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Maize lethal necrosis viruses and other maize viruses in Rwanda.

ABSTRACT: Maize lethal necrosis (MLN) is emergent in East Africa, first reported in 2011 in Kenya, and is devastating to maize production in the region. MLN is caused by coinfection of maize with the emergent maize chlorotic mottle virus (MCMV) and any of several maize-infecting potyviruses endemic in East Africa and worldwide. Here, we examined the distribution of MCMV and sugarcane mosaic virus (SCMV), the major viruses contributing to MLN in Rwanda. These and other viruses in maize across Rwanda were further characterized by deep sequencing. When identified, MCMV had high titres and minimal sequence variability, whereas SCMV showed moderate titres and high sequence variability. Deep sequencing also identified maize streak virus and other maize-associated viruses, including a previously described polerovirus, maize yellow mosaic virus, and barley yellow dwarf virus, diverse maize-associated totiviruses, maize-associated pteridovirus, Zea mays chrysovirus 1, and a maize-associated betaflexivirus. Detection of each virus was confirmed in maize samples by reverse transcription polymerase chain reaction.

SUBMITTER: Asiimwe T

PROVIDER: S-EPMC9291312 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description: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.

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Maize lethal necrosis viruses and other maize viruses in Rwanda.

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