Identification of quantitative trait Loci for resistance to southern leaf blight and days to anthesis in a maize recombinant inbred line population

ABSTRACT A recombinant inbred line population derived from a cross between the maize lines NC300 (resistant) and B104 (susceptible) was evaluated for resistance to southern leaf blight (SLB) disease caused by Cochliobolus heterostrophus race O and for days to anthesis in four environments (Clayton, NC, and Tifton, GA, in both 2004 and 2005). Entry mean and average genetic correlations between disease ratings in different environments were high (0.78 to 0.89 and 0.9, respectively) and the overall entry mean heritability for SLB resistance was 0.89. When weighted mean disease ratings were fitted to a model using multiple interval mapping, seven potential quantitative trait loci (QTL) were identified, the two strongest being on chromosomes 3 (bin 3.04) and 9 (bin 9.03-9.04). These QTL explained a combined 80% of the phenotypic variation for SLB resistance. Some time-point-specific SLB resistance QTL were also identified. There was no significant correlation between disease resistance and days to anthesis. Six putative QTL for time to anthesis were identified, none of which coincided with any SLB resistance QTL.     

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.     

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.     

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.     

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.     

Comparative Quantitative Trait Loci Mapping of Partial Resistance to Puccinia sorghi Across Four Populations of European Flint Maize

ABSTRACT We mapped and characterized quantitative trait loci (QTL) for partial resistance to Puccinia sorghi and investigated consistency across different European flint maize populations. Four independent populations, containing 280 F(3) lines (AxB(I)), 120 F(5) lines (AxB(II)), 131 F(4) lines (AxC), and 133 F(4) lines (CxD) were produced from four European elite flint inbreds (A, B, C, and D) and genotyped at 89, 151, 104, and 122 restriction fragment length polymorphism marker loci, respectively. All F(n) lines were evaluated in field trials with two replications in three or five (AxB(I)) environments. Genotypic variance was highly significant for rust ratings in all populations, and heritabilities exceeded 0.64. Between 4 and 13 QTL were detected in individual populations using composite interval mapping, explaining between 33 and 71% of the phenotypic variance. Twenty QTL were distributed over all ten chromosomes, without preference to chromosomes 3, 4, 6, and 10, which harbor qualitatively acting Rp loci. In most cases, gene action was additive or partially dominant. Four pairs of QTL displayed significant digenic epistatic interactions, and QTL-environment interactions were observed frequently. Approximately half of the QTL were consistent between AxB(I) and AxB(II) or AxC and CxD; fewer were consistent between AxB(I) and AxC or CxD. In European flint maize germ plasm, conventional selection for partial rust resistance seems to be more promising than marker-assisted selection.     

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.     

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.     

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 Associated with Seedling Resistance to Isolates of Puccinia coronata in Oat

ABSTRACT In our previous report, quantitative trait loci (QTL) for field adult plant resistance to crown rust were identified in an oat population of 152 F(5:6) recombinant inbred lines from the cross of 'Ogle' (susceptible)/MAM17-5 (resistant). The objectives of the present study were to identify in the same population, the number, genomic location, and effect of QTL and digenic QTL epistasis associated with greenhouse seedling resistance to isolates of Puccinia coronata to determine if the QTL detected are isolate-specific and to compare them with previously detected QTL for field resistance. Reaction type was scored on greenhouse seedlings inoculated with three isolates. Composite interval mapping was conducted to identify genomic regions associated with resistance using a framework map of 272 molecular markers. Two QTL, Pcq1 and Pcq2, were identified for resistance to each of the three isolates. Pcq1, the major QTL controlling field resistance, did not confer detectable greenhouse seedling resistance when present singly; however, Pcq1 did serve as an enhancer of seedling resistance when it was combined with Pcq2. The final model explained 76.5, 77.9, and 79.3% of total phenotypic variation for resistance to isolates MNB248, MNB249, and MNB251, respectively. Race-specificity of quantitative resistance remains to be further examined.     

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.     

Relationships among resistances to fusarium and Aspergillus ear rots and contamination by fumonisin and aflatoxin in maize

ABSTRACT Fusarium verticillioides, F. proliferatum, and Aspergillus flavus cause ear rots of maize and contaminate the grain with mycotoxins (fumonisin or aflatoxin). The objective of this study was to investigate the relationships between resistance to Fusarium and Aspergillus ear rots and fumonisin and aflatoxin contamination. Based on a previous study of 143 recombinant inbred lines from the cross NC300 x B104, 24 lines with the highest and 24 lines with the lowest mean fumonisin concentration were selected for further evaluation. Paired plots of each line were inoculated with F. verticillioides and F. proliferatum or with A. flavus in replicated trials in 2004 and 2005 in Clayton, NC, and College Station, TX. The low-fumonisin group had significantly lower levels of fumonisin, aflatoxin, and Fusarium and Aspergillus ear rots. Across year-location environments, all four traits were significantly correlated; the genotypic correlation (r(G)) ranged from r(G) = 0.88 (aflatoxin and Aspergillus ear rot) to r(G) = 0.99 (Fusarium and Aspergillus ear rots). Quantitative trait loci (QTLs) were identified and their effects estimated. Two QTLs affected both toxin concentrations, one QTL affected both ear rots, and one QTL affected Aspergillus and Fusarium rots and fumonisin. These results suggest that at least some of the genes involved in resistance to ear rots and mycotoxin contamination are identical or genetically linked.     

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.     

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.     

In the eye of the beholder: the effect of rater variability and different rating scales on QTL mapping

The agronomic importance of developing durably resistant cultivars has led to substantial research in the field of quantitative disease resistance (QDR) and, in particular, mapping quantitative trait loci (QTL) for disease resistance. The assessment of QDR is typically conducted by visual estimation of disease severity, which raises concern over the accuracy and precision of visual estimates. Although previous studies have examined the factors affecting the accuracy and precision of visual disease assessment in relation to the true value of disease severity, the impact of this variability on the identification of disease resistance QTL has not been assessed. In this study, the effects of rater variability and rating scales on mapping QTL for northern leaf blight resistance in maize were evaluated in a recombinant inbred line population grown under field conditions. The population of 191 lines was evaluated by 22 different raters using a direct percentage estimate, a 0-to-9 ordinal rating scale, or both. It was found that more experienced raters had higher precision and that using a direct percentage estimation of diseased leaf area produced higher precision than using an ordinal scale. QTL mapping was then conducted using the disease estimates from each rater using stepwise general linear model selection (GLM) and inclusive composite interval mapping (ICIM). For GLM, the same QTL were largely found across raters, though some QTL were only identified by a subset of raters. The magnitudes of estimated allele effects at identified QTL varied drastically, sometimes by as much as threefold. ICIM produced highly consistent results across raters and for the different rating scales in identifying the location of QTL. We conclude that, despite variability between raters, the identification of QTL was largely consistent among raters, particularly when using ICIM. However, care should be taken in estimating QTL allele effects, because this was highly variable and rater dependent.     

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.     

弱光胁迫下黄瓜霜霉病抗性评价与分析

为明确弱光胁迫下黄瓜霜霉病田间发病规律及遗传特性,筛选抗霜霉病黄瓜品种,以15份黄瓜自交系为试材,在弱光条件下通过子叶接菌诱导寄主植株发病,同时结合田间发病率及病情指数调查进行复合抗性鉴定,进而筛选抗病组合,并对其分离世代进行抗性鉴定与遗传特征分析。结果表明,供试15份材料中共筛选出4个典型品系HB1、HB2、HB3和HB4,其病情指数分别是14.17、28.71、63.33和78.33,分别属于高抗、抗病、感病和高感病类型。这4个亲本的F1代及分离世代群体中霜霉病抗性与亲本抗性均存在正相关关系,抗性亲本的后代表现出较强的抗性;F2代群体病株分离现象比较明显,呈偏态分布,有明显的主基因+多基因存在特征,表明弱光胁迫下黄瓜霜霉病受主基因+多基因控制,主基因效应值较大。经田间抗病性鉴定分析,初步筛选出组合HB12、HB13和HB21为抗霜霉病组合,可用于后续抗病品种的选育。     

Genome-wide association study of resistance to rough dwarf disease in maize

Maize rough dwarf disease (MRDD), caused by the Maize rough dwarf virus (MRDV) is highly prevalent across summer at maize-growing areas in China. To investigate the genetic architecture underlying this viral disease, a set of 236 Chinese maize inbred lines was evaluated for resistance to MRDD in 2010 and 2011. Based on 41,101 single-nucleotide polymorphism (SNP) markers with minor allele frequencies (MAF) greater than 5 %, a genome-wide association study (GWAS) was employed to identify genomic loci for resistance to MRDD. A total of 73 SNPs were found to be associated with resistance to MRDD at a significance threshold of -log10 (P)?>?4 controlling the false discovery rate (FDR) at α?=?0.1. Fourteen of these SNPs were detected in both of the two environments tested. A total of 48 SNPs were identified in linkage disequilibrium (LD) blocks containing candidate resistance genes, including protein kinase genes. Using the pedigree information and whole-genome SNP analysis of five highly resistant inbred lines derived from the hybrid ‘P78599’, nine derivative fragments harbouring SNPs associated with MRDD resistance were detected. One 81.57 Mb fragment in particular located in bin 8.03, which contained six SNPs associated with MRDD resistance, and included the major quantitative trait loci (QTL) that had been identified in the previous study. These results suggest that the SNPs and fragments associated with MRDD resistance, especially those in bin 8.03, could be used for fine mapping of resistance genes and developing resistant varieties in maize.     

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.     

Pyramiding of partial disease resistance genes has a predictable,but diminishing,benefit to efficacy

Partial resistance genes often need to be ‘pyramided’ into a crop cultivar to obtain commercially acceptable levels of disease resistance. Analysis of data from four different wheat mapping populations, segregating for partial resistance to four contrasting foliar pathogens, showed a diminishing benefit to disease control from increasing the numbers of resistance loci in wheat lines. To test whether a general function could describe the efficacy benefit from pyramiding, a simple multiplicative survival model (MSM) was used to predict disease severities on mapping population lines carrying various combinations of two, three or four resistance loci. The effectiveness of each resistance locus was expressed as the disease severity in lines carrying resistance alleles at one locus, as a proportion of the severity in lines carrying no detectable resistance alleles. The predicted severity from any given combination of multiple resistance loci was calculated as the product of the proportional severities for the relevant single loci. A regression line fitted to transformed observed against predicted values explained 93% of the variation, with a slope and intercept not significantly different from 1 and 0, respectively. MSM may therefore provide a simple method to test contrasting types of partial resistance and search for synergistic combinations. The analysis suggests that diminishing returns are a general feature of partial resistance to foliar pathogens in wheat, a finding that is likely to apply to other crop pathosystems. Identifying and combining ever more QTL is likely to provide limited gains. The consequences of these findings for QTL analysis are described.