Molecular mapping of rsp1, rsp2, and rsp3 genes conferring resistance to septoria speckled leaf blotch in barley

ABSTRACT Septoria speckled leaf blotch (SSLB) caused by Septoria passerinii is a common disease in barley. SSLB resistance genes Rsp1, Rsp2, and Rsp3 have previously been identified in the United States Department of Agriculture National Small Grains collection accessions CIho 14300, CIho 4780, and CIho 10644, respectively. Populations of 100 to 120 F(2) individuals were evaluated for SSLB resistance in the greenhouse. Inheritance was evaluated in F(2:3)-derived families in the field. Partial molecular maps for three Rsp genes were constructed on F(2) and F(2:3) families derived from crosses between Robust and the resistant accessions CIho 14300, CIho 4780, and CIho 10644. The resistant locus Rsp1 was mapped to the short arm of chromosome 3H with two flanking diversity arrays technology (DArT) markers, bPb-6978 (8.9 cM) and bPb-9945 (16.3 cM), and two random amplified polymorphic DNA (RAPD) markers, OPC2(441R) (3.0 cM) and UBC285(158R) (4.3 cM). The genes Rsp2 and Rsp3 were positioned on the short arm of barley chromosome 1H with two restriction fragment length polymorphism (RFLP), six DArT, and three RAPD markers. An RFLP marker, MWG938, and an RAPD marker, OPAH5(545C), were tightly associated with Rsp2 at a distance of 0 cM. Five DArT markers spanning the short arm of 1H surrounded Rsp3 at a distance of 2.3 and 5.8 cM, while two RAPD markers-OPBA12(314C) (2.4 cM) in coupling and OPB17(451R) (3.5 cM) in repulsion-flanked Rsp3. Molecular marker data associated with Rsp2 and Rsp3 indicated that the two genes are closely linked on chromosome 1HS. A total of 17 of 154 simple sequence repeats (SSRs) tested were associated with Rsp genes on chromosome 1H and 3H, and they were also integrated into genetic linkage maps of the three F(2) Robust populations. Knowledge about the map position of Rsp genes on barley chromosomes will be useful for breeding for SSLB resistance in barley and eventual gene cloning.     

Molecular mapping and marker-assisted selection of genes for septoria speckled leaf blotch resistance in barley

ABSTRACT Septoria speckled leaf blotch (SSLB), caused by Septoria passerinii, has emerged as one of the most important foliar diseases of barley in the Upper Midwest region of the United States. To map and tag genes for SSLB resistance, we developed two populations derived from the resistant accessions CIho 4780 and CIho 10644 and the susceptible malting cv. Foster. Segregation analysis of F(2) plants or F(2:3) families from the Foster/CIho 4780 and Foster/CIho 10644 populations revealed that a single dominant gene conferred resistance at the seedling stage. Bulked segregant analysis identified an amplified fragment length polymorphism marker, E-ACT/M-CAA-170, that co-segregated with the SSLB resistance gene Rsp2 in the Foster/CIho 4780 F(2) population. Southern hybridization analysis with DNA from the wheat/barley addition lines localized E-ACT/M-CAA-170 on the short arm of the barley chromosome 5(1H). Restriction fragment length polymorphism analysis with DNA clones previously mapped to the short arm of chromosome 5(1H) placed Rsp2 at a position flanked by the markers Act8 and ksuD14. A sequence-characterized amplified region (SCAR) marker (E-ACT/M-CAA-170a) was developed that co-segregated with not only Rsp2 in the Foster/CIho 4780 population but also resistance gene Rsp3 in the Foster/CIho 10644 population. This result indicates that Rsp3 is closely linked to Rsp2 on the short arm of chromosome 5(1H). The utility of SCAR marker E-ACT/M-CAA-170a for selecting Rsp2 in two different breeding populations was validated.     

Novel septoria speckled leaf blotch resistance loci in a barley doubled-haploid population

The genetics of resistance to Septoria speckled leaf blotch (SSLB), caused by Septoria passerinii, was studied in the Leger × CIho9831 barley doubled-haploid population. The 140 lines in the population segregated as 102 resistant and 38 susceptible, approximating a 3:1 ratio. A recombination map was developed using diversity arrays technology and other molecular markers. Quantitative trait locus (QTL) analysis demonstrated that resistance is primarily conferred either by having the CIho9831 allele at a QTL on 6HS or by having the CIho9831 allele at both of two QTLs on 3H and 2HL. In addition, ≈1/16 of the lines were resistant for unidentified reasons. This model predicts a resistant/susceptible ratio of 11:5, which fits the phenotypic observations. Minor QTLs were detected on 2HS and 1H. DNA sequences of linked markers suggest that the 6HS, 3H, and 2HS QTLs are part of resistance gene clusters and that the 6HS and 3H QTLs share homology. The 6HS QTL is identical to or closely linked to the SSLB resistance locus Rsp4 and the 1H QTL to the Rsp2 or Rsp3 locus. The 3H and 2HS QTLs are unique and offer new opportunities for pyramiding resistance genes through marker-assisted breeding for resistance to S. passerinii.     

Inheritance and molecular mapping of barley genes conferring resistance to wheat stripe rust

ABSTRACT Most barley cultivars are resistant to stripe rust of wheat that is caused by Puccinia striiformis f. sp. tritici. The barley cv. Steptoe is susceptible to all identified races of P. striiformis f. sp. hordei (PSH), the barley stripe rust pathogen, but is resistant to most P. striiformis f. sp. tritici races. To determine inheritance of the Steptoe resistance to P. striiformis f. sp. tritici, a cross was made between Steptoe and Russell, a barley cultivar susceptible to some P. striiformis f. sp. tritici races and all tested P. striiformis f. sp. hordei races. Seedlings of parents and F(1), BC(1), F(2), and F(3) progeny from the barley cross were tested with P. striiformis f. sp. tritici races PST-41 and PST-45 under controlled greenhouse conditions. Genetic analyses of infection type data showed that Steptoe had one dominant gene and one recessive gene (provisionally designated as RpstS1 and rpstS2, respectively) for resistance to races PST-41 and PST-45. Genomic DNA was extracted from the parents and 150 F(2) plants that were tested for rust reaction and grown for seed of F(3) lines. The infection type data and polymorphic markers identified using the resistance gene analog polymorphism (RGAP) technique were analyzed with the Mapmaker computer program to map the resistance genes. The dominant resistance gene in Steptoe for resistance to P. striiformis f. sp. tritici races was mapped on barley chromosome 4H using a linked microsatellite marker, HVM68. A linkage group for the dominant gene was constructed with 12 RGAP markers and the microsatellite marker. The results show that resistance in barley to the wheat stripe rust pathogen is qualitatively inherited. These genes might provide useful resistance against wheat stripe rust when introgressed into wheat from barley.     

Molecular Mapping of the rps1.a Recessive Gene for Resistance to Stripe Rust in BBA 2890 Barley

ABSTRACT Stripe rust, caused by Puccinia striiformis f. sp. hordei, is one of the most important diseases of barley in the south-central and western United States. Growing resistant cultivars is the best approach for controlling the disease. The barley genotype BBA 2890 has all-stage resistance against all races of P. striiformis f. sp. hordei (PSH) identified thus far in the United States. The resistance in BBA 2890 is controlled by a single recessive gene, rps1.a. The objectives of this study were to identify resistance gene analog polymorphism (RGAP) markers for the all-stage resistance gene rps1.a, to map the gene on a barley chromosome using chromosome-specific simple sequence repeat (SSR) markers, and to determine the presence or absence of the flanking RGAP markers for the gene in 24 barley genotypes. Seedlings of the parents and 200 F(8) recombinant inbred lines (RILs) were tested for resistance to pathogen races PSH-14, PSH-48, and PSH-54 in the greenhouse in 2005. Genomic DNA was extracted from the parents and 150 F(8) RILs. The RGAP technique was used to identify molecular markers for the rps1.a gene. Twelve primer pairs generating repeatable polymorphic bands were selected for genotyping the 150 F(8) RILs. A genetic linkage group was constructed for the resistance gene with 13 RGAP markers and four chromosome-specific SSR markers. The four SSR markers mapped the gene on the long arm of barley chromosome 3H. The closest RGAP marker for the resistant allele was within a genetic distance of 2.1 centimorgans (cM). The closest marker for the susceptible allele was 6.8 cM away from the locus. The two closest RGAP markers for the resistant allele detected polymorphisms in 67 and 71% of the 24 barley genotypes when used individually, and detected polymorphism in 88% of the genotypes when used in combination. This information should be useful in incorporating the resistance gene into barley cultivars and in pyramiding the gene with other resistance genes for superior stripe rust resistance.     

Amplified fragment length polymorphism markers linked to a major quantitative trait locus controlling scab resistance in wheat

ABSTRACT Scab is a destructive disease of wheat. To accelerate development of scab-resistant wheat cultivars, molecular markers linked to scab resistance genes have been identified by using recombinant inbred lines (RILs) derived by single-seed descent from a cross between the resistant wheat cultivar Ning 7840 (resistant to spread of scab within the spike) and the susceptible cultivar Clark. In the greenhouse, F(5), F(6), F(7), and F(10) families were evaluated for resistance to spread of scab within a spike by injecting about 1,000 conidiospores of Fusarium graminearum into a central spikelet. Inoculated plants were kept in moist chambers for 3 days to promote initial infection and then transferred to greenhouse benches. Scab symptoms were evaluated four times (3, 9, 15, and 21 days after inoculation). The frequency distribution of scab severity indicated that resistance to spread of scab within a spike was controlled by a few major genes. DNA was isolated from both parents and F(9) plants of the 133 RILs. A total of 300 combinations of amplified fragment length polymorphism (AFLP) primers were screened for polymorphisms using bulked segregant analysis. Twenty pairs of primers revealed at least one polymorphic band between the two contrasting bulks. The segregation of each of these bands was evaluated in the 133 RILs. Eleven AFLP markers showed significant association with scab resistance, and an individual marker explained up to 53% of the total variation (R(2)). The markers with high R(2) values mapped to a single linkage group. By interval analysis, one major quantitative trait locus for scab resistance explaining up to 60% of the genetic variation for scab resistance was identified. Some of the AFLP markers may be useful in marker-assisted breeding to improve resistance to scab in wheat.     

Identification of resistance to new virulent races of rust in sunflowers and validation of DNA markers in the gene pool

Sunflower rust, caused by Puccinia helianthi, is a prevalent disease in many countries throughout the world. The U.S. Department of Agriculture (USDA)-Agricultural Research Service, Sunflower Research Unit has released rust resistant breeding materials for several decades. However, constantly coevolving rust populations have formed new virulent races to which current hybrids have little resistance. The objectives of this study were to identify resistance to race 336, the predominant race in North America, and to race 777, the most virulent race currently known, and to validate molecular markers known to be linked to rust resistance genes in the sunflower gene pool. A total of 104 entries, including 66 released USDA inbred lines, 14 USDA interspecific germplasm lines, and 24 foreign germplasms, all developed specifically for rust resistance, were tested for their reaction to races 336 and 777. Only 13 of the 104 entries tested were resistant to both races, whereas another six were resistant only to race 336. The interspecific germplasm line, Rf ANN-1742, was resistant to both races and was identified as a new rust resistance source. A selection of 24 lines including 19 lines resistant to races 777 and/or 336 was screened with DNA markers linked to rust resistance genes R(1), R(2), R(4u), and R(5). The results indicated that the existing resistant lines are diverse in rust resistance genes. Durable genetic resistance through gene pyramiding will be effective for the control of rust.     

小麦抗白粉病基因Pm13及Pm4累加体的分子标记辅助选择

 利用Pm4的STS-PCR标记及Pm13的SCAR标记,检测含Pm4b的YW243与含Pm13抗性基因品系杂交的F₃代的抗感单株,初步筛选到累加了Pm4b及Pm13两个抗性基因的植株R1、R4;并分别对R1和R4自交后代(F₄代)的15个抗病单株进行跟踪检测,得到13株累加体,而另外2株仅具Pm4b基因。本研究说明分子标记是检测抗病基因累加体、辅助育种的有效手段。     

Identification of Random Amplified Polymorphic DNA Markers Linked to the Co-4 Resistance Gene to Colletotrichum lindemuthianum in Common Bean

ABSTRACT New cultivars of the common bean (Phaseolus vulgaris) with durable resistance to anthracnose can be developed by pyramiding major resistance genes using marker-assisted selection. To this end, it is necessary to identify sources of resistance and molecular markers tightly linked to the resistance genes. The objectives of this work were to study the inheritance of resistance to anthracnose in the cultivar TO (carrying the Co-4 gene), to identify random amplified polymorphic DNA (RAPD) markers linked to Co-4, and to introgress this gene in the cultivar Rudá. Populations F(1), F(2), F(2:3), BC(1)s, and BC(1)r from the cross Rudá x TO were inoculated with race 65 of Colletotrichum lindemuthianum, causal agent of bean anthracnose. The phenotypic ratios (resistant/susceptible) were 3:1 in the F(2) population, 1:1 in the BC(1)s, and 1:0 in the BC(1)r, confirming that resistance to anthracnose in the cultivar TO was monogenic and dominant. Six RAPD markers linked to the Co-4 gene were identified, four in the coupling phase: OPY20(830C) (0.0 centimorgan [cM]), OPC08(900C) (9.7 cM), OPI16(850C) (14.3 cM), and OPJ01(1,380C) (18.1 cM); and two in the repulsion phase: OPB03(1,800T) (3.7 cM) and OPA18(830T) (17.4 cM). OPY20(830C) and OPB03(1,800T), used in association as a codominant pair, allowed the identification of the three genotypic classes with a high degree of confidence. Marker OPY20(830C), which is tightly linked to Co-4, is being used to assist in breeding for resistance to anthracnose.     

Identification and Molecular Mapping of a Gene in Wheat Conferring Resistance to Mycosphaerella graminicola

ABSTRACT Septoria tritici leaf blotch (STB), caused by the ascomycete Mycosphaerella graminicola (anamorph Septoria tritici), is an economically important disease of wheat. Breeding for resistance to STB is the most effective means to control this disease and can be facilitated through the use of molecular markers. However, molecular markers linked to most genes for resistance to STB are not yet available. This study was conducted to test for resistance in the parents of a standard wheat mapping population and to map any resistance genes identified. The population consisted of 130 F(10) recombinant-inbred lines (RILs) from a cross between the synthetic hexaploid wheat W7984 and cv. Opata 85. Genetic analysis indicated that a single major gene controls resistance to M. graminicola in this population. This putative resistance gene is now designated Stb8 and was mapped with respect to amplified fragment length polymorphism (AFLP) and microsatellite markers. An AFLP marker, EcoRI-ACG/MseI-CAG5, was linked in repulsion with the resistance gene at a distance of approximately 5.3 centimorgans (cM). Two flanking microsatellite markers, Xgwm146 and Xgwm577, were linked to the Stb8 gene on the long arm of wheat chromosome 7B at distances of 3.5 and 5.3 cM, respectively. The microsatellite markers identified in this study have potential for use in marker-assisted selection in breeding programs and for pyramiding of Stb8 with other genes for resistance to M. graminicola in wheat.     

Molecular mapping of the crown rust resistance gene rpc1 in barley

ABSTRACT Crown rust of barley, caused by Puccinia coronata var. hordei, occurs sporadically and sometimes may cause yield and quality reductions in the Great Plains region of the United States and Canada. The incompletely dominant resistance allele Rpc1 confers resistance to P. coronata in barley. Two generations, F(2) and F(2:3), developed from a cross between the resistant line Hor2596 (CIho 1243) and the susceptible line Bowman (PI 483237), were used in this study. Bulked segregant analysis combined with random amplified polymorphic DNA (RAPD) primers were used to identify molecular markers linked to Rpc1. DNA genotypes produced by 500 RAPD primers, 200 microsatellites (SSRs), and 71 restriction fragment length polymorphism (RFLP) probes were applied to map Rpc1. Of these, 15 RAPD primers identified polymorphisms between resistant and susceptible bulks, and 62 SSR markers and 32 RFLP markers identified polymorphisms between the resistant and susceptible parents. The polymorphic markers were applied to 97 F(2) individuals and F(2:3) families. These markers identified 112 polymorphisms and were used for primary linkage mapping to Rpc1 using Map Manager QT. Two RFLP and five SSR markers spanning the centromere on chromosome 3H and one RAPD marker (OPO08-700) were linked with Rpc1 and, thus, used to construct a 30-centimorgan (cM) linkage map containing the Rpc1 locus. The genetic distance between Rpc1 and the closest marker, RAPD OPO08-700, was 2.5 cM. The linked markers will be useful for incorporating this crown rust resistance gene into barley breeding lines.     

Genetic analysis and molecular mapping of wheat genes conferring resistance to the wheat stripe rust and barley stripe rust pathogens

ABSTRACT Stripe rust is one of the most important diseases of wheat and barley worldwide. On wheat it is caused by Puccinia striiformis f. sp. tritici and on barley by P. striiformis f. sp. hordei Most wheat genotypes are resistant to P. striiformis f. sp. hordei and most barley genotypes are resistant to P. striiformis f. sp. tritici. To determine the genetics of resistance in wheat to P. striiformis f. sp. hordei, crosses were made between wheat genotypes Lemhi (resistant to P. striiformis f. sp. hordei) and PI 478214 (susceptible to P. striiformis f. sp. hordei). The greenhouse seedling test of 150 F(2) progeny from the Lemhi x PI 478214 cross, inoculated with race PSH-14 of P. striiformis f. sp. hordei, indicated that Lemhi has a dominant resistance gene. The single dominant gene was confirmed by testing seedlings of the F(1), BC(1) to the two parents, and 150 F(3) lines from the F(2) plants with the same race. The tests of the F(1), BC(1), and F(3) progeny with race PSH-48 of P. striiformis f. sp. hordei and PST-21 of P. striiformis f. sp. tritici also showed a dominant gene for resistance to these races. Cosegregation analyses of the F(3) data from the tests with the two races of P. striiformis f. sp. hordei and one race of P. striiformis f. sp. tritici suggested that the same gene conferred the resistance to both races of P. striiformis f. sp. hordei, and this gene was different but closely linked to Yr21, a previously reported gene in Lemhi conferring resistance to race PST-21 of P. striiformis f. sp. tritici. A linkage group consisting of 11 resistance gene analog polymorphism (RGAP) markers was established for the genes. The gene was confirmed to be on chromosome 1B by amplification of a set of nullitetrasomic Chinese Spring lines with an RGAP marker linked in repulsion with the resistance allele. The genetic information obtained from this study is useful in understanding interactions between inappropriate hosts and pathogens. The gene identified in Lemhi for resistance to P. striiformis f. sp. hordei should provide resistance to barley stripe rust when introgressed into barley cultivars.     

Improved Selection with Newly Identified RAPD Markers Linked to Resistance Gene to Four Pathotypes of Colletotrichum lindemuthianum in Common Bean

ABSTRACT Three F(2) populations derived from crosses between the resistant cultivar AB 136 and the susceptible cultivar Michelite (MiA), and one F(2) population derived from a cross between AB 136 and Mexico 222 (MeA), were used to identify markers linked to anthracnose resistance genes present in cultivar AB 136. Primer OPZ04 produced a DNA band (OPZ04(560)) linked in coupling phase to the resistance gene for pathotype 89 (8.5 +/- 0.025 cM) in one population derived from the cross MiA. In the same population, primer OPZ09 produced one band (OPZ09(950)) linked in repulsion phase (20.4 +/- 0.014 cM) to the same resistance gene. The simultaneous use of markers in coupling and in repulsion phases allowed the identification of the three genotypic classes. In the other two populations from cross MiA, OPZ04(560) was linked in coupling phase to resistance genes for pathotypes 73 (2.9 +/- 0.012 cM) and 81 (2.8 +/- 0.017 cM). In population MeA, OPZ04(560) was linked in coupling phase (7.5 +/- 0.033 cM) to resistance to pathotype 64. These data suggest that a single gene or complex locus of linked resistance genes present in cultivar AB 136 confers resistance to all four pathotypes of C. lindemuthianum.     

Resistance in Lycopersicon esculentum Intraspecific Crosses to Race T1 Strains of Xanthomonas campestris pv. vesicatoria Causing Bacterial Spot of Tomato

ABSTRACT We used molecular markers to identify quantitative trait loci (QTL) that confer resistance in the field to Xanthomonas campestris pv. vesicatoria race T1, a causal agent of bacterial spot of tomato. An F(2) population derived from a cross between Hawaii 7998 (H 7998) and an elite breeding line, Ohio 88119, was used for the initial identification of an association between molecular markers and resistance as measured by bacterial populations in individual plants in the greenhouse. Polymorphism in this cross between a Lycopersicon esculentum donor of resistance and an elite L. esculentum parent was limited. The targeted use of a core set of 148 polymerase chain reaction-based markers that were identified as polymorphic in L. esculentum x L. esculentum crosses resulted in the identification of 37 markers that were polymorphic for the cross of interest. Previous studies using an H 7998 x L. pennellii wide cross implicated three loci, Rx1, Rx2, and Rx3, in the hypersensitive response to T1 strains. Markers that we identified were linked to the Rx1 and Rx3 loci, but no markers were identified in the region of chromosome 1 where Rx2 is located. Single marker-trait analysis suggested that chromosome 5, near the Rx3 locus, contributed to reduced bacterial populations in lines carrying the locus from H 7998. The locus on chromosome 5 explained 25% of the phenotypic variation in bacterial populations developing in infected plants. An advanced backcross population and subsequent inbred backcross lines developed using Ohio 88119 as a recurrent parent were used to confirm QTL associations detected in the F(2) population. Markers on chromosome 5 explained 41% of the phenotypic variation for resistance in replicated field trials. In contrast, the Rx1 locus on chromosome 1 did not play a role in resistance to X. campestris pv. vesicatoria race T1 strains as measured by bacterial populations in the greenhouse or symptoms in the field. A locus from H 7998 on chromosome 4 was associated with susceptibility to disease and explained 11% of the total phenotypic variation. Additional variation in resistance was explained by plant maturity (6%), with early maturing families expressing lower levels of resistance, and plant habit (6%), with indeterminate plants displaying more resistance. The markers linked to Rx3 will be useful in selection for resistance in elite x elite crosses.     

Validation of a QTL for resistance to ascochyta blight linked to resistance to fusarium wilt race 5 in chickpea (<Emphasis Type="Italic">Cicer arietinum</Emphasis> L.)

Ascochyta blight caused by Ascochyta rabiei and fusarium wilt caused by Fusarium oxysporum. f. sp. ciceris are the two most serious diseases of chickpea (Cicer arietinum). Quantitative trait loci (QTL) or genes for ascochyta blight resistance and a cluster of resistance genes for several fusarium wilt races (foc1, foc3, foc4 and foc5) located on LG2 of the chickpea map have been reported independently. In order to validate these results and study the linkage relationship between the loci that confer resistance to blight and wilt, an intraspecific chickpea recombinant inbred lines (RIL) population that segregates for resistance to both diseases was studied. A new LG2 was established using sequence tagged microsatellite sites (STMS) markers selected from other chickpea maps. Resistance to race 5 of F. oxysporum (foc5) was inherited as a single gene and mapped to LG2, flanked by the STMS markers TA110 (6.5 cM apart) and TA59 (8.9 cM apart). A QTL for resistance to ascochyta blight (QTL_AR3) was also detected on LG2 using evaluation data obtained separately in two cropping seasons. This genomic region, where QTL_AR3 is located, was highly saturated with STMS markers. STMS TA194 appeared tightly linked to QTL_AR3 and was flanked by the STMS markers TR58 and TS82 (6.5 cM apart). The genetic distance between foc5 and QTL_AR3 peak was around 24 cM including six markers within this interval. The markers linked to both loci could facilitate the pyramiding of resistance genes for both diseases through MAS.     

Marker-assisted selection for disease resistance in wheat and barley breeding

Marker-assisted selection (MAS) provides opportunities for enhancing the response from selection because molecular markers can be applied at the seedling stage, with high precision and reductions in cost. About each of 50 genes conferring monogenic resistances and hundreds of quantitative trait loci (QTL) for quantitative disease resistances have been reported in wheat and barley. For detecting single-major gene resistance, MAS could be easily applied, but is often not necessary because the resistances are selected phenotypically. In quantitative disease resistances, MAS would be very useful, but the individual QTL often have small effects. Additionally, only a few monogenic resistances are durable and only a few QTL with high effects have been successfully transferred into elite breeding material. Further economic and biological constraints, e.g., a low return of investment in small-grain cereal breeding, lack of diagnostic markers, and the prevalence of QTL-background effects, hinder the broad implementation of MAS. Examples in which MAS has been successfully applied to practical breeding are the wheat rust resistance genes Lr34 and Yr36, the eyespot resistance gene Pch1, the recessive resistance genes rym4/rym5 to barley yellow mosaic viruses, mlo to barley powdery mildew, and two QTL for resistance to Fusarium head blight in wheat (Fhb1 and Qfhs.ifa-5A). Newly identified broad-spectrum resistance genes/QTL conferring resistance to multiple taxa of pathogens offer additional perspectives for MAS. In the future, chip-based, high-throughput genotyping platforms and the introduction of genomic selection will reduce the current problems of integrating MAS in practical breeding programs and open new avenues for a molecular-based resistance breeding.     

Chromosomal location and genetic relationship of leaf rust resistance genes rph9 and rph12 in barley

ABSTRACT Barley lines Hor 2596 and Triumph are the sources of leaf rust resistance genes Rph9 and Rph12, respectively. An allelism test was performed with F(2) progeny of the cross Triumph/Hor 2596 inoculated with Puccinia hordei. No recombinants were found in a population of 3,858 progeny, indicating Rph9 and Rph12 are alleles. Molecular and morphological markers were used to identify the chromosomal location of these genes in the crosses Bowman/Hor 2596 and Triumph/I91-533-va. A linkage was detected between Rph9 and the flanking sequence-tagged site (STS) markers ABC155 and ABG3 on chromosome 7(5H) at a distance of 20.6 and 20.1 centimorgans (cM), respectively, and to the microsatellite marker dehydrin-9 (HVDHN9) at a distance of 10.2 cM in the Bowman/ Hor 2596 cross. Analysis of isozymes in bulks of the same population showed that Rph9 may be closely linked to the Est9 locus on chromosome 7(5H). The Rph12 locus was linked to the morphological trait locus va (controlling variegated leaf color) on chromosome 7(5H) at a distance of 22.6 cM in the Triumph/I91-533-va cross. Rph12 also was linked with STS marker ABC155 (24.4 cM) and RAPD marker OPA19 (1.5) (17.8 cM). These data indicate that Hor 2596 and Triumph carry a leaf rust resistance gene at the same locus on the long arm of chromosome 7(5H) of barley.     

Identification of a quantitative trait locus for high-temperature adult-plant resistance against Puccinia striiformis f. sp. hordei in 'Bancroft' barley

Sustainable control of plant diseases can be achieved by developing cultivars with durable resistance. 'Bancroft' barley has durable high-temperature, adult-plant (HTAP) resistance to stripe rust caused by Puccinia striiformis f. sp. hordei. The objectives of this study were to determine the inheritance of the HTAP resistance in Bancroft, develop molecular markers for the HTAP resistance using the resistance gene analog polymorphism (RGAP) technique, map the HTAP resistance quantitative trait locus or loci (QTL) on barley chromosomes, and determine the usefulness of the RGAP markers in other barley cultivars for marker-assisted selection. The parents and F(4) recombinant inbred lines (RIL) and the parents and F(5) RIL were evaluated in 2004 and 2005 in one and three field sites, respectively, in Washington State. Infection type (IT) and disease severity (DS) were recorded three times at each location during each growing season. Area under the disease progress curve (AUDPC) was calculated for each parent and RIL based on the DS data. Genetic analyses of IT data of the parents, F(1), and F(2) tested in the adult-plant stage under controlled high-temperature cycle in the greenhouse and the parents, F(4), and F(5) RIL in the field indicated that one dominant gene controlled the HTAP resistance in Bancroft. Using 119 F(5:6) RIL and IT data, a linkage map on chromosome arm 3HL was constructed with eight RGAP markers and three simple sequence repeat (SSR) markers. Using the QTL analysis, a QTL for HTAP resistance was mapped with the DS and AUDPC data on the same chromosome location as with the IT data. The QTL explained >70% of the total phenotypic variation for the DS and AUDPC. The heritability of the HTAP resistance based on the AUDPC data was 76%. The two markers most close to the QTL peak detected polymorphisms in 84 and 88% of 25 barley genotypes that do not have the Bancroft HTAP resistance when used individually, and detected polymorphism in 100% of the genotypes when used in combination, indicating that the markers could be used in incorporating the HTAP resistance into these barley genotypes to improve the level and durability of resistance to stripe rust.     

Molecular Marker Analysis of Soybean Plant Introductions with Resistance to Phytophthora sojae

ABSTRACT Molecular analysis of sources of resistance to plant pathogens should expedite and confirm novel gene discovery and consequently the development of disease resistant cultivars. Recently, soybean plant introductions (PIs) were identified that contain putative novel Rps genes for resistance to Phytophthora sojae. The number of resistance genes that confer resistance to P. sojae isolates OH17 (1b,1d,2,3a,3b,3c,4,5,6,7) and OH25 (1a,1b,1c,1k,7) was then determined in several of the PIs. The objective of this study was to determine if the Rps genes present in these PIs were associated with eight described Rps loci that have been mapped on soybean molecular linkage groups F, G, J, and N. Nine F(2:3) soybean populations were genotyped with simple sequence repeat (SSR) markers linked to previously mapped Rps loci. The nine PI populations all had SSR markers associated (P < 0.01) with resistance to P. sojae isolate OH17 in the Rps1 region. Rps1c is a likely candidate in eight PIs but novel genes may also be possible, while novel genes may confer resistance in one PI to P. sojae isolate OHI7. Two or more Rps genes, including some that are potentially novel, confer resistance to P. sojae isolate OH25 in eight of the populations. However, based on the response to these two isolates, virulence already exists for at least some of the novel genes identified in this study.     

Sources and genetics of crown rust resistance in barley

ABSTRACT Crown rust, caused by Puccinia coronata var. hordei, is a new disease threat to barley in the Great Plains region of the United States. Deployment of resistant cultivars is the only economically viable option for the control of this disease. Thus, the objective of this study was to investigate the sources and genetics of crown rust resistance in barley. A geographically diverse sample of barley germ plasm collected around the world (526 accessions total) was evaluated at the seedling stage to P. coronata var. hordei, and only 10 accessions (1.9% of the total) were found resistant. These 10 accessions were also resistant at the adult plant stage in a greenhouse test. Three F(2) populations (Bowman x Hor2596, MR x Hor2596, and MD x Hor2596) were developed to study the inheritance of crown rust resistance in the resistant line Hor2596 (CIho 1243). A close fit to a 3:1 ratio of resistant/susceptible plants was observed in all three populations and is consistent with the segregation of a single resistance gene. F(1) plants from the Bowman x Hor2596 population exhibited slightly higher infection types than the resistant parent, indicating incomplete dominance. The locus symbol Rpc1 and allele symbol Rpc1.a were recommended for the crown rust resistance gene in Hor2596. An attempt was made to associate the Rpc1 locus with one of the seven barley chromosomes by analyzing linkage data with previously mapped morphological markers in crosses with multiple recessive (MR) and multiple dominant (MD) morphological marker stocks. However, no close linkages were detected between Rpc1 and the 20 morphological markers present in the marker stocks. The resistant accessions identified in this study should be useful to breeders for developing barley germ plasm with crown rust resistance.