Quantitative Trait Loci Analysis and Mapping of Seedling Resistance to Stagonospora nodorum Leaf Blotch in Wheat

ABSTRACT Stagonospora nodorum leaf blotch is an economically important foliar disease in the major wheat-growing areas of the world. In related work, we identified a host-selective toxin (HST) produced by the S. nodorum isolate Sn2000 and determined the chromosomal location of the host gene (Snn1) conditioning sensitivity to the toxin using the International Triticeae Mapping Initiative mapping population and cytogenetic stocks. In this study, we used the same plant materials to identify quantitative trait loci (QTL) associated with resistance to fungal inoculations of Sn2000 and investigate the role of the toxin in causing disease. Disease reactions were scored at 5, 7, and 10 days postinoculation to evaluate changes in the degree of effectiveness of individual QTL. A major QTL was identified on the short arm of chromosome 1B, which coincided with the snn1 toxin-insensitivity gene. This locus explained 58% of the phenotypic variation for the 5-day reading but decreased to 27% for the 10-day reading, indicating that the toxin is most effective in the early stages of the interaction. In addition, relatively minor QTL were identified on chromosomes 3AS, 3DL, 4AL, 4BL, 5DL, 6AL, and 7BL, but not all minor QTL were significant for all readings and their effects varied. Multiple regression models explained from 68% of the phenotypic variation for the 5-day reading to 36% for the 10-day reading. The Chinese Spring nullisomic 1B tetrasomic 1D line and the Chinese Spring-Triticum dicoccoides disomic 1B chromosome substitution line, which were insensitive to SnTox1, were more resistant to the fungus than the rest of the nullisomictetrasomic and disomic chromosome substitution lines. Our results indicate that the toxin produced by isolate Sn2000 is a major virulence factor.     

Gene Flow and Sexual Reproduction in the Wheat Glume Blotch Pathogen Phaeosphaeria nodorum (Anamorph Stagonospora nodorum)

ABSTRACT Restriction fragment length polymorphisms (RFLPs) were used to characterize the genetic structures of three field populations of Phaeosphaeria nodorum from Texas, Oregon, and Switzerland. Data from seven nuclear RFLP loci were used to estimate gene diversity and genetic distances and to make indirect measures of gene flow between populations. Three of the seven RFLP loci differed significantly in allele frequencies across populations. On average, 96% of the total gene diversity was found within populations. There was little evidence for population subdivision, suggesting that gene flow was not restricted among populations. Based on an average population differentiation of 0.04, we estimated that the exchange of 11 migrants among populations per generation would be needed to account for the present level of population subdivision. Genotype diversity based on DNA fingerprints was at a maximum for the Swiss population, whereas populations in Texas and Oregon had lower genotype diversities. Many multilocus haplotypes were found in each population. Ninety-five percent of RFLP allele pairs were in gametic equilibrium. The data were consistent with random mating within each population.     

Genetic Analysis of Sensitivity to a Pyrenophora tritici-repentis Necrosis-Inducing Toxin in Durum and Common Wheat

ABSTRACT The fungus Pyrenophora tritici-repentis produces a toxin (Ptr ToxA) that causes rapid cell necrosis in sensitive wheat genotypes. A single recessive gene (tsn1) on chromosome 5BL in common wheat confers insensitivity to this toxin. Our objectives were to analyze the allelic relationships of genotypes that have shown insensitivity to a P. tritici-repentis necrosis-inducing toxin, map the gene for insensitivity to the necrosis-inducing factor produced by P. tritici-repentis in a durum wheat population, and determine the reaction to P. tritici-repentis of aneuploid genotypes that do not contain the gene. Greenhouse-grown plants of seven populations from crosses of insensitive genotypes; an F(2) population of durum wheat; and 'Chinese Spring' aneuploid, substitution, and deletion lines were infiltrated with Ptr ToxA. All crosses involving insensitive genotypes failed to produce sensitive progeny, indicating that the same gene is present in these genotypes. The gene for insensitivity in the durum population was mapped to the same region on 5BL as in common wheat using restriction fragment length polymorphism markers. 'Chinese Spring', its homoeologous group 5 nullisomic-tetrasomic stocks, and 5BL deletion lines were insensitive to the toxin. Substitution of a 5B chromosome from sensitive genotypes into 'Chinese Spring' resulted in sensitivity. Therefore, insensitivity is not conferred by a gene product per se, but rather conferred by absence of a gene for sensitivity.     

Control of Stagonospora nodorum and Septoria tritici in Wheat by Pre-treatment with Drechslera teres, a Non-host Pathogen

A field study is described which explored the possibility of controlling Stagonospora nodorum and Septoria tritici on wheat using a barley pathogen, Drechslera teres. Pre-treatment of wheat cv. Hussar flag leaves with D. teres resulted in a significant reduction in disease caused by S. nodorum and S. tritici, resulting in a significant increase in grain yield. When cv. Brigadier leaves were treated with D. teres prior to inoculation with S. nodorum there was an initial increase in disease expression whilst D. teres had no effect on symptoms produced by S. tritici on cv. Brigadier. There was significantly less disease on leaves of cvs. Hussar and Brigadier pre-treated with D. teres prior to inoculation with an equal mixture of S. nodorum and S. tritici compared to plants pre-treated with water. It is concluded that D. teres and other non-host pathogens show potential as biological control agents for S. nodorum and S. tritici.     

A Rainfall-Based Model for Predicting the Regional Incidence of Wheat Seed Infection by Stagonospora nodorum in New York

ABSTRACT Our goal was to develop a simple model for predicting the incidence of wheat seed infection by Stagonospora nodorum across western and central New York in any given year. The distribution of the incidence of seed infection by S. nodorum across the region was well described by the beta-binomial probability distribution (parameters p and theta). Mean monthly rainfalls in May and in June across western and central New York were used to predict p. The binary power law was used to predict theta. The model was validated with independent data collected from New York. The predicted distribution of seed infection incidence was not statistically different from the actual distribution of the incidence of seed infection.     

Sensitivity of Wheat Genotypes to a Toxic Fraction Produced by Cephalosporium gramineum and Correlation with Disease Susceptibility

ABSTRACT Cephalosporium stripe is an important disease of winter wheat (Triticum aestivum) in several areas of the world, especially where stubble mulch and early seeding are practiced to maintain soil moisture and prevent erosion. We developed a procedure to mass-produce a toxic fraction produced by Cephalosporium gramineum through a modification of the method of Kobayashi and Ui. Exposure of excised wheat leaves to a concentration of 60 mul/ml of the toxic fraction for 72 h produced distinct wilting symptoms that allowed us to distinguish toxin-sensitive wheat genotypes in a repeatable manner. Twenty wheat genotypes belonging to four distinct germ plasm groups (common, club, durum, and synthetic) were evaluated. Variation in toxin sensitivity of wheat genotypes was mostly at the level of the germ plasm group, and all differences among the four germ plasm groups were highly significant (P < 0.001) based on linear contrasts. Seventeen winter wheat genotypes representing the common, club, and durum germ plasm groups were planted in C. gramineum-infested fields at two locations. The logarithm of the percentage of tillers showing whitehead symptoms at each of the two locations was significantly (P < 0.0001) correlated with wilting symptoms measured by the toxin assay (r = 0.80 and 0.84). The common wheat genotypes were all sensitive to the toxic fraction, but showed a substantial range of disease reactions in the field. However, we found no case of a toxin-insensitive genotype being susceptible in the field. These results suggest that toxin insensitivity may be an important mechanism of resistance to Cephalosporium stripe, but that other mechanisms are operative as well. The toxin assay may be useful as an initial screening procedure to reduce the number of genotypes to be tested in the field.     

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.     

High Genetic Similarity Among Populations of Phaeosphaeria nodorum Across Wheat Cultivars and Regions in Switzerland

ABSTRACT Phaeosphaeria nodorum was sampled from nine wheat fields across a 30-km transect representing three geographical regions in Switzerland to determine the scale of genetic differentiation among subpopulations. Three different wheat cultivars were sampled three times to determine whether differences in host genotype correlated with differences among corresponding pathogen populations. Seven restriction fragment length polymorphism (RFLP) loci and one DNA fingerprint were assayed for each of the 432 isolates in the collection. DNA fingerprints differentiated 426 unique genotypes. Though absolute differences were small, five RFLP loci exhibited significant differences in allele frequencies across the nine sub-populations. Gene diversity within all subpopulations was high (H(T) = 0.51), but only 3% of the total genetic variation was distributed among the nine subpopulations. When subpopulations were grouped according to geographical region or host cultivar, less than 1% of the genetic variation was distributed among groups, suggesting widespread gene flow and the absence of pathogen adaptation to specific wheat cultivars. Tests for gametic equilibrium within subpopulations and across the entire Swiss population supported the hypothesis of random mating.     

Identification and Molecular Mapping of a Gene Conferring Resistance to Pyrenophora tritici-repentis Race 3 in Tetraploid Wheat

ABSTRACT Race 3 of the fungus Pyrenophora tritici-repentis, causal agent of tan spot, induces differential symptoms in tetraploid and hexaploid wheat, causing necrosis and chlorosis, respectively. This study was conducted to examine the genetic control of resistance to necrosis induced by P. tritici-repentis race 3 and to map resistance genes identified in tetraploid wheat (Triticum turgidum). A mapping population of recombinant inbred lines (RILs) was developed from a cross between the resistant genotype T. tur-gidum no. 283 (PI 352519) and the susceptible durum cv. Coulter. Based on the reactions of the Langdon-T. dicoccoides (LDN[DIC]) disomic substitution lines, chromosomal location of the resistance genes was determined and further molecular mapping of the resistance genes for race 3 was conducted in 80 RILs of the cross T. turgidum no. 283/Coulter. Plants were inoculated at the two-leaf stage and disease reaction was assessed 8 days after inoculation based on lesion type. Disease reaction of the LDN(DIC) lines and molecular mapping on the T. turgidum no. 283/Coulter population indicated that the gene, designated tsn2, conditioning resistance to race 3 is located on the long arm of chromosome 3B. Genetic analysis of the F(2) generation and of the F(4:5) and F(6:7) families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.     

Molecular Mapping of the Stb4 Gene for Resistance to Septoria tritici Blotch in Wheat

ABSTRACT Breeding wheat for resistance is the most effective means to control Septoria tritici blotch (STB), caused by the ascomycete Mycosphaerella graminicola (anamorph Septoria tritici). At least eight genes that confer resistance to STB in wheat have been identified. Among them, the Stb4 locus from the wheat cv. Tadinia showed resistance to M. graminicola at both seedling and adult-plant stages. However, no attempt has been made to map the Stb4 locus in the wheat genome. A mapping population of 77 F10 recombinant-inbred lines (RILs) derived from a three-way cross between the resistant cv. Tadinia and the susceptible parent (Yecora Rojo x UC554) was evaluated for disease resistance and molecular mapping. The RILs were tested with Argentina isolate I 89 of M. graminicola for one greenhouse season in Brazil during 1999, with an isolate from Brazil (IPBr1) for one field season in Piracicaba (Brazil) during 2000, and with Indiana tester isolate IN95-Lafayette-1196-WW-1-4 in the greenhouse during 2000 and 2001. The ratio of resistant:susceptible RILs was 1:1 in all three tests, confirming the single-gene model for control of resistance to STB in Tadinia. However, the patterns of resistance and susceptibility were different between the Indiana isolate and those from South America. For example, the ratio of RILs resistant to both the Indiana and Argentina isolates, resistant to one but susceptible to the other, and susceptible to both isolates was approximately 1:1:1:1, indicating that Tadinia may contain at least two genes for resistance to STB. A similar pattern was observed between the Indiana and Brazil isolates. The gene identified with the Indiana tester isolate was assumed to be the same as Stb4, whereas that revealed by the South American isolates may be new. Bulked-segregant analysis was used to identify amplified fragment length polymorphism (AFLP) and microsatellite markers linked to the presumed Stb4 gene. The AFLP marker EcoRI-ACTG/MseI-CAAA5 and microsatellite Xgwm111 were closely linked to the Stb4 locus in coupling at distances of 2.1 and 0.7 centimorgans (cM), respectively. A flanking marker, AFLP EAGG/ M-CAT10, was 4 cM from Stb4. The Stb4 gene was in a potential supercluster of resistance genes near the centromere on the short arm of wheat chromosome 7D that also contained Stb5 plus five previously identified genes for resistance to Russian wheat aphid. The microsatellite marker Xgwm111 identified in this study may be useful for facilitating the transfer of Stb4 into improved cultivars of wheat.     

Geminate Particle Morphology of Sweet Potato Leaf Curl Virus in Partially Purified Preparation and Its Serological Relationship to Two Begomoviruses by Western Blotting

Sweet potato leaf curl virus (SPLCV) is a possible member of the genus Begomovirus; however, the presence of typical geminate particles in sap has not been confirmed. We attempted to observe SPLCV virions by partially purifying the virus using an enzyme-assisted procedure. The observed virions in the partially purified preparations were typical geminate particles with a size of ca. 18×30nm. This virus preparation was subjected to western blot analysis using antisera against Bean golden mosaic virus (BGMV) and Mungbean yellow mosaic virus (MYMV). SPLCV reacted with both antisera. Specific bands appeared to be slightly larger than the 30-kDa marker protein and were considered to be SPLCV coat protein. This western blot analysis revealed for the first time a serelogical relationship between SPLCV and the two well-characterized begomoviruses. Received 28 June 1999/ Accepted in revised form 17 November 1999     

Identification and Mapping of Quantitative Trait Loci Conditioning Resistance to Southern Leaf Blight of Maize Caused by Cochliobolus heterostrophus Race O

ABSTRACT A random set of recombinant inbred (RI) lines (F2:7) derived from the cross of the inbred lines Mo17 (resistant) and B73 (susceptible) were evaluated for resistance to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O. The RI lines were genotyped at a total of 234 simple sequence repeat, restriction fragment length polymorphism, or isozyme loci. Field plots of the RI lines were inoculated artificially with an aggressive isolate of C. heterostrophus race O in each of two growing seasons in North Carolina. Lines were rated for percent SLB severity two (1996) or three (1995) times during the grain-filling period. Data also were converted to area under the disease progress curve (AUDPC) and analyzed using the composite interval mapping option of the PLABQTL program. When means of disease ratings over years were fitted to models, a total of 11 quantitative trait loci (QTLs) were found to condition resistance to SLB, depending upon which disease ratings were used in the analyses. When the AUDPC data were combined and analyzed over environments, seven QTLs, on chromosomes 1, 2, 3, 4, 7, and 10 were found to come from the resistant parent Mo17. An additional QTL for resistance on chromosome 1 came from the susceptible parent B73. The eight identified QTLs accounted for 46% of the phenotypic variation for resistance. QTL x environment interactions often were highly significant but, with one exception, were the result of differences in the magnitude of QTL effects between years and not due to changes in direction of effects. QTLs on the long arm of chromosome 1 and chromosomes 2 and 3 had the largest effects, were the most consistently detected, and accounted for most of the phenotypic variance. No significant additive x additive epistatic effects were detected. These data support earlier reports of the polygenic inheritance of resistance to SLB of maize.     

Identification of a Chlorosis-Inducing Toxin from Pyrenophora tritici-repentis and the Chromosomal Location of an Insensitivity Locus in Wheat

ABSTRACT Culture filtrate from Pyrenophora tritici-repentis race 1 isolate 78-62 contained a genotype-specific toxin which elicited extensive chlorosis on sensitive wheat genotypes. This toxin was partially purified using gel filtration, ion exchange, and reversed-phase chromatography. The chlorosis toxin was found to be a polar, nonionic, low-molecular-weight molecule. Wheat genotypes infiltrated with crude culture filtrate and partially purified chlorosis toxin exhibited the same chlorotic symptoms seen with conidial inoculations of isolate 78-62. All tested wheat genotypes that exhibited extensive chlorosis to the toxin also exhibited extensive chlorosis to conidial inoculations, and all wheat genotypes insensitive to the toxin did not exhibit extensive chlorosis to conidial inoculations. The recombinant inbred population derived from the cross W-7984 x Opata 85 segregated for chlorosis induction from infiltration with partially purified chlorosis toxin from isolate 78-62. The locus identified by the marker XGli1, associated with resistance to conidial inoculations from race 1 isolates Pti2 and 78-62 and race 3 isolate D308, also was associated with insensitivity to infiltration of crude culture filtrate and partially purified chlorosis toxin. The marker XGli1, located on the short arm of chromosome 1A, is linked to the insensitivity locus within 5.7 cM. We propose that this chlorosis toxin be designated Ptr ToxC.     

一个小麦csAtPR5-类似基因的克隆、鉴定和表达分析

 小麦(Triticum aestivumL.)品系‘兰考90(6)’在2AL染色体臂上携带1个隐性抗白粉病基因,暂命名为PmLK906。以‘中国春’/‘兰考90(6)21-12’杂交F₃代纯合株系构建的抗、感cDNA池为探针进行小麦基因芯片杂交,结果表明与粗山羊草(Aegilops tauschii)csAtPR5类似的基因在抗病池中的表达量比感病池中约高2^4.2倍。随后,从‘兰考90(6)21-12’中成功克隆了一个2 125 bp的全长csAtPR5-类似基因cDNA序列,暂命名为TaAetPR5(GenBank登录号:EU082094)。TaAet-PR5与csAtPR5的cDNA序列有93%的相同。TaAetPR5编码1个由657个氨基酸组成的多肽,与csAtPR5有88%的相同。蛋白推导分析表明TaAetPR5的分子量为74.5 kDa,pI 6.82,可能是一个可溶性的球蛋白,存在于细胞核中的可能性是95%。接种小麦白粉病菌(Blumeria graminisf.sp.tritici)后12至72 h,‘兰考90(6)21-12’幼苗叶片中的TaAetPR5基因转录水平不断提高。感白粉病的‘中国春’中没有检测到TaAetPR5基因。     

Role of Light and Malate in the Decreased Sensitivity of cms-T Cytoplasm Maize Leaves to Bipolaris maydis Race T Toxin

ABSTRACT Leaf segments from Texas male sterile (cms-T) cytoplasm maize isolines exposed to light (50 muM s(-1) m(-2)) for 8 h or more before or after being infiltrated with the Bipolaris maydis race T toxin (T-toxin) leaked significantly less electrolytes when immersed in distilled water (DW) for 24 to 48 h than did dark-treated leaf segments. No comparable effect of light on toxin-induced electrolyte leakage was observed with normal (N) cytoplasm isolines. Toxin-treated cms-T leaf segments incubated in DW for three consecutive 12-h periods of alternating light and dark showed significantly greater electrolyte leakage than leaf segments incubated in continuous light for 36 h and significantly less leakage than segments incubated in continuous dark for 36 h.Exposure of cms-T, but not N, cytoplasm leaves to 25 or 50 muM malic acid decreased their sensitivity to T-toxin in the dark to a level similar to that observed when leaves were incubated in the light without malic acid. The potency of T-toxin appeared to be unaffected by its exposure to light. The loss of electrolytes from T-toxin-treated cms-T cytoplasm leaf segments was at approximately the level seen with light or malate when 25 muM H(2)O(2) was added to the DW bathing solution. Evaluation of the data points to the possibility that H(2)O(2) might be involved with the altered sensitivity of cms-T cytoplasm leaves to T-toxin caused by either light or malate.     

Restriction Fragment Length Polymorphism Mapping of Resistance to Two Races of Pyrenophora tritici-repentis in Adult and Seedling Wheat

ABSTRACT Resistance to the chlorosis factor of tan spot of wheat, caused by the ascomycete Pyrenophora tritici-repentis, has been reported to be quantitative and a single quantitative trait loci (QTL), QTsc.ndsu-1A, explained 35% of the variation for resistance to a single isolate in seedlings of recombinant inbred (RI) lines derived from the cross W-7984/Opata 85. The objectives of this study were to determine the number and locations of genes conditioning resistance to the same isolate in adult plants of this population and three isolates in seedlings of wheat RI lines derived from the cross W-7976/Trenton. An extensive restriction fragment length polymorphism map exists for the W-7984/Opata 85 population, and markers significantly associated (P < 0.01) with resistance to tan spot were selected to analyze the W-7976/Trenton population. A multiple regression model accounted for 49% of the variation for resistance in adult plants with QTsc.ndsu-1A, explaining 26% of the variation. QTsc.ndsu-1A explained 47, 58, and 64% of the variation for resistance in seedlings to isolates Pti2, 78-62, and D308, respectively. These results showed that the QTL for tan spot resistance on chromosome 1AS was effective in both seedlings and adult plants and against isolates from different races of P. tritici-repentis.     

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.     

Genetic Control of Resistance to Tan Necrosis Induced by Pyrenophora tritici-repentis, Races 1 and 2, in Spring and Winter Wheat Genotypes

ABSTRACT The symptoms of tan spot of wheat, caused by Pyrenophora triticirepentis, include a tan necrosis component and an extensive chlorosis component. Since tan spot has become the major component of the leafspotting disease complex of wheat in western Canada, the need for resistant cultivars has increased. This study was conducted to determine whether the resistance to tan spot found in a diverse set of spring and winter wheat genotypes was due to resistance genes not previously reported. The genetic control of resistance to necrosis induced by P. triticirepentis race 1 and race 2 was determined, under controlled environmental conditions, for spring wheat genotypes Erik and 86ISMN 2137 and winter wheat genotypes Hadden, Red Chief, and 6B-365. Plants were inoculated at the two-leaf stage and disease reaction was assessed based on lesion type. Tests of the F(1) and F(2) generations, and of F(2:3) and F(2:8) families, indicated that one recessive gene controlled resistance to the necrosis component of tan spot caused by both race 1 and race 2 in each cross studied. Lack of segregation in crosses between the resistant cultivars indicated that the resistance gene was the same in all of the cultivars.     

Generation and Molecular Mapping of a Sequence Characterized Amplified Region Marker Linked with the Bct Gene for Resistance to Beet curly top virus in Common Bean

ABSTRACT A random amplified polymorphic DNA (RAPD) marker directly linked (0.0 cM) with a resistance gene was identified in a snap bean recombinant inbred population (Moncayo x Primo) consisting of 94 F(5:7) recombinant inbred lines that had uniform segregation for disease reaction to Beet curly top virus (BCTV) across three field locations. Resistance was conditioned by a single dominant allele tentatively designated Bct. Seven hundred and fifty decamer primers were screened to obtain the linked RAPD marker that was then converted to a sequence characterized amplified region (SCAR) marker SAS8.1550. The SCAR mapped within a cluster of resistance genes on linkage group B7 of the core map. A survey of 103 BCTV-resistant and -susceptible snap and dry bean genotypes was conducted using SAS8.1550. Results showed that the SCAR would be highly useful for marker-assisted selection of Bct in snap and dry bean originating from the Andean gene pool. Marker-assisted selection for Bct will expedite the development of BCTV-resistant cultivars and minimize the need for cumbersome pathogen tests.