Genetic mapping of gray leaf spot resistance genes in maize

[摘要] ENGLISH ABSTRACT: Gray leaf spot (GLS) of maize, caused by the fungus Cercospora zeae-maydis,can reduce grain yields by up to 60% and it is now recognized as one of the mostsignificant yield-limiting diseases of maize in many parts of the world. The mostsustainable and long-term management strategy for GLS will rely heavily on thedevelopment of high-yielding, locally adapted GLS resistant hybrids.Molecular markers could be useful to plant breeders to indirectly select for genesaffecting GLS resistance and to identify resistance genes without inoculation andat an early stage of plant development. Only two studies in the USA haveexamined quantitative trait loci (QTL) association with GLS resistance.The aim of this study was to map GLS resistance genes in a resistant Seed CoLTD, Zimbabwean inbred line. Molecular markers linked to the GLS resistanceQTL were identified by using the amplified fragment length polymorphism (AFLP)technique together with bulked segregant analysis. Eleven polymorphic AFLPfragments were identified and converted to sequence-specific PCR (polymerasechain reaction) markers. Eight of the 11 converted AFLP markers were added tothe maize marker database of the University of Stellenbosch.Five of the 8 converted AFLP markers were polymorphic between the resistantand the susceptible parent. They were amplified on the DNA of 230 plants of asegregating F2 population and linkage analysis was performed withMAPMAKER/EXP. Two linkage groups consisting of two markers each, with alinkage distance of 10.4 cM (LOD 22.83) and 8.2 cM (LOD 55.41) between thetwo markers, were identified. QTL mapping with MAPMAKER/QTL confirmed thepresence of QTL in both linkage groups. Two publicly available recombinant inbred families (Burr et a/., 1988) were usedto localize the converted AFLP markers on the genetic map of maize. The QTL,which were identified with the AFLP markers, were mapped to chromosomes 1and 5. Another AFLP marker was mapped to chromosome 2 and a further tochromosome 3.To obtain more precise localizations of the QTL on chromosomes 1 and 5,sequence-tagged site markers and microsatellite markers were used. Themarkers were amplified on the DNA of the 230 plants of the F2 population andlinkage analysis was performed with MAPMAKER/EXP. The order of the markerswas in agreement with the UMC map of the Maize Genome Database. Intervalmapping using MAPMAKERlQTL and composite interval mapping using QTLCartographer were performed. The QTL on chromosome 1 had a LOD score of21 and was localized in bin 1.05/06. A variance of 37% was explained by theQTL. Two peaks were visible for the QTL on chromosome 5, one was localized inbin 5.03/04 and the other in bin 5.05/06. Both peaks had a LOD score of 5 and11% of the variance was explained by the QTL.To test the consistency of the detected QTL, the markers flanking each QTLwere amplified on selected plants of two F2 populations planted in consecutiveyears and regression analysis was performed. Both the QTL on chromosome 1and the QTL on chromosome 5 were detected in these populations. Furthermore,the presence of a QTL on chromosome 3 was confirmed with these populations.A variance of 8 -10% was explained by the QTL on chromosome 3.In this study, a major GLS resistance QTL was thus mapped on chromosomes 1and two minor GLS resistance QTL were mapped on chromosomes 3 and 5using a resistant Seed Co LTD, Zimbabwean inbred line. Markers were identifiedwhich could be used in a marker-assisted selection program to select for the GLSresistance QTL.

[发布机构] Stellenbosch University