QTL mapping for test weight by using F(2:3) population in maize.

Test weight is an important trait in maize breeding. Understanding the genetic mechanism of test weight is important for effective selection of maize test weight improvement. In this study, quantitative trait loci (QTL) for maize test weight were identified. In the years 2007 and 2008, a F(2:3) population along with the parents Chang7-2 and Zheng58 were planted in Zhengzhou, People's Republic of China. Significant genotypic variation for maize test weight was observed in both years. Based on the genetic map containing 180 polymorphic SSR markers with an average linkage distance of 11.0 cM, QTL for maize test weight were analysed by mixed-model composite interval mapping. Five QTL, including four QTL with only additive effects, were identified on chromosomes 1, 2, 3, 4 and 5, and together explained 25.2% of the phenotypic variation. Seven pairs of epistatic interactions were also detected, involving 11 loci distributed on chromosomes 1, 2, 3, 4, 5 and 7, respectively, which totally contributed 18.2% of the phenotypic variation. However, no significant QTL x environment (QxE) interaction and epistasis x environment interaction effects were detected. The results showed that besides the additive QTL, epistatic interactions also formed an important genetic basis for test weight in maize.

A new QTL for resistance to Fusarium ear rot in maize.

Understanding the inheritance of resistance to Fusarium ear rot is a basic prerequisite for an efficient resistance breeding in maize. In this study, 250 recombinant inbred lines (RILs) along with their resistant (BT-1) and susceptible (N6) parents were planted in Zhengzhou with three replications in 2007 and 2008. Each line was artificially inoculated using the nail-punch method. Significant genotypic variation in response to Fusarium ear rot was detected in both years. Based on a genetic map containing 207 polymorphic simple sequence repeat (SSR) markers with average genetic distances of 8.83 cM, the ear rot resistance quantitative trait loci (QTL) were analyzed by composite interval mapping with a mixed model (MCIM) across the environments. In total, four QTL were detected on chromosomes 3, 4, 5, and 6. The resistance allele at each of these four QTL was contributed by resistant parent BT-1, and accounted for 2.5-10.2% of the phenotypic variation. However, no significant epistasis interaction effect was detected after a two-dimensional genome scan. Among the four QTL, one QTL with the largest effect on chromosome 4 (bin 4.06) can be suggested to be a new locus for resistance to Fusarium ear rot, which broadens the genetic base for resistance to the disease and can be used for further genetic improvement in maize-breeding programs.

Identification of QTL for maize resistance to common smut by using recombinant inbred lines developed from the Chinese hybrid Yuyu22.

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.

Identification and molecular tagging of two complementary dominant resistance genes to maize dwarf mosaic virus.

Maize dwarf mosaic is one of the devastating and widespread viral diseases in the world. So far, only a few genes were identified and mapped in the resistant materials. A new resistant elite inbred line Siyi was identified with resistance to maize dwarf mosaic virus strain B at early and adult stage. Two complementary dominant genes conditioned the resistance, with a new genetic model, of the maize inbred line were found at adult stage by the genetic analysis based on parents, F1, F2 and backcrosses in two years. The microsatellite analysis of a F2 population from the cross between Siyi and Mo17 was used to identify the two resistance genes on chromosome 3 and 6 respectively by 87 pairs of microsatellite markers. The linkage distance between phi029 and the one resistance gene on chromosome 3 is 14.5 cM, and phi126 to the other on chromosome 6 is 7.2 cM.