Fine Mapping of a New Major QTL-qGLS8 for Gray Leaf Spot Resistance in Maize.
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ABSTRACT:
SUBMITTER: Qiu H
PROVIDER: S-EPMC8484643 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND: Gray leaf spot (GLS) is a globally important foliar disease of maize. Cercospora zeina, one of the two fungal species that cause the disease, is prevalent in southern Africa, China, Brazil and the eastern corn belt of the USA. Identification of QTL for GLS resistance in subtropical germplasm is important to support breeding programmes in developing countries where C.?zeina limits production of this staple food crop. RESULTS: A maize RIL population (F7:S6) from a cross between CML444 and SC Malawi was field-tested under GLS disease pressure at five field sites over three seasons in KwaZulu-Natal, South Africa. Thirty QTL identified from eleven field trials (environments) were consolidated to seven QTL for GLS resistance based on their expression in at least two environments and location in the same core maize bins. Four GLS resistance alleles were derived from the more resistant parent CML444 (bin 1.10, 4.08, 9.04/9.05, 10.06/10.07), whereas the remainder were from SC Malawi (bin 6.06/6.07, 7.02/7.03, 9.06). QTLs in bin 4.08 and bin 6.06/6.07 were also detected as joint QTLs, each explained more than 11% of the phenotypic variation, and were identified in four and seven environments, respectively. Common markers were used to allocate GLS QTL from eleven previous studies to bins on the IBM2005 map, and GLS QTL "hotspots" were noted. Bin 4.08 and 7.02/7.03 GLS QTL from this study overlapped with hotspots, whereas the bin 6.06/6.07 and bin 9.06 QTLs appeared to be unique. QTL for flowering time (bin 1.07, 4.09) in this population did not correspond to QTL for GLS resistance. CONCLUSIONS: QTL mapping of a RIL population from the subtropical maize parents CML444 and SC Malawi identified seven QTL for resistance to gray leaf spot disease caused by C.?zeina. These QTL together with QTL from eleven studies were allocated to bins on the IBM2005 map to provide a basis for comparison. Hotspots of GLS QTL were identified on chromosomes one, two, four, five and seven, with QTL in the current study overlapping with two of these. Two QTL from this study did not overlap with previously reported QTL.
| S-EPMC4059882 | biostudies-other
Project description:Key messageA major QTL for angular leaf spot resistance in the common bean accession G5686 was fine-mapped to a region containing 36 candidate genes. Markers have been developed for marker-assisted selection. Common bean (Phaseolus vulgaris L.) is an important grain legume and an essential protein source for human nutrition in developing countries. Angular leaf spot (ALS) caused by the pathogen Pseudocercospora griseola (Sacc.) Crous and U. Braun is responsible for severe yield losses of up to 80%. Breeding for resistant cultivars is the most ecological and economical means to control ALS and is particularly important for yield stability in low-input agriculture. Here, we report on a fine-mapping approach of a major quantitative trait locus (QTL) ALS4.1(GS, UC) for ALS resistance in a mapping population derived from the resistant genotype G5686 and the susceptible cultivar Sprite. 180 F3 individuals of the mapping population were evaluated for ALS resistance and genotyped with 22 markers distributed over 11 genome regions colocating with previously reported QTL for ALS resistance. Multiple QTL analysis identified three QTL regions, including one major QTL on chromosome Pv04 at 43.7 Mbp explaining over 75% of the observed variation for ALS resistance. Additional evaluation of 153 F4, 89 BC1F2 and 139 F4/F5/BC1F3 descendants with markers in the region of the major QTL delimited the region to 418 kbp harboring 36 candidate genes. Among these, 11 serine/threonine protein kinases arranged in a repetitive array constitute promising candidate genes for controlling ALS resistance. Single nucleotide polymorphism markers cosegregating with the major QTL for ALS resistance have been developed and constitute the basis for marker-assisted introgression of ALS resistance into advanced breeding germplasm of common bean.
| S-EPMC4544502 | biostudies-literature
Project description:Key messageA major QTL of qRtsc8-1 conferring TSC resistance was identified and fine mapped to a 721 kb region on chromosome 8 at 81 Mb, and production markers were validated in breeding lines. Tar spot complex (TSC) is a major foliar disease of maize in many Central and Latin American countries and leads to severe yield loss. To dissect the genetic architecture of TSC resistance, a genome-wide association study (GWAS) panel and a bi-parental doubled haploid population were used for GWAS and selective genotyping analysis, respectively. A total of 115 SNPs in bin 8.03 were detected by GWAS and three QTL in bins 6.05, 6.07, and 8.03 were detected by selective genotyping. The major QTL qRtsc8-1 located in bin 8.03 was detected by both analyses, and it explained 14.97% of the phenotypic variance. To fine map qRtsc8-1, the recombinant-derived progeny test was implemented. Recombinations in each generation were backcrossed, and the backcross progenies were genotyped with Kompetitive Allele Specific PCR (KASP) markers and phenotyped for TSC resistance individually. The significant tests for comparing the TSC resistance between the two classes of progenies with and without resistant alleles were used for fine mapping. In BC5 generation, qRtsc8-1 was fine mapped in an interval of ~ 721 kb flanked by markers of KASP81160138 and KASP81881276. In this interval, the candidate genes GRMZM2G063511 and GRMZM2G073884 were identified, which encode an integral membrane protein-like and a leucine-rich repeat receptor-like protein kinase, respectively. Both genes are involved in maize disease resistance responses. Two production markers KASP81160138 and KASP81160155 were verified in 471 breeding lines. This study provides valuable information for cloning the resistance gene, and it will also facilitate the routine implementation of marker-assisted selection in the breeding pipeline for improving TSC resistance.
| S-EPMC9110495 | biostudies-literature
Project description:Gray leaf spot is a maize foliar disease with worldwide distribution and can drastically reduce the production in susceptible genotypes. Published works indicate that resistance to gray leaf spot is a complex trait controlled by multiple genes, with additive effect and influenced by environment. The aim of this study was to identify genomic regions, including putative genes, associated with resistance to gray leaf spot under natural conditions of disease occurrence. A genome wide association study was conducted with 355,972 single nucleotide polymorphism markers on a phenotypic data composed by 157 tropical maize inbred lines, evaluated at Maringá -Brazil. Seven single nucleotide polymorphisms were significantly associated with gray leaf spot, some of which were localized to previously reported quantitative trait loci regions. Three gene models linked to the associated single nucleotide polymorphism were expressed at flowering time and tissue related with gray leaf spot infection, explaining a considerable proportion of the phenotypic variance, ranging from 0.34 to 0.38. The gene model GRMZM2G073465 (bin 10.07) encodes a cysteine protease3 protein, gene model GRMZM2G007188 (bin 1.02) expresses a rybosylation factor-like protein and the gene model GRMZM2G476902 (bin 4.08) encodes an armadillo repeat protein. These three proteins are related with plant defense pathway. Once these genes are validated in next studies, they will be useful for marker-assisted selection and can help improve the understanding of maize resistance to gray leaf spot.
| S-EPMC6023161 | biostudies-literature
Project description:Leaf width (LW) influences canopy architecture of population-cultured maize and can thus contribute to density breeding. In previous studies, almost all maize LW-related mutants have extreme effect on leaf development or accompanied unfavorable phenotypes. In addition, the identification of quantitative trait loci (QTLs) has been resolution-limited, with cloning and fine-mapping rarely performed. Here, we constructed a bin map for 670 recombinant inbred lines (RILs) using ?1.2 billion 100-bp re-sequencing reads. QTL analysis of the LW trait directly narrowed the major effect QTL, qLW4, to a ?270-kb interval. A fine-mapping population and near-isogenic lines (NILs) were quickly constructed using a key RIL harboring heterozygous genotypes across the qLW4 region. A recombinant-derived progeny testing strategy was subsequently used to further fine-map qLW4 to a 55-kb interval. Examination of NILs revealed that qLW4 has a completely dominant effect on LW, with no additional effect on leaf length. Candidate gene analysis suggested that this locus may be a novel LW controlling allele in maize. Our findings demonstrate the advantage of large-population high-density bin mapping, and suggest a strategy for efficiently fine-mapping or even cloning of QTLs. These results should also be helpful for further dissection of the genetic mechanism of LW variation, and benefit maize density breeding.
| S-EPMC5816676 | biostudies-literature
Project description:Maize grain contamination with aflatoxin from Aspergillus flavus (A. flavus) is a serious health hazard to animals and humans. To map the quantitative trait loci (QTLs) associated with resistance to A. flavus, we employed a powerful approach that differs from previous methods in one important way: it combines the advantages of the genome-wide association analysis (GWAS) and traditional linkage mapping analysis. Linkage mapping was performed using 228 recombinant inbred lines (RILs), and a highly significant QTL that affected aflatoxin accumulation, qAA8, was mapped. This QTL spanned approximately 7 centi-Morgan (cM) on chromosome 8. The confidence interval was too large for positional cloning of the causal gene. To refine this QTL, GWAS was performed with 558,629 single nucleotide polymorphisms (SNPs) in an association population comprising 437 maize inbred lines. Twenty-five significantly associated SNPs were identified, most of which co-localised with qAA8 and explained 6.7% to 26.8% of the phenotypic variation observed. Based on the rapid linkage disequilibrium (LD) and the high density of SNPs in the association population, qAA8 was further localised to a smaller genomic region of approximately 1500 bp. A high-resolution map of the qAA8 region will be useful towards a marker-assisted selection (MAS) of A. flavus resistance and a characterisation of the causal gene.
| S-EPMC5037484 | biostudies-other
Project description:Gray leaf spot (GLS), caused by Cercospora zeae-maydis and Cercospora zeina, is one of the most important diseases of maize worldwide. The pathogen has a necrotrophic lifestyle and no major genes are known for GLS. Quantitative resistance, although poorly understood, is important for GLS management. We used genetic mapping to refine understanding of the genetic architecture of GLS resistance and to develop hypotheses regarding the mechanisms underlying quantitative disease resistance (QDR) loci. Nested association mapping (NAM) was used to identify 16 quantitative trait loci (QTL) for QDR to GLS, including seven novel QTL, each of which demonstrated allelic series with significant effects above and below the magnitude of the B73 reference allele. Alleles at three QTL, qGLS1.04, qGLS2.09, and qGLS4.05, conferred disease reductions of greater than 10%. Interactions between loci were detected for three pairs of loci, including an interaction between iqGLS4.05 and qGLS7.03. Near-isogenic lines (NILs) were developed to confirm and fine-map three of the 16 QTL, and to develop hypotheses regarding mechanisms of resistance. qGLS1.04 was fine-mapped from an interval of 27.0 Mb to two intervals of 6.5 Mb and 5.2 Mb, consistent with the hypothesis that multiple genes underlie highly significant QTL identified by NAM. qGLS2.09, which was also associated with maturity (days to anthesis) and with resistance to southern leaf blight, was narrowed to a 4-Mb interval. The distance between major leaf veins was strongly associated with resistance to GLS at qGLS4.05. NILs for qGLS1.04 were treated with the C. zeae-maydis toxin cercosporin to test the role of host-specific toxin in QDR. Cercosporin exposure increased expression of a putative flavin-monooxygenase (FMO) gene, a candidate detoxification-related gene underlying qGLS1.04. This integrated approach to confirming QTL and characterizing the potential underlying mechanisms advances the understanding of QDR and will facilitate the development of resistant varieties.
| S-EPMC4357430 | biostudies-literature
Project description:BackgroundKernel weight and size are important components of grain yield in cereals. Although some information is available concerning the map positions of quantitative trait loci (QTL) for kernel weight and size in maize, little is known about the molecular mechanisms of these QTLs. qGW4.05 is a major QTL that is associated with kernel weight and size in maize. We combined linkage analysis and association mapping to fine-map and identify candidate gene(s) at qGW4.05.ResultsQTL qGW4.05 was fine-mapped to a 279.6-kb interval in a segregating population derived from a cross of Huangzaosi with LV28. By combining the results of regional association mapping and linkage analysis, we identified GRMZM2G039934 as a candidate gene responsible for qGW4.05. Candidate gene-based association mapping was conducted using a panel of 184 inbred lines with variable kernel weights and kernel sizes. Six polymorphic sites in the gene GRMZM2G039934 were significantly associated with kernel weight and kernel size.ConclusionThe results of linkage analysis and association mapping revealed that GRMZM2G039934 is the most likely candidate gene for qGW4.05. These results will improve our understanding of the genetic architecture and molecular mechanisms underlying kernel development in maize.
| S-EPMC4828868 | biostudies-literature
Project description:Kernel size is an important agronomic trait for grain yield in maize. The purpose of this study is to map QTLs and predict candidate genes for kernel size in maize. A total of 199 F2 and its F2 : 3 lines from the cross between SG5/SG7 were developed. A composite interval mapping (CIM) method was used to detect QTLs in three environments of F2 and F2 : 3 populations. The result showed that a total of 10 QTLs for kernel size were detected, among which were five QTLs for kernel length (KL) and five QTLs for kernel width (KW). Two stable QTLs, qKW-1, and qKL-2, were mapped in all three environments. Three QTLs, qKL-1, qKW-1, and qKW-2, were overlapped with the QTLs identified from previous studies. In order to validate and fine map qKL-2, near-isogenic lines (NILs) were developed by continuous backcrossing between SG5 as the donor parent and SG7 as the recurrent parent. Marker-assisted selection was conducted from BC2F1 generation with molecular markers near qKL-2. A secondary linkage map with six markers around the qKL-2 region was developed and used for fine mapping of qKL-2. Finally, qKL-2 was confirmed in a 1.95 Mb physical interval with selected overlapping recombinant chromosomes on maize chromosome 9 by blasting with the Zea_Mays_B73 v4 genome. Transcriptome analysis showed that a total of 11 out of 40 protein-coding genes differently expressed between the two parents were detected in the identified qKL-2 interval. GRMZM2G006080 encoding a receptor-like protein kinase FERONIA, was predicted as a candidate gene to control kernel size. The work will not only help to understand the genetic mechanisms of kernel size of maize but also lay a foundation for further fine mapping and even cloning of the promising loci.
| S-EPMC7728991 | biostudies-literature
Project description:Gray leaf spot (GLS) is one of the major maize foliar diseases in sub-Saharan Africa. Resistance to GLS is controlled by multiple genes with additive effect and is influenced by both genotype and environment. The objectives of the study were to dissect the genetic architecture of GLS resistance through linkage mapping and genome-wide association study (GWAS) and assessing the potential of genomic prediction (GP). We used both biparental populations and an association mapping panel of 410 diverse tropical/subtropical inbred lines that were genotyped using genotype by sequencing. Phenotypic evaluation in two to four environments revealed significant genotypic variation and moderate to high heritability estimates ranging from 0.43 to 0.69. GLS was negatively and significantly correlated with grain yield, anthesis date, and plant height. Linkage mapping in five populations revealed 22 quantitative trait loci (QTLs) for GLS resistance. A QTL on chromosome 7 (qGLS7-105) is a major-effect QTL that explained 28.2% of phenotypic variance. Together, all the detected QTLs explained 10.50, 49.70, 23.67, 18.05, and 28.71% of phenotypic variance in doubled haploid (DH) populations 1, 2, 3, and F3 populations 4 and 5, respectively. Joint linkage association mapping across three DH populations detected 14 QTLs that individually explained 0.10-15.7% of phenotypic variance. GWAS revealed 10 significantly (p < 9.5 × 10-6) associated SNPs distributed on chromosomes 1, 2, 6, 7, and 8, which individually explained 6-8% of phenotypic variance. A set of nine candidate genes co-located or in physical proximity to the significant SNPs with roles in plant defense against pathogens were identified. GP revealed low to moderate prediction correlations of 0.39, 0.37, 0.56, 0.30, 0.29, and 0.38 for within IMAS association panel, DH pop1, DH pop2, DH pop3, F3 pop4, and F3 po5, respectively, and accuracy was increased substantially to 0.84 for prediction across three DH populations. When the diversity panel was used as training set to predict the accuracy of GLS resistance in biparental population, there was 20-50% reduction compared to prediction within populations. Overall, the study revealed that resistance to GLS is quantitative in nature and is controlled by many loci with a few major and many minor effects. The SNPs/QTLs identified by GWAS and linkage mapping can be potential targets in improving GLS resistance in breeding programs, while GP further consolidates the development of high GLS-resistant lines by incorporating most of the major- and minor-effect genes.
| S-EPMC7667048 | biostudies-literature