Luhua Li1,2, Xicui Yang3, Zhongni Wang4, Mingjian Ren1,2, Chang An1,2, Susong Zhu4, Ruhong Xu5,6. 1. College of Agriculture, Guizhou University, Guiyang, 550025, China. 2. Guizhou Sub-center of National Wheat Improvement Center, Guiyang, 550025, China. 3. Guizhou Agricultural Technology Extension Station, Guiyang, 550001, China. 4. Guizhou Rice Research Institute, Guizhou Academy of Agricultural Science, Guiyang, 550006, China. 5. College of Agriculture, Guizhou University, Guiyang, 550025, China. xrhgz@163.com. 6. Guizhou Sub-center of National Wheat Improvement Center, Guiyang, 550025, China. xrhgz@163.com.
Abstract
BACKGROUND: Wheat (Triticum aestivum L.) powdery mildew (Pm), which caused by Blumeria graminis f. sp. tritici (Bgt), is a destructive disease worldwide that causes severe yield losses in wheat. Resistant wheat cultivars easily lose their ability to effectively resist newly emerged Bgt strains; therefore, identifying new resistance genes is necessary for breeding resistant cultivars. METHODS AND RESULTS: Guizi 1 (GZ1) is a Chinese wheat cultivar with moderate and stable resistance to Pm. Genetic analysis indicated that the Pm resistance of GZ1 was controlled by a single dominant gene, designated PmGZ1. In total, 110 F2 individual plants and their 2 parents were subjected to genotyping by sequencing (GBS), which yielded 23,134 high-quality single-nucleotide polymorphisms (SNPs). The SNP distributions across the 21 chromosomes ranged from 134 on chromosome 6D to 6288 on chromosome 3B. Chromosome 6A has 1866 SNPs, among which 16 are physically located between positions 307,802,221 and 309,885,836 in an approximate 2.3-cM region; this region also had the greatest SNP density. The average map distance between SNP markers was 0.1 cM. A quantitative trait locus (QTL) with a significant epistatic effect on Pm resistance was mapped to chromosome 6A. The logarithm of odds (LOD) value of PmGZ1 was 34.8, and PmGZ1 was located within the confidence interval marked by chr6a-307802221 and chr6a-309885836. Moreover, 74.7% of the phenotypic variance was explained by PmGZ1. Four candidate genes (which encoded two TaAP2-A and two actin proteins) were annotated maybe as resistance genes. CONCLUSIONS: The present results provide valuable information for wheat genetic improvement, QTL fine mapping, and candidate gene validation.
BACKGROUND: Wheat (Triticum aestivum L.) powdery mildew (Pm), which caused by Blumeria graminis f. sp. tritici (Bgt), is a destructive disease worldwide that causes severe yield losses in wheat. Resistant wheat cultivars easily lose their ability to effectively resist newly emerged Bgt strains; therefore, identifying new resistance genes is necessary for breeding resistant cultivars. METHODS AND RESULTS: Guizi 1 (GZ1) is a Chinese wheat cultivar with moderate and stable resistance to Pm. Genetic analysis indicated that the Pm resistance of GZ1 was controlled by a single dominant gene, designated PmGZ1. In total, 110 F2 individual plants and their 2 parents were subjected to genotyping by sequencing (GBS), which yielded 23,134 high-quality single-nucleotide polymorphisms (SNPs). The SNP distributions across the 21 chromosomes ranged from 134 on chromosome 6D to 6288 on chromosome 3B. Chromosome 6A has 1866 SNPs, among which 16 are physically located between positions 307,802,221 and 309,885,836 in an approximate 2.3-cM region; this region also had the greatest SNP density. The average map distance between SNP markers was 0.1 cM. A quantitative trait locus (QTL) with a significant epistatic effect on Pm resistance was mapped to chromosome 6A. The logarithm of odds (LOD) value of PmGZ1 was 34.8, and PmGZ1 was located within the confidence interval marked by chr6a-307802221 and chr6a-309885836. Moreover, 74.7% of the phenotypic variance was explained by PmGZ1. Four candidate genes (which encoded two TaAP2-A and two actin proteins) were annotated maybe as resistance genes. CONCLUSIONS: The present results provide valuable information for wheat genetic improvement, QTL fine mapping, and candidate gene validation.