SummaryImprovement of grain yield is an essential long-term goal of maize (Zea mays) breeding to meet continual and increasing food demands worldwide, but the genetic basis remains unclear.We used 10 different recombination inbred line (RIL) populations genotyped with highdensity markers and phenotyped in multiple environments to dissect the genetic architecture of maize ear traits.Three methods were used to map the quantitative trait loci (QTLs) affecting ear traits. We found 17-34 minor-or moderate-effect loci that influence ear traits, with little epistasis and environmental interactions, totally accounting for 55.4-82% of the phenotypic variation. Four novel QTLs were validated and fine mapped using candidate gene association analysis, expression QTL analysis and heterogeneous inbred family validation.The combination of multiple different populations is a flexible and manageable way to collaboratively integrate widely available genetic resources, thereby boosting the statistical power of QTL discovery for important traits in agricultural crops, ultimately facilitating breeding programs.
Maize (Zea mays) is a major staple crop. Maize kernel size and weight are important contributors to its yield. Here, we measured kernel length, kernel width, kernel thickness, hundred kernel weight, and kernel test weight in 10 recombinant inbred line populations and dissected their genetic architecture using three statistical models. In total, 729 quantitative trait loci (QTLs) were identified, many of which were identified in all three models, including 22 major QTLs that each can explain more than 10% of phenotypic variation. To provide candidate genes for these QTLs, we identified 30 maize genes that are orthologs of 18 rice (Oryza sativa) genes reported to affect rice seed size or weight. Interestingly, 24 of these 30 genes are located in the identified QTLs or within 1 Mb of the significant single-nucleotide polymorphisms. We further confirmed the effects of five genes on maize kernel size/weight in an independent association mapping panel with 540 lines by candidate gene association analysis. Lastly, the function of ZmINCW1, a homolog of rice GRAIN INCOMPLETE FILLING1 that affects seed size and weight, was characterized in detail. ZmINCW1 is close to QTL peaks for kernel size/weight (less than 1 Mb) and contains significant single-nucleotide polymorphisms affecting kernel size/weight in the association panel. Overexpression of this gene can rescue the reduced weight of the Arabidopsis (Arabidopsis thaliana) homozygous mutant line in the AtcwINV2 gene (Arabidopsis ortholog of ZmINCW1). These results indicate that the molecular mechanisms affecting seed development are conserved in maize, rice, and possibly Arabidopsis.Maize (Zea mays) is one of the most important crops and is cultivated worldwide as a source of staple food, animal feed, and industrial materials. According to the Food and Agriculture Organization, the production of maize was 1,016.7 million tons in 2013, which was far more than rice (Oryza sativa) and wheat (Triticum aestivum; 745.7 and 713.1 million tons, respectively). Yield improvement is a central goal of maize breeding. Kernel size and weight are two significant components of maize yield, and many attempts have been made to elucidate the genetic basis of kernel size and weight.Many studies have mapped quantitative trait loci (QTLs) for natural variations in kernel size and weight. (2015) mapped 28 QTLs in a test cross population. Most of these studies used two diverse inbred lines to develop the segregating population and used a limited number of genetic markers to construct the linkage map, which greatly limited the resolution and power to detect rare and/or small-effect QTLs. Large-scale QTL mapping studies including more diverse genetic backgrounds and dense genetic markers would provide more insight into the number and effect of QTLs controlling the natural variations of kernel size and weight in maize.
BackgroundNorthern corn leaf blight (NCLB) caused by Exserohilum turcicum is a destructive disease in maize. Using host resistance to minimize the detrimental effects of NCLB on maize productivity is the most cost-effective and appealing disease management strategy. However, this requires the identification and use of stable resistance genes that are effective across different environments.ResultsWe evaluated a diverse maize population comprised of 999 inbred lines across different environments for resistance to NCLB. To identify genomic regions associated with NCLB resistance in maize, a genome-wide association analysis was conducted using 56,110 single-nucleotide polymorphism markers. Single-marker and haplotype-based associations, as well as Anderson-Darling tests, identified alleles significantly associated with NCLB resistance. The single-marker and haplotype-based association mappings identified twelve and ten loci (genes), respectively, that were significantly associated with resistance to NCLB. Additionally, by dividing the population into three subgroups and performing Anderson-Darling tests, eighty one genes were detected, and twelve of them were related to plant defense. Identical defense genes were identified using the three analyses.ConclusionAn association panel including 999 diverse lines was evaluated for resistance to NCLB in multiple environments, and a large number of resistant lines were identified and can be used as reliable resistance resource in maize breeding program. Genome-wide association study reveals that NCLB resistance is a complex trait which is under the control of many minor genes with relatively low effects. Pyramiding these genes in the same background is likely to result in stable resistance to NCLB.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-015-0589-z) contains supplementary material, which is available to authorized users.
Broad-spectrum resistance has great values for crop breeding. However, its mechanisms are largely unknown. Here, we report the cloning of a maize NLR gene, RppK, for resistance against southern corn rust (SCR) and its cognate Avr gene, AvrRppK, from Puccinia polysora (the causal pathogen of SCR). The AvrRppK gene has no sequence variation in all examined isolates. It has high expression level during infection and can suppress pattern-triggered immunity (PTI). Further, the introgression of RppK into maize inbred lines and hybrids enhances resistance against multiple isolates of P. polysora, thereby increasing yield in the presence of SCR. Together, we show that RppK is involved in resistance against multiple P. polysora isolates and it can recognize AvrRppK, which is broadly distributed and conserved in P. polysora isolates.
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