Identification of QTL for maize resistance to common smut by using recombinant inbred lines developed from the Chinese hybrid Yuyu22
文献类型: 外文期刊
第一作者: Ding, Jun-qiang
作者: Ding, Jun-qiang;Chander, Subhash;Li, Jian-sheng;Wang, Xiao-ming
作者机构:
关键词: maize;QTL mapping;SSR markers;Ustilago maydis
期刊名称:JOURNAL OF APPLIED GENETICS ( 影响因子:3.24; 五年影响因子:2.756 )
ISSN: 1234-1983
年卷期: 2008 年 49 卷 2 期
页码:
收录情况: SCI
摘要: Common smut in maize, caused by Ustilago maydis, reduces grain yield greatly. Agronomic and chemical approaches to control such diseases are often impractical or ineffective. Resistance breeding could be an efficient approach to minimize the losses caused by common smut. In this study, quantitative trait loci (QTL) for resistance to common smut in maize were identified. In 2005, a recombinant inbred line (RIL) population along with the resistant (Zong 3) and susceptible (87-1) parents were planted in Beijing and Zhengzhou. Significant genotypic variation in resistance to common smut was observed at both locations after artificial inoculation by injecting inoculum into the whorl of plants with a modified hog vaccinator. Basing on a genetic map containing 246 polymorphic SSR markers with an average linkage distance of 9.11 cM, resistance QTL were analysed by composite interval mapping. Six additive-effect QTL associated with resistance to common smut were identified on chromosomes 3 (three QTL), 5 (one QTL) and 8 (two QTL), and explained 3.2% to 12.4% of the phenotypic variation. Among the 6 QTL, 4 showed significant QTL x environment (Q x E) interaction effects, which accounted for 1.2% to 2.5% of the phenotypic variation. Nine pairs of epistatic interactions were also detected, involving 18 loci distributed on all chromosomes except 2, 6 and 10, which contributed 0.8% to 3.0% of the observed phenotypic variation. However, no significant epistasis x environment interactions were detected. In total, additive QTL effects and Q x E interactions explained 38.8% and 8.0% of the phenotypic variation, respectively. Epistatic effects contributed 15% of the phenotypic variation. The results showed that besides the additive QTL, both epistasis and Q x E interactions formed an important genetic basis for the resistance to Ustilogo maydis in maize.
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