Quantitative trait Loci mapping of resistance to sugarcane mosaic virus in maize

ABSTRACT Sugarcane mosaic virus (SCMV) is an important virus disease of maize (Zea mays) in Europe. In this study, we mapped and characterized quantitative trait loci (QTL) affecting resistance to SCMV in a maize population consisting of 219 F(3) or immortalized F(2) families from the cross of two European maize inbreds, D32 (resistant) x D145 (susceptible). Resistance was evaluated in replicated field trials across two environments under artificial inoculation. The method of composite interval mapping was employed for QTL detection with a linkage map based on 87 restriction fragment length polymorphism and 7 mapped microsatellite markers. Genotypic and genotype x environment interaction variances for SCMV resistance were highly significant in the population. Heritabilities ranged from 0.77 to 0.94 for disease scores recorded on seven consecutive dates. Five QTL for SCMV resistance were identified on chromosomes 1, 3, 5, 6, and 10 in the joint analyses. Two major QTL on chromosomes 3 and 6 were detected consistently in both environments. Significant epistatic effects were found among some of these QTL. A simultaneous fit with all QTL in the joint analyses explained between 70 and 77% of the phenotypic variance observed at various stages of plant development. Resistance to SCMV was correlated with plant height and days to anthesis.     

Quantitative Trait Loci in Sweet Corn Associated with Partial Resistance to Stewart's Wilt, Northern Corn Leaf Blight, and Common Rust

ABSTRACT Partial resistance to Stewart's wilt (Erwina stewartii, syn. Pantoea stewartii), northern corn leaf blight (NCLB) (Exserohilum turcicum), and common rust (Puccinia sorghi) was observed in an F(2:3) population developed from a cross between the inbred sweet corn lines IL731a and W6786. The objective of this study was to identify quantitative trait loci (QTL) associated with partial resistance using restriction fragment length polymorphic markers. Phenotypic data were collected for 2 years for Stewart's wilt, NCLB, and common rust but, due to significant family-environment interaction, analysis was conducted individually on data from each year. In 2 years of evaluation for the three diseases, a total of 33 regions in the maize genome were associated with partial resistance describing from 5.9 to 18% of the total phenotypic variability. Of six regions common in both years, three were associated with partial resistance to Stewart's wilt (chromosomes 4:07, 5:03, and 6:04), one was associated with NCLB (chromosome 9:05), and two were associated with common rust (chromosomes 2:04 and 3:04). The rust QTL on 3S mapped to within 20 cM of the rp3 locus and explained 17.7% of the phenotypic variability. Some of the QTL associated with partial resistance to the three diseases have been reported previously, and some are described here for the first time. Results suggest it may be possible to consolidate QTL from various elite backgrounds in a manner analogous to the pyramiding of major resistance genes. We also report here on two QTL associated with anthocyanin production on chromosomes 10:6 and 5:03 in the general location of the a2 gene.     

Quantitative trait loci for resistance to fusarium head blight and deoxynivalenol accumulation in Wangshuibai wheat under field conditions

Wangshuibai is a Chinese landrace wheat with a high level of resistance to fusarium head blight (FHB) and deoxynivalenol (DON) accumulation. Using an F7 population of recombinant inbred lines (RILs) derived from the cross between Wangshuibai and Annong 8455 for molecular mapping of quantitative trait loci (QTL) for FHB resistance, the proportion of scabbed spikelets (PSS) and DON content were assessed under field conditions. Composite interval mapping revealed that two and three QTL were significantly associated with low PSS and low DON content, respectively, over 2 years. QTL on chromosomes 3B and 2A explained 17 and 11·5%, respectively, of the phenotypic variance for low PSS, whereas QTL on chromosomes 5A, 2A and 3B explained 12·4, 8·5 and 6·2%, respectively, of the phenotypic variance for low DON content. The 3B QTL appeared to be associated mainly with low PSS, and the 5A QTL primarily with low DON content in Wangshuibai. The 2A QTL had minor effects on both low PSS and DON content. Microsatellite and AFLP markers linked to these QTL should be useful for marker-assisted selection of QTL for low PSS and low DNA content from Wangshuibai.     

Selection for quantitative trait loci associated with resistance to Stewart's wilt in sweet corn

The objectives of this research were to identify quantitative trait loci (QTL) for Stewart's wilt resistance from a mapping population derived from a sweet corn hybrid that is highly resistant to Pantoea stewartii and to determine if marker-based selection for those QTL could substantially improve Stewart's wilt resistance in a population derived from a cross of resistant lines and a highly susceptible sweet corn inbred. Three significant QTL for Stewart's wilt resistance on chromosomes 2 (bin 2.03), 5 (bin 5.03), and 6 (bin 6.06/6.07) explained 31% of the genetic variance in a population of 110 F(3:4) families derived from the sweet corn hybrid Bonus. The three QTL appeared to be additive in their effects on Stewart's wilt ratings. Based on means of families that were either homozygous or heterozygous for marker alleles associated with the resistance QTL, the QTL on chromosomes 2 and 6 appeared to have dominant or partially dominant gene action, while the QTL on chromosome 5 appeared to be recessive. A population of 422 BC(2)S(2) families was derived from crosses of a sweet corn inbred highly susceptible to Stewart's wilt, Green Giant Code 88 (GG88), and plants from two F(3:4) families (12465 and 12467) from the Bonus mapping population that were homozygous for marker alleles associated with Stewart's wilt resistance at the three QTL. Mean Stewart's wilt ratings for BC(2)S(2) families were significantly (P < 0.05) lower for families that were homozygous for the bnlg1902 marker allele (bin 5.03) from resistant lines 12465 or 12467 than for families that were heterozygous at this marker locus or homozygous for the bnlg1902 marker allele from GG88. Resistance associated with this QTL was expressed only if F(3:5) or BC(2)S(2) families were homozygous for marker alleles associated with the resistant inbred parent (P(1)). Marker alleles identified in the F(3:5) mapping population that were in proximity to the resistance QTL on chromosomes 2 and 6 were not polymorphic in crosses of GG88 with 12465 and 12467. Selection for other polymorphic marker loci adjacent to these two regions did not improve Stewart's wilt resistance of BC(2)S(2) families.     

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 quantitative trait Loci for resistance to southern leaf blight and days to anthesis in two maize recombinant inbred line populations

The genetic architecture underlying resistance in maize to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O is not well understood. The objective of this study was to identify loci contributing to SLB resistance in two recombinant inbred line populations and to compare these to SLB resistance loci in other populations. The two populations used were derived from crosses between maize inbred lines H99 and B73 (HB population-142 lines) and between B73 and B52 (BB population-186 lines). They were evaluated for SLB resistance and for days from planting to anthesis (DTA) in 2005 and 2006. Two replications arranged as randomized complete blocks were assessed in each year for each population. Entry mean heritabilities for disease resistance were high for both populations (0.876 and 0.761, respectively). Quantitative trait loci (QTL) for SLB resistance were identified in bins 3.04 (two QTL), 6.01, and 8.05 in the HB population and in bin 2.07 in the BB population. No overlap of DTA and SLB resistance QTL was observed, nor was there any phenotypic correlation between the traits. A comparison of the results of all published SLB resistance QTL studies suggested that bins 3.04 and 6.01 are 'hotspots' for SLB resistance QTL.     

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.     

Inheritance of resistance to aflatoxin production and Aspergillus ear rot of corn from the cross of inbreds b73 and oh516

ABSTRACT Our objective was to determine the value of corn (Zea mays) inbred Oh516 as a source of resistance to Aspergillus ear rot and aflatoxin accumulation in grain. Types and magnitudes of gene action associated with resistance were determined with generation means analysis. Molecular markers associated with resistance were identified from BCP(1)S(1) families developed from the cross of the susceptible inbred B73 and Oh516. In 2001 and 2002, B73 (P(1)), Oh516 (P(2)), and the F(1), F(2), F(3), BCP(1), BCP(2), and BCP(1)S(1) generations were evaluated for aflatoxin concentration in grain, percent bright greenish yellow fluorescence (BGYF), and severity of Aspergillus ear rot following inoculation in Urbana, IL. BCP(1)S(1) families testcrossed with LH185 also were evaluated at three locations in 2002. Molecular marker-quantitative trait loci (QTL) associations with all traits were determined with single factor analysis of variance. Dominance gene action was associated with aflatoxin concentration in grain and percent BGYF. QTL associated with aflatoxin accumulation in grain were identified on chromosomes 2, 3, and 7 (bins 2.01 to 2.03, 2.08, 3.08, and 7.06). Alleles from inbred Oh516 on chromosomes 2, 3, and 7 should improve resistance of commercially used, B73-type inbreds.     

Tagging and validation of a major quantitative trait locus for leaf rust resistance and leaf tip necrosis in winter wheat cultivar forno

ABSTRACT A major leaf rust (Puccinia triticina) resistance quantitative trait locus (QTL) (QLrP.sfr-7DS) previously has been described on chromosome 7DS in the winter wheat (Triticum aestivum) cv. Forno. It was detected in a population of single-seed descent (SSD) lines derived from the cross Arina x Forno. QLrP.sfr-7DS conferred a durable and slow-rusting resistance phenotype, co-segregated with a QTL for leaf tip necrosis (LTN) and was mapped close to Xgwm295 at a very similar location as the adult plant leaf rust resistance gene Lr34 found in some spring wheat lines. Here, we describe the validation of this QTL by mapping it to the same chromosomal region close to Xgwm295 on chromosome 7DS in a population of SSD lines from the winter wheat x spelt (T. spelta) cross Forno x Oberkulmer. In both populations, the log of the likelihood ratio curves for leaf rust resistance and LTN peaked at identical or very similar locations, indicating that both traits are due to the same gene. We have improved the genetic map in the target region of QLrP.sfr-7DS using microsatellite and expressed sequence tag (EST) markers. Two EST loci (Xsfr.BF473324 and Xsfr.BE493812) define a genetic interval of 7.6 centimorgans containing QLrP.sfr-7DS, a considerably more precise genetic location for this QTL than previously described both in spring and winter wheat. The identified genetic interval is physically located in the distal 39% of chromosome 7DS. Single-marker analysis identified Xsfr.BF473324 and Xgwm1220 as the most informative loci for QLrP.sfr-7DS and QLtn.sfr-7DS. In the rice genome, the two ESTs flanking the QLrP.sfr-7DS/QLtn.sfr-7DS chromosomal segment in wheat are conserved on chromosome 6S in a region colinear with wheat chromosome 7DS. There, they define a physical region of three rice bacterial artificial chromosomes spanning approximately 300 kb.     

Two Loci from Lycopersicon hirsutum LA407 Confer Resistance to Strains of Clavibacter michiganensis subsp. michiganensis

ABSTRACT We used molecular markers to identify quantitative trait loci (QTL) that contribute to resistance to bacterial canker of tomato caused by Clavibacter michiganensis subsp. michiganensis. Resistance was first identified as a marker-trait association in an inbred backcross (IBC) population derived from crossing Lycopersicon hirsutum accession (LA407) with L. esculentum. Single-marker QTL analysis suggested that at least two loci originating from L. hirsutum LA407, Rcm 2.0 on chromosome 2 and Rcm 5.1 on chromosome 5, contribute to resistance in replicated trials. Two segregating F(2) populations were developed by crossing resistant inbred backcross lines (IBLs) to elite L. esculentum lines and used to confirm QTL associations detected in the IBC population. In these populations, realized heritability estimates were higher for selection based on maximal disease than for selection based on disease progression. Realized heritability in the population carrying Rcm 2.0 was 0.63 and 0.14, respectively, for each selection criteria. Realized heritability estimates were 0.85 for selection based on maximal disease and 0.37 for selection based on disease progression in a population carrying Rcm 5.1. The disease response of F(3) families selected for resistance suggested that both Rcm 2.0 and Rcm 5.1 confer resistance to bacterial strains in the repetitive sequence-based polymerase chain reaction DNA fingerprint classes A and C. Markers linked to Rcm 2.0 explained up to 56% of the total phenotypic variation for resistance in one population, and markers linked to Rcm 5.1 explained up to 73% of the total phenotypic variation for resistance in a separate population.     

Main effects, epistasis, and environmental interactions of quantitative trait Loci for fusarium head blight resistance in a recombinant inbred population

ABSTRACT Chinese Spring Sumai 3 chromosome 7A disomic substitution line (CS-SM3-7ADS) is highly resistant to Fusarium head blight (FHB), and an F(7) population of recombinant inbred lines derived from the cross CS-SM3-7ADS x Annong 8455 was evaluated for resistance to FHB to investigate main effects, epistasis, and environmental interactions of quantitative trait loci (QTLs) for FHB resistance. A molecular linkage map consists of 501 simple sequence repeat and amplified fragment length polymorphism markers. A total of 10 QTLs were identified with significant main effects on the FHB resistance using MapQTL and QTLMapper software. Among them, CS-SM3-7ADS carries FHB-resistance alleles at five QTLs on chromosomes 2D, 3B, 4D, and 6A. One QTL on 3BS had the largest effect and explained 30.2% of the phenotypic variance. Susceptible QTLs were detected on chromosomes 1A, 1D, 4A, and 4B. A QTL for enhanced FHB resistance was not detected on chromosome 7A of CS-SM3-7ADS; therefore, the increased FHB resistance in CS-SM3-7ADS was not due to any major FHB-resistance QTL on 7A of Sumai 3, but more likely was due to removal of susceptible alleles of QTLs on 7A of Chinese Spring. QTLMapper detected nine pairs of additive-additive interactions at 17 loci that explained 26% phenotypic variance. QTL-environment interactions explained 49% of phenotypic variation, indicating that the environments significantly affected the expression of the QTLs, especially these epistasis QTLs. Adding FHB-enhancing QTLs or removal of susceptible QTLs both may significantly enhance the degree of wheat resistance to FHB in a wheat cultivar.     

Analysis of quantitative trait Loci for resistance to southern leaf blight in juvenile maize

ABSTRACT A set of 192 maize recombinant inbred lines (RILs), derived from a cross between the inbred lines Mo17 and B73, were evaluated as 3-week-old seedlings in the greenhouse for resistance to southern leaf blight, caused by Cochliobolus heterostrophus race O. Six significant (LOD >3.1) quantitative trait loci (QTL) were identified for disease resistance, located on chromosomes 1, 2, 3, 6, 7, and 8. Results were compared with a previous study that had used the same RIL population and pathogen isolate, but had examined resistance in mature rather than juvenile plants. There was a very weak but significant correlation between the overall resistance phenotypes of the RILs scored as mature and juvenile plants. Two QTL were found in similar positions on chromosomes 1 and 3 at both growth stages. Other QTL were specific to one growth stage or the other. Twenty-three of these RILs, together with the parental lines, were inoculated in the greenhouse with four C. heterostrophus isolates. Results indicated that the quantitative resistance observed was largely isolate non-specific.     

Quantitative trait loci for adult-plant resistance to Mycosphaerella graminicola in two winter wheat populations

Septoria tritici blotch (STB) is one of the most important leaf spot diseases in wheat worldwide. The goal of this study was to detect chromosomal regions for adult-plant resistance in large winter wheat populations to STB. Inoculation by two isolates with virulence to Stb6 and Stb15, both present in the parents, was performed and STB severity was visually scored plotwise as percent coverage of flag leaves with pycnidia-bearing lesions. 'Florett'/'Biscay' and 'Tuareg'/'Biscay', each comprising a cross of a resistant and a susceptible cultivar, with population sizes of 316 and 269 F(7:8) recombinant inbred lines, respectively, were phenotyped across four and five environments and mapped with amplified fragment length polymorphism, diversity array technology, and simple sequence repeat markers covering polymorphic regions of ≈1,340 centimorgans. Phenotypic data revealed significant (P < 0.01) genotypic differentiation for STB, heading date, and plant height. Entry-mean heritabilities (h(2)) for STB were 0.73 for 'Florett'/'Biscay' and 0.38 for 'Tuareg'/'Biscay'. All correlations between STB and heading date as well as between STB and plant height were low (r = -0.13 to -0.20). In quantitative trait loci (QTL) analysis, nine and six QTL were found for STB ratings explaining, together, 55 and 51% of phenotypic variation in 'Florett'/'Biscay' and 'Tuareg'/'Biscay', respectively. Genotype-environment and QTL-environment interactions had a large impact. Two major QTL were detected consistently across environments on chromosomes 3B and 6D from 'Florett' and chromosomes 4B and 6B from 'Tuareg', each explaining 12 to 17% of normalized adjusted phenotypic variance. These results indicate that adult-plant resistance to STB in both mapping populations was of a quantitative nature.     

Quantitative trait loci for Fusarium head blight resistance in a recombinant inbred population of Wangshuibai/Wheaton

Use of diverse sources of Fusarium head blight (FHB)-resistant germplasm in breeding may significantly improve wheat resistance to FHB. Wangshuibai is an FHB-resistant Chinese landrace unrelated to cv. Sumai 3, the most commonly used FHB-resistant source. In all, 139 F(6) recombinant inbred lines were developed from a cross between Wangshuibai and an FHB-susceptible cultivar, Wheaton, to map quantitative trait loci (QTL) for wheat resistance to initial infection (type I resistance), spread of FHB symptoms within a spike (type II resistance), and deoxynivalenol (DON) accumulation (type III resistance) in infected grain. The experiments were conducted in a greenhouse at Manhattan, KS from 2003 to 2005. More than 1,300 simple-sequence repeat and amplified fragment length polymorphism markers were analyzed in this population. Five QTL for type I resistance were detected on chromosomes 3AS, 3BS, 4B, 5AS, and 5DL after spray inoculation; seven QTL for type II resistance were identified on chromosomes 1A, 3BS, 3DL, 5AS, 5DL, and 7AL after point inoculation; and seven QTL for type III resistance were detected on chromosomes 1A, 1BL, 3BS, 5AS, 5DL, and 7AL with the data from both inoculation methods. These QTL jointly explained up to 31.7, 64, and 52.8% of the phenotypic variation for the three types of FHB resistance, respectively. The narrow-sense heritabilities were low for type I resistance (0.37 to 0.41) but moderately high for type II resistance (0.45 to 0.61) and type III resistance (0.44 to 0.67). The QTL on the distal end of 3BS, 5AS, and 5DL contributed to all three types of resistance. Two QTL, on 7AL and 1A, as well as one QTL near the centromere of 3BS (3BSc), showed effects on both type II and type III resistance. Selection for type II resistance may simultaneously improve type I and type III resistance as well. The QTL for FHB resistance identified in Wangshuibai have potential to be used to pyramid FHB-resistance QTL from different sources.     

小麦抗条锈病一致性数量性状位点(MQTL)图谱构建

 小麦条锈病是造成小麦减产和品质劣化的最重要病害,定位小麦染色体上一致性条锈病抗性基因/位点/区段是小麦条锈病抗性分子育种的重要基础。本研究对至今分子标记和遗传定位的342个条锈病抗性基因/位点/区段进行数据搜集整理,借助Maccaferr和Andrzej的参考图谱,基于元分析技术进行Meta-QTL(MQTL)检测,共获得194个小麦抗条锈病MQTL,包括74个与严重度(Disease severity, DS)相关,46个与反应型(Infection type, IT)相关、19个与病程曲线下面积相关(Area under disease progress curve, AUDPC)、28个与DS和IT共相关、6个与DS和AUDPC共相关、15个与IT和AUDPC共相关、6个与其他条锈病抗性性状相关。这些抗条锈病一致性QTL定位于小麦21条染色体上,呈非均匀分布,且部分MQTL集中成簇。通过与已发表的正式命名抗条锈病基因比较分析,发现大多数正式命名基因定位于MQTL簇区段,说明这些MQTL簇区段很可能是控制小麦条锈病抗性热点区域。控制小麦抗条锈病一致性QTL遗传图谱的构建为小麦条锈病抗性基因精细定位及抗病育种提供了遗传信息参考依据。     

小麦抗条锈病一致性数量性状位点(MQTL)图谱构建

 小麦条锈病是造成小麦减产和品质劣化的最重要病害,定位小麦染色体上一致性条锈病抗性基因/位点/区段是小麦条锈病抗性分子育种的重要基础。本研究对至今分子标记和遗传定位的342个条锈病抗性基因/位点/区段进行数据搜集整理,借助Maccaferr和Andrzej的参考图谱,基于元分析技术进行Meta-QTL(MQTL)检测,共获得194个小麦抗条锈病MQTL,包括74个与严重度(Disease severity, DS)相关,46个与反应型(Infection type, IT)相关、19个与病程曲线下面积相关(Area under disease progress curve, AUDPC)、28个与DS和IT共相关、6个与DS和AUDPC共相关、15个与IT和AUDPC共相关、6个与其他条锈病抗性性状相关。这些抗条锈病一致性QTL定位于小麦21条染色体上,呈非均匀分布,且部分MQTL集中成簇。通过与已发表的正式命名抗条锈病基因比较分析,发现大多数正式命名基因定位于MQTL簇区段,说明这些MQTL簇区段很可能是控制小麦条锈病抗性热点区域。控制小麦抗条锈病一致性QTL遗传图谱的构建为小麦条锈病抗性基因精细定位及抗病育种提供了遗传信息参考依据。     

Molecular mapping of the major resistance quantitative trait locus qHS2.09 with simple sequence repeat and single nucleotide polymorphism markers in maize

The major quantitative trait locus (QTL) qHS2.09 plays an important role in resistance to head smut during maize breeding and production. In this study, a near-isogenic line (NIL), L34, which harbors the major QTL qHS2.09 in bin 2.09, was developed using a resistant donor 'Mo17' in a susceptible genetic background 'Huangzao4'. Using 18,683 genome-wide polymorphic loci, this major QTL was finely mapped into an interval of ≈1.10 Mb, flanked by single nucleotide polymorphism (SNP) markers PZE-102187307 and PZE-102188421. Moreover, the favorable allele from 'Mo17' for SNP PZE-102187611 in this interval that was most significantly associated with resistance to head smut (P = 1.88 E-10) and accounted for 39.7 to 44.4% of the phenotypic variance in an association panel consisting of 80 inbred lines. With combined linkage and association mapping, this major QTL was finally located between SNP PZE-102187486 and PZE-102188421 with an interval of ≈1.00 Mb. Based on the pedigrees of 'Mo17' and its derivatives widely used in temperate maize breeding programs, the favorable haplotype from 'Mo17' is shown to be the main source of resistance to head smut in these lines. Therefore, the SNPs closely linked to the major QTL qHS2.09, detected in both linkage and association mapping, and could be useful for marker-assisted selection in maize breeding programs.     

Mapping and Comparative Analysis of QTL for Crown Rust Resistance in an Italian x Perennial Ryegrass Population

ABSTRACT Crown rust (Puccinia coronata f. sp. lolli) is a serious fungal foliar disease of perennial ryegrass (Lolium perenne L.) and Italian ryegrass (L. multiflorum Lam.), which are important forage and turf species. A number of quantitative trait loci (QTL) for crown rust resistance previously were identified in perennial ryegrass under growth chamber or greenhouse conditions. In this study, we conducted a QTL mapping for crown rust resistance in a three-generation Italian x perennial ryegrass interspecific population under natural field conditions at two locations over 2 years. Through a comparative mapping analysis, we also investigated the syntenic relationships of previously known crown rust resistance genes in other ryegrass germplasms and oat, and genetic linkage between crown rust resistance QTL and three lignin genes: LpOMT1, LpCAD2, and LpCCR1. The interspecific mapping population of 156 progeny was developed from a cross between two Italian x perennial ryegrass hybrids, MFA and MFB. Because highly susceptible reactions to crown rust were observed from all perennial ryegrass clones, including two grandparental clones and eight clones from different pedigrees tested in this study, two grandparent clones from Italian ryegrass cv. Floregon appeared to be a source of the resistance. Two QTL on linkage groups (LGs) 2 and 7 in the resistant parent MFA map were detected consistently regardless of year and location. The others, specific to year and location, were located on LGs 3 and 6 in the susceptible parent MFB map. The QTL on LG2 was likely to correspond to those previously reported in three unrelated perennial ryegrass mapping populations; however, the other QTL on LGs 3, 6, and 7 were not. The QTL on LG7 was closely located in the syntenic genomic region where genes Pca cluster, Pcq2, Pc38, and Prq1b resistant to crown rust (P. coronata f. sp. avenae) in oat (Avena sativa L.) were previously identified. Similarly, the QTL on LG3 was found in a syntenic region with oat genes resistant to crown rust isolates PC54 and PC59. This indicates that the ortholoci for resistance genes to different formae speciales of crown rust might be present between two distantly related grass species, ryegrass and oat. In addition, we mapped four restriction fragment length polymorphism loci for three key ryegrass lignin genes encoding caffeic acid-O-methyltransferase, cinnamyl alcohol dehydrogenase, and cinnamoyl CoA-reductase on LG7. These loci were within a range of 8 to 17 centimorgans from the QTL on LG7, suggesting no tight linkage between them. The putative ortholoci for those lignin biosynthesis genes were identified on segments of rice (Oryza sativa L.) chromosomes 6 and 8, which are the counterparts of ryegrass LG7. Results from the current study facilitate understanding of crown rust resistance and its relationship with lignin biosynthesis, and also will benefit ryegrass breeders for improving crown rust resistance through marker-assisted selection.     

Histopathology provides a phenotype by which to characterize stripe rust resistance genes in wheat

The expression of the resistance phenotypes of QPst.jic‐2D and QPst.jic‐4B, two quantitative trait loci (QTL) for stripe rust resistance in wheat cv. Alcedo, were assessed relative to plant growth stage, while a histopathology analysis was undertaken to characterize the cellular interaction between Puccinia striiformis f. sp. tritici (the causal agent of stripe rust) and each QTL. QPst.jic‐2D expressed a partial resistant phenotype at seedling growth stages, with the level of resistance increasing as the wheat plant matured, conferring a disease‐free phenotype at heading. QPst.jic‐4B, however, did not express a resistant phenotype until booting (growth stage 41 on the Zadoks scale), displaying its full resistant phenotype at heading. Microscopic examination in flag leaves showed that infection sites formed in all genotypes tested, with full infection‐site establishment being observed by 36 h post‐inoculation (hpi). In lines carrying both QPst.jic‐2D and QPst.jic‐4B, as well as the parental cv. Alcedo, no microcolony formation, defined by the appearance of runner hyphae, was observed. Microcolony formation was observed in lines carrying only one, or neither QTL. Cell death associated with infection sites was observed for all genotypes, although the timing of first appearance and the extent of the cell death response varied considerably. In lines carrying both QPst.jic‐2D and QPst.jic‐4B cell death did not extend beyond one to three cells. In lines carrying only one QTL more extensive cell death was observed and cell death appeared later in lines with QPst.jic‐4B than QPst.jic‐2D. Cell death was also occasionally observed in lines without either QTL, although only at 264 hpi.     

The genetic architecture of disease resistance in maize: a synthesis of published studies

ABSTRACT Fifty publications on the mapping of maize disease resistance loci were synthesized. These papers reported the locations of 437 quantitative trait loci (QTL) for disease (dQTL), 17 resistance genes (R-genes), and 25 R-gene analogs. A set of rules was devised to enable the placement of these loci on a single consensus map, permitting analysis of the distribution of resistance loci identified across a variety of maize germplasm for a number of different diseases. The confidence intervals of the dQTL were distributed over all 10 chromosomes and covered 89% of the genetic map to which the data were anchored. Visual inspection indicated the presence of clusters of dQTL for multiple diseases. Clustering of dQTL was supported by statistical tests that took into account genome-wide variations in gene density. Several novel clusters of resistance loci were identified. Evidence was also found for the association of dQTL with maturity-related QTL. It was evident from the distinct dQTL distributions for the different diseases that certain breeding schemes may be more suitable for certain diseases. This review provides an up-to-date synthesis of reports on the locations of resistance loci in maize.