Ding Jun-qiang, Wang Xiao-ming, Chander Subhash, Li Jian-sheng
National Maize Improvement Centre of China, China Agriculture University, China.
J Appl Genet. 2008;49(2):147-54. doi: 10.1007/BF03195608.
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 Ustilago maydis in maize.
由玉米黑粉菌引起的玉米普通黑粉病会大幅降低粮食产量。采用农艺和化学方法防治此类病害往往不切实际或效果不佳。抗性育种可能是将普通黑粉病造成的损失降至最低的有效方法。在本研究中，鉴定了玉米对普通黑粉病抗性的数量性状位点（QTL）。2005年，在北京和郑州种植了一个重组自交系（RIL）群体以及抗性亲本（综3）和感病亲本（87-1）。通过用改良的猪疫苗接种器将接种物注入植株叶腋进行人工接种后，在两个地点均观察到对普通黑粉病抗性的显著基因型变异。基于一张包含246个多态性SSR标记、平均连锁距离为9.11 cM的遗传图谱，通过复合区间作图分析抗性QTL。在第3号染色体（3个QTL）、第5号染色体（1个QTL）和第8号染色体（2个QTL）上鉴定出6个与普通黑粉病抗性相关的加性效应QTL，它们解释了3.2%至12.4%的表型变异。在这6个QTL中，有4个表现出显著的QTL×环境（Q×E）互作效应，占表型变异的1.2%至2.5%。还检测到9对上位性互作，涉及分布在除2、6和10号染色体外的所有染色体上的18个位点，它们对观察到的表型变异的贡献为0.8%至3.0%。然而，未检测到显著的上位性×环境互作。总体而言，加性QTL效应和Q×E互作分别解释了38.8%和8.0%的表型变异。上位性效应贡献了15%的表型变异。结果表明，除了加性QTL外，上位性和Q×E互作均构成了玉米对玉米黑粉菌抗性的重要遗传基础。
