Analysis of Heterosis and Quantitative Trait Loci for Kernel Shape Related Traits Using Triple Testcross Population in Maize

文献类型： 外文期刊

第一作者： Jiang, Lu

作者： Jiang, Lu;Ge, Min;Zhao, Han;Zhang, Tifu;Jiang, Lu

作者机构：

期刊名称：PLOS ONE （ 影响因子：3.24； 五年影响因子：3.788 ）

ISSN： 1932-6203

年卷期： 2015 年 10 卷 4 期

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收录情况： SCI

摘要： Kernel shape related traits (KSRTs) have been shown to have important influences on grain yield. The previous studies that emphasize kernel length (KL) and kernel width (KW) lack a comprehensive evaluation of characters affecting kernel shape. In this study, materials of the basic generations (B73, Mo17, and B73 x Mo17), 82 intermated B73 x Mo17 (IBM) individuals, and the corresponding triple testcross (TTC) populations were used to evaluate heterosis, investigate correlations, and characterize the quantitative trait loci (QTL) for six KSRTs: KL, KW, length to width ratio (LWR), perimeter length (PL), kernel area (KA), and circularity (CS). The results showed that the mid-parent heterosis (MPH) for most of the KSRTs was moderate. The performance of KL, KW, PL, and KA exhibited significant positive correlation with heterozygosity but their Pearson's R values were low. Among KSRTs, the strongest significant correlation was found between PL and KA with R values was up to 0.964. In addition, KW, PL, KA, and CS were shown to be significant positive correlation with 100-kernel weight (HKW). 28 QTLs were detected for KSRTs in which nine were augmented additive, 13 were augmented dominant, and six were dominance x additive epistatic. The contribution of a single QTL to total phenotypic variation ranged from 2.1% to 32.9%. Furthermore, 19 additive x additive digenic epistatic interactions were detected for all KSRTs with the highest total R-2 for KW(78.8%), and nine dominance x dominance digenic epistatic interactions detected for KL, LWR, and CS with the highest total R-2 (55.3%). Among significant digenic interactions, most occurred between genomic regions not mapped with main-effect QTLs. These findings display the complexity of the genetic basis for KSRTs and enhance our understanding on heterosis of KSRTs from the quantitative genetic perspective.

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