Dataset Information

Genetic dissection of resistance to gray leaf spot by genome-wide association study in a multi-parent maize population.

ABSTRACT:

Background

Understanding the genetic mechanisms underlying gray leaf spot (GLS) resistance in maize is crucial for breeding GLS-resistant inbred lines and commercial hybrids. Genome-wide association studies (GWAS) and gene functional annotation are valuable methods for identifying potential SNPs (single nucleotide polymorphism) and candidate genes associated with GLS resistance in maize.

Results

In this study, a total of 757 lines from five recombinant inbred line (RIL) populations of maize at the F₇ generation were used to construct an association mapping panel. SNPs obtained through genotyping-by-sequencing (GBS) were used to perform GWAS for GLS resistance using a linear mixture model in GEMMA. Candidate gene screening was performed by analyzing the 10 kb region upstream and downstream of the significantly associated SNPs linked to GLS resistance. Through GWAS analysis of multi-location phenotypic data, we identified ten candidate genes that were consistently detected in two locations or from one location along with best linear unbiased estimates (BLUE). One of these candidate genes, Zm00001d003257 that might impact GLS resistance by regulating gibberellin content, was further identified through haplotype-based association analysis, candidate gene expression analysis, and previous reports.

Conclusions

The discovery of the novel candidate gene provides valuable genomic resources for elucidating the genetic mechanisms underlying GLS resistance in maize. Additionally, these findings will contribute to the development of new genetic resources by utilizing molecular markers to facilitate the genetic improvement and breeding of maize for GLS resistance.

SUBMITTER: Hu C

PROVIDER: S-EPMC10759574 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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Publications

Genetic dissection of resistance to gray leaf spot by genome-wide association study in a multi-parent maize population.

Hu Can C Kuang Tianhui T Shaw Ranjan K RK Zhang Yudong Y Fan Jun J Bi Yaqi Y Jiang Fuyan F Guo Ruijia R Fan Xingming X

BMC plant biology 20240102 1

<h4>Background</h4>Understanding the genetic mechanisms underlying gray leaf spot (GLS) resistance in maize is crucial for breeding GLS-resistant inbred lines and commercial hybrids. Genome-wide association studies (GWAS) and gene functional annotation are valuable methods for identifying potential SNPs (single nucleotide polymorphism) and candidate genes associated with GLS resistance in maize.<h4>Results</h4>In this study, a total of 757 lines from five recombinant inbred line (RIL) population ...[more]

PMID: 38163896

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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.

Project description:BackgroundGray 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.ResultsA 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.ConclusionsQTL 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.

Project description:Key messageUsing QTL mapping and GWAS, two candidate genes (Zm00001d051039 and Zm00001d051147) were consistently identified across the three different environments and BLUP values. GWAS analysis identified the candidate gene, Zm00001d044845. These genes were subsequently validated to exhibit a significant association with maize gray leaf spot (GLS) resistance. Gray leaf spot (GLS) is a major foliar disease of maize (Zea mays L.) that causes significant yield losses worldwide. Understanding the genetic mechanisms underlying gray leaf spot resistance is crucial for breeding high-yielding and disease-resistant varieties. In this study, eight tropical and subtropical germplasms were crossed with the temperate germplasm Ye107 to develop a nested association mapping (NAM) population comprising 1,653 F2:8 RILs, consisting of eight recombinant inbred line (RIL) subpopulations, using the single-seed descent method. The NAM population was evaluated for GLS resistance in three different environments, and genotyping by sequencing of the NAM population generated 593,719 high-quality single-nucleotide polymorphisms (SNPs). Linkage analysis and genome-wide association studies (GWASs) were conducted to identify candidate genes regulating GLS resistance in maize. Both analyses identified 25 QTLs and 149 SNPs that were significantly associated with GLS resistance. Candidate genes were screened 20 Kb upstream and downstream of the significant SNPs, and three novel candidate genes (Zm00001d051039, Zm00001d051147, and Zm00001d044845) were identified. Zm00001d051039 and Zm00001d051147 were located on chromosome 4 and co-localized in both linkage (qGLS4-1 and qGLS4-2) and GWAS analyses. SNP-138,153,206 was located 0.499 kb downstream of the candidate gene Zm00001d051039, which encodes the protein IN2-1 homolog B, a homolog of glutathione S-transferase (GST). GSTs and protein IN2-1 homolog B scavenge reactive oxygen species under various stress conditions, and GSTs are believed to protect plants from a wide range of biotic and abiotic stresses by detoxifying reactive electrophilic compounds. Zm00001d051147 encodes a probable beta-1,4-xylosyltransferase involved in the biosynthesis of xylan in the cell wall, enhancing resistance. SNP-145,813,215 was located 2.69 kb downstream of the candidate gene. SNP-5,043,412 was consistently identified in three different environments and BLUP values and was located 8.788 kb downstream of the candidate gene Zm00001d044845 on chromosome 9. Zm00001d044845 encodes the U-box domain-containing protein 4 (PUB4), which is involved in regulating plant immunity. qRT-PCR analysis showed that the relative expression levels of the three candidate genes were significantly upregulated in the leaves of the TML139 (resistant) parent, indicating that these three candidate genes could be associated with resistance to GLS. The findings of this study are significant for marker-assisted breeding aimed at enhancing resistance to GLS in maize and lay the foundation for further elucidation of the genetic mechanisms underlying resistance to gray leaf spot in maize and breeding of new disease-resistant varieties.

Dataset Information

Genetic dissection of resistance to gray leaf spot by genome-wide association study in a multi-parent maize population.

Background

Results

Conclusions

Publications

Genetic dissection of resistance to gray leaf spot by genome-wide association study in a multi-parent maize population.

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