Mapping and Validation of Major Quantitative Trait Loci (Qtl) for Maize Lethal Necrosis (Mln) Resistance in Maize

Abstract

Maize lethal necrosis (MLN) is a viral disease caused by dual infection of two viruses Maize chlorotic mottle virus (MCMV) and Sugarcane mosaic virus (SCMV) resulting in devastating effects on maize production. The prevalence of MLN in Kenya and neighbouring countries poses a great challenge to maize production and increases the risk of food insecurity in the region. Maize is susceptible to MLN from the seedling stage to maturity, and the management and control of the disease is costly to smallholder farmers. Development of host plant resistance will be an effective method of MLN control. Little is known about the causal genes and molecular mechanisms underlying the resistance. To identify genetic loci associated with MLN resistance, two independent sets of mapping populations were developed. From a set five F2 bi-parental mapping populations, the most resistant and most susceptible individuals were genotyped and marker-trait association analysis was performed through GWAS. Genome-Wide Association Mapping (GWAS) revealed a major effect QTL on chromosome 6 (qMLN_06.157) that was significantly associated (P < 1 X 10-8) with MLN resistance. Candidate genes within the QTL interval consists of genes involved in plant tolerance to stresses with functional activities in plant defence pathways. While using seven independent segregating populations, the favourable allele from KS23 at qMLN_06.157 was validated and fine-mapped to a 0.4cM interval (~125kb in the B73 v4 reference map). Candidate gene analysis using maize reference genome, B73, revealed a eukaryotic transcription initiation factor, GRMZM2G073535 within this interval. Transcription initiation factors have previously been shown to be involved in plant viral resistance. Eight polymorphic sites (SNPs) within or adjacent to the target window have been identified which co-segregate with MLN. This study provides important insights into the genetic architecture underlying resistance to MLN, establishes a tenable target for gene editing in GRMZM2G073535, and presents a useful set of polymorphic SNPs to be used in breeding for MLN resistance.