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Maize head smut, caused by Sporisorium reilianum f. sp. Zea, is a kind of fungal diseases, which has seriously limited the maize production and development. Molecular breeding for improving disease resistance against various pathogens is an effective approach to increase the quality and quantity of maize, and mine disease resistance genes and functional marker associated with resistance are the theoretical premises of disease resistance in molecular breeding.In recent years, with the development of high-throughput genotyping technology and the theory of association analysis, genome-wide association studies (GWAS) are performed in more and more plants. At present, little information is available about the genetic study against S. reilianum in maize. The present study aims at localization of genes involved in head smut resistance and exploration the possible mechanism of resistance against S. reilianum in maize, via combination high density analysis techniques in whole genome with genome-wide association analysis. The main results are as follows:1. When assessing linkage disequilibrium (LD), a serial spacing between two loci on the same chromosome of0.1kb,0.2kb,0.5kb,1kb,2kb,5kb,10kb,30kb,50kb,100kb,300kb,500kb,1Mb,3Mb,5Mb,40Mb,50Mb, and100Mb respectively, were considered. A sharp decline in the r2value was observed as the physical distance increased among each chromosome and all the chromosomes. Linkage disequilibrium decay for each chromosome is also different. The level of LD decay was faster in chr.10than in chr.l. The average r2for all chromosomes was estimated at-200kb, when the value of the cut off for r2was set to0.1.2. To correct for false positives, six models were selected, which referred to the population structure (Q, PCA) and kinship (K). The general linear model (GLM) included the Q model controlling for Q, the PCA model controlling for PCA, and a model that did not control for Q and PCA. The mixed linear model (MLM) comprised the K model controlling for K, the Q+K model controlling for both Q and K, and the PCA+K model controlling for both PCA and K. The results were better from the Q+k model than those from other models.3. In the present study,19association loci were found to be distributed over10chromosomes. One loci in chrl, chr3, chr4and chr10. Eight loci overlapped with previous studies. Most of SNP locations were adjacent to genes. These genes were classified into three groups including R genes such as NBS-LRR homologous gene in chr8, disease response genes such as encoding tubby-like protein gene in chr4, and other genes possibly functioning in plant disease resistance such as Antifreeze gene in2.04bin. These could reflect a complicated molecular mechanism of maize resistance to head smut.4. Candidate gene association in a region expanding SNP4to400kb from both ends was performed to ascertain whether a true association signal exists in2.09bin.1.6Mb of sequence from a panel of144maize inbred lines was obtained, including231SNPs and82Indels. Nine loci showed significant associations with resistance to head smut. These nine loci all belonged to the gene GRMZM2G166566.5. In the analysis of genome-wide association results, NBS type disease resistance genes were found. Therefore, in maize inbred line B73genome, gene number, type and phylogenetic relationship for NBS candidate disease resistance gene were analyzed, and these findings provided useful information on the understanding of the maize genome structure, genome expansion and new genes generation.
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