Genome Wide Association And Linkage Analysis Of Resistance To Rough Dwarf Disease In Maize

Maize (Zea mays L.) is an important crop which serves as food and forage. It plays ansignificant role in agricultural and economic development. However, the production of maize wasdisturbed by a lot of biotic stress. Maize rough dwarf disease (MRDD) is a kind of viral disease allover the world, which is caused by maize rough dwarf virus (MRDV), or rice black-streakeddwarf virus (RBSDV), and is transmitted by the insect vector Laodelphax striatellus Fallen. In the1970s, MRDD caused serious loss in maize production in beijing and hebei province. Now, it isone of the most serious diseases in the Yellow-Huai river region which is very important for maizeproduction. The currently agricultural measures protecting maize production are inclined to causeenvironmental pollution, and have little effects. So the most effective measures to conquer MRDDare to breed and plant resistant varieties. In this study, genome wide association and linkageanalysis were used to explore the genetic architecture of resistance to MRDD，and to find themajor resistant quantitative trait loci (QTL) or genes. The main results were as fellows：1A total of236maize inbred lines with rich diversity were evaluated for resistance to MRDD in2010and2011, respectively. Using41101high quality SNP with minor allele frequencies(MAF) greater than5%, a genome wide association analysis (GWAS) was conducted toinvestigate the genetic architecture underlying this viral disease. As a result, a total of73SNPwere found to be associated with resistance to MRDD at a significant threshold of-log10(P)>4controlling false discovery rate (FDR) at α=0.1, single SNP could explain phenotypicvariance from2.68%to6.18%. Fourteen out of these SNP were detected in both environments.They distributed across chromosome bin5.03, bin7.02, bin8.03, bin10.02, and bin10.03, andSNP PZE-108052072and PZE-108057211were located in bin8.03. A total of48SNP wereidentified in LD blocks (r2>0.1) with candidate resistance genes, and32were included bycandidate genes, including GRMZM2G413544and GRMZM2G405760.2Using41101SNP to analysis5highly resistant inbred lines derived from the hybrid ‘P78599’,nine derivative fragments harboring SNP associated with MRDD resistance were detected,which were not harbored by the susceptible line ‘Ye478’. The r2within these fragments weregreater than0.1. The length of these fragments varied from48.84Kb to81.57Mb with anaverage of9351.03Kb. The fragment with a length of81.57Mb, which was located in bin8.03and contained6SNP associated with MRDD resistance, included the major resistant QTL thathad been identified in previous studies.3Three F2populations (assigned as F2-1, F2-2, and F2-5) were constructed with a cross betweenthe susceptible line ’B73’ and the resistant line ‘NL203’ which was selected from therecombinant inbred line population developed from the line ‘X178’ crossed with the line ‘B73’.(1) Based on F2-1, the linkage map of chromosome8was constructed, which contained9SSRmarkers with a length of35.28cM. After evaluation for resistance to MRDD through artificial inoculation, one QTL was detected between the marker umc1617and phi121in bin8.03with apeak LOD of5.1, which could explain11%phenotypic variance;(2) Based on F2-2, the linkagemap of chromosome8was constructed, which contained10markers with a length of38.36cM.The order of markers was consistant with that in IBM2008neighbor map. After evaluationthrough artificial inoculation, one QTL was identified between the marker umc1617and phi121with a peak LOD of6.18, which could explain11%phenotypic variance;(3) Based on F2-5, thelinkage map of chromosome8was constructed containing18markers with a length of153.81cM. After evaluation for resistance to MRDD through natural infection, two QTL were detectedwithin the interval of umc1139-bnlg1194and umc1735-phi121, respectively. The QTL in thefirst interval could explain3.99%phenotypic variance, and another could explain25.71%phenotypic variance.