |
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TOPNOTESABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The goal of this research was to identify SSR markers linked to the Rps1 to Rps6 loci. Linkages were found for all but Rps5, but only the linkages (all P < 0.05) of Satt584, Satt530, Satt152, and Satt159 with the Rps1 locus, and the linkage (P < 0.09) of Satt472 with the Rps4 locus, were close enough to be possibly useful in MAS applications. Linkages of p = 0.05 or less are generally required for efficient MAS, although this restriction can be relaxed if two markers flanking the locus of interest are available (Tanksley, 1983). Low SSR polymorphism between the Harosoy and NIL parents precluded the identification of exceptionally tight linkages for each Rps locus (see later discussion). However, the SSR–Rps linkages that were detected in this study were useful in other ways. First, we directly confirmed the SSR map position of those Rps loci whose map positions on the soybean SSR map were heretofore inferred on the basis of map positions of multi-locus RFLP markers linked to those Rps loci (Diers et al, 1992; Cregan et al., 1999). With this study we have established that the Rps1, Rps2, Rps3, and Rps4 loci clearly belong to the SSR linkage groups N, J, F, & G, respectively. Second, we were able to identify a LG-G map position for Rps6, the only Rps locus not yet positioned on the SSR map. Our linkages of SSRs with Rps4 and Rps6, and the linkage of T005 to both Rps4 and Rps5 (Diers et al., 1992), suggests that these three loci may all be linked on LG-G. The literature is not clear as to whether complementation tests were ever performed to determine if Rps4, Rps5, and Rps6 are an allelic series at one monogenic locus (like the multi-allelic Rps1 locus), or are a cluster of closely linked, but recombinably separate loci (Athow et al., 1980; Buzzell and Anderson, 1981; Athow and Laviolette, 1982; Diers et al., 1992). Both kinds are evident in other species. For example, the L gene conferring rust resistance in flax consists of at least 13 different alleles at one locus that differ by point mutations as well as major structural changes (Ellis et al., 1999). In contrast, at least 10 separate DM genes, mapping to a single cluster, confer resistance to downy mildew in lettuce (Meyers et al., 1998), and in barley, the Mla locus for powdery mildew resistance consists of a cluster of several linked genes and at least 11 Resistance Gene Analogs (Wei et al, 1999). The soybean genomic segment containing the Rps4, Rps5, & Rps6 genes would seem to be worthy of further research in that regard.
The ideal MAS scenario would be one in which each Rps allele for resistance is completely linked to an SSR allele not present in the elite germplasm pool, so that MAS would be applicable to any mating of the donor parent to a recurrent (elite) parent. Moreover, for every Rps locus with multiple alleles, each of its alleles would ideally be linked to a different SSR allele, thereby allowing the identification, in resistant x resistant matings, of those progeny possessing each desired resistance allele. The opportunity for both of the above scenarios exists. Narvel et al. (2000), in a survey of 40 plant introductions (PIs) and 39 elite lines with 74 SSRs, observed a total of 397 different SSR alleles, of which 138 were detected in the PIs only (i.e., not present in the elite lines). More than 85% of the PI-specific 138 alleles had a frequency of 0.25 or less.
Two obstacles were encountered in our search for such SSR–Rps linkages. First, there was often a paucity of markers in the genomic regions containing resistance alleles. For example, SSR markers were scarce in the LG-J region containing Rps2, and in the LG-G region containing Rps4, Rps5, and Rps6 (Cregan et al., 1999). This situation is improving as more SSR markers are currently being added to the SSR-sparse regions of the soybean genetic map (Cregan, 2001, unpublished data). Second, when SSRs were abundant in a genomic region, parental SSR polymorphism was often low. This was the case for the LG-F region containing Rps3 (Cregan et al., 1999), where only four of the many available SSRs were polymorphic in our Rps3 population. The only practical solution to this parental monomorphism problem is to sample more parents by creating more than one cross segregating for a given resistance gene.
The SSR genotyping of just those F2 individuals homozygous recessive for a gene of interest proved to be a convenient and efficient means of confirming (or refuting) the tightest putative linkages, which were the ones of interest. Since only the homozygous recessives of an F2 population undergo SSR genotyping, the cost of genotyping is but a quarter of that needed to genotype the entire F2 population. Thus, for approximately the same cost of creating one segregating population in which all 100 F2 individuals were SSR genotyped, one could create four different segregating populations of 100 F2s each (from mating one donor Rps parent to four divergent rps parents) and SSR genotype only the four sets of approximately 25 homozygous recessives. In this way, the probability of encountering parental polymorphism in the genomic region of interest would be greater. The trade-off is that the 100 F2 individuals in each of four populations would still have to be phenotyped to identify the 25 homozygous recessives.
Finally, we would recommend SSR genotyping of the F2 homozygous recessive class to soybean geneticists who, on the basis of a classical inheritance study, have identified a new classical gene for a qualitatively scored trait. If the leaf tissue is not available, then one could save seed of the parents and seed of (at least) 25 of the F2 or F3 homozygous recessives. SSR genotyping could be performed on these homozygous recessives, which could lead to the positioning of the new gene on the SSR map. Putting such genes on the map as they are discovered might be of interest to geneticists wishing to clone particular genes of interest. Moreover, when genes affecting the same trait are known to exist, the Soybean Genetics Committee requires allelism tests before the approval of a symbol for a new gene is granted. Comparison of the map position of a new gene with the map positions of existing genes would help the geneticist to determine which of the many possible complementation tests are truly necessary.
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TOPNOTESABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Received for publication September 18, 2000.
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TOPNOTESABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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