Abstract
Key messageAnalysis 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.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.
Highlights
Maize chlorotic mottle virus (MCMV) is one of the most destructive pathogens, and it interacts synergistically with many members of the Potyviridae family: the potyviruses sugarcane mosaic virus (SCMV), maize dwarf mosaic virus (MDMV), and wheat streak mosaic virus (WSMV), resulting in maize lethal necrosis (MLN) (Wangai et al 2012; Braidwood et al 2018; Redinbaugh and Lucy 2018)
A considerable variation was observed in the disease severity (DS) and area under the disease progress curve (AUDPC) values of MCMV and MLN in all three DH populations and in the IMAS panel (Fig. 1, Table 1)
Most of the elite inbred lines and commercial hybrids are susceptible to MCMV and MLN (De Groote et al 2016)
Summary
Maize chlorotic mottle virus (MCMV) is one of the most destructive pathogens, and it interacts synergistically with many members of the Potyviridae family: the potyviruses sugarcane mosaic virus (SCMV), maize dwarf mosaic virus (MDMV), and wheat streak mosaic virus (WSMV), resulting in maize lethal necrosis (MLN) (Wangai et al 2012; Braidwood et al 2018; Redinbaugh and Lucy 2018). In sub-Saharan Africa (SSA), MCMV as one of the causal agents of MLN was first reported in Kenya (Wangai et al 2012). Both MCMV and MLN were reported in Tanzania, the Democratic Republic of Congo (Lukanda et al 2014), Rwanda (Adams et al 2014), Ethiopia and Uganda (Mahuku et al 2015), resulting in significant yield loss and affecting the food security and livelihoods of smallholder farmers in eastern and central Africa. In eastern Africa, MCMV was found in co-infections with SCMV that cause MLN (Gowda et al 2015; Beyene et al 2017)
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