Key message Analysis of the genetic architecture of MCMV and MLN resistance in maize doubled-haploid populations revealed QTLs with major effects on chromosomes 3 and 6 that were consistent across genetic backgrounds and environments. Two major-effect QTLs, qMCMV3 - 108/qMLN3 - 108 and qMCMV6 - 17/qMLN6 - 17 , were identified as conferring resistance to both MCMV and MLN. Abstract Maize lethal necrosis (MLN) is a serious threat to the food security of maize-growing smallholders in sub-Saharan Africa. The ability of the maize chlorotic mottle virus (MCMV) to interact with other members of the Potyviridae causes severe yield losses in the form of MLN. The objective of the present study was to gain insights and validate the genetic architecture of resistance to MCMV and MLN in maize. We applied linkage mapping to three doubled-haploid populations and a genome-wide association study (GWAS) on 380 diverse maize lines. For all the populations, phenotypic variation for MCMV and MLN was significant, and heritability was moderate to high. Linkage mapping revealed 13 quantitative trait loci (QTLs) for MCMV resistance and 12 QTLs conferring MLN resistance. One major-effect QTL, qMCMV3 - 108/qMLN3 - 108 , was consistent across populations for both MCMV and MLN resistance. Joint linkage association mapping (JLAM) revealed 18 and 21 main-effect QTLs for MCMV and MLN resistance, respectively. Another major-effect QTL, qMCMV6 - 17/qMLN6 - 17 , was detected for both MCMV and MLN resistance. The GWAS revealed a total of 54 SNPs (MCMV-13 and MLN-41) significantly associated ( P ≤ 5.60 × 10 −05 ) with MCMV and MLN resistance. Most of the GWAS-identified SNPs were within or adjacent to the QTLs detected through linkage mapping. The prediction accuracy for within populations as well as the combined populations is promising; however, the accuracy was low across populations. Overall, MCMV resistance is controlled by a few major and many minor-effect loci and seems more complex than the genetic architecture for MLN resistance. Electronic supplementary material The online version of this article (10.1007/s00122-019-03360-x) contains supplementary material, which is available to authorized users.
Contrast between marker-assisted backcross (MABC) and doubled haploid (DH) methods in transferring genes for resistance to maize lethal necrosis (MLN) in maize (Zea mays L.) is not well understood. The MLN is caused by co-infection of maize plant by maize chlorotic mottle virus and sugarcane mosaic virus. Two maize panels consisting of four BC 3 F 2 and six DH populations, separately developed through markerassisted selection from crosses between susceptible CIMMYT lines and MLN-resistant donor parent (KS23-6), were used in the current study. The two populations were of different population structures with unequal sizes. Experiments were conducted under artificial MLN inoculations for two seasons in 2018. Analyses of variance revealed significant variations among genotypes in both panels (p ≤ 0.001). Levene's and Welch's tests found that variances and means of the BC 3 F 2 and DH populations were highly unequal (p ≤ 0.001). The study identified genotypes with reduced MLN infections in both populations; however, lower means for MLN severity and area under disease progress curve (AUDPC) values, and higher heritability estimates were obtained in the DH populations than in the BC 3 F 2 populations. Additionally, the DH populations showed higher relative genetic gains for resistance to MLN compared with the BC 3 F 2 populations. The current study detected superiority of DH over MABC populations for breeding for resistance to MLN. Nevertheless, the results observed in the present study warrant further investigations using the same genetic materials with identical population sizes.
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