Maize lethal necrosis (MLN) occurs when maize chlorotic mottle virus (MCMV) and sugarcane mosaic virus (SCMV) co-infect maize plant. Yield loss of up to 100% can be experienced under severe infections. Identification and validation of genomic regions and their flanking markers can facilitate marker assisted breeding for resistance to MLN. To understand the status of previously identified quantitative trait loci (QTL)in diverse genetic background, F3 progenies derived from seven bi-parental populations were genotyped using 500 selected kompetitive allele specific PCR (KASP) SNPs. The F3 progenies were evaluated under artificial MLN inoculation for three seasons. Phenotypic analyses revealed significant variability (P ≤ 0.01) among genotypes for responses to MLN infections, with high heritability estimates (0.62 to 0.82) for MLN disease severity and AUDPC values. Linkage mapping and joint linkage association mapping revealed at least seven major QTL (qMLN3_130 and qMLN3_142, qMLN5_190 and qMLN5_202, qMLN6_85 and qMLN6_157 qMLN8_10 and qMLN9_142) spread across the 7-biparetal populations, for resistance to MLN infections and were consistent with those reported previously. The seven QTL appeared to be stable across genetic backgrounds and across environments. Therefore, these QTL could be useful for marker assisted breeding for resistance to MLN.

Maize lethal necrosis (MLN), resulting from co-infection by maize chlorotic mottle virus (MCMV) and sugarcane mosaic virus (SCMV) can cause up to 100% yield losses in maize in Africa under serious disease conditions. Maize improvement through conventional backcross (BC) takes many generations but can significantly be shortened when molecular tools are utilized in the breeding process. We used a donor parent (KS23-6) to transfer quantitative trait loci (QTL) for resistance to MLN into nine adapted but MLN susceptible lines. Nurseries were established in Kiboko, Kenya during 2015–2017 seasons and BC3F2 progeny were developed using marker assisted backcrossing (MABC) approach. Six single nucleotide polymorphism (SNP) markers linked to QTL for resistance to MLN were used to genotype 2,400 BC3F2 lines using Kompetitive Allele Specific PCR (KASP) platform. We detected that two of the six QTL had major effects for resistance to MLN under artificial inoculation field conditions in 56 candidate BC3F2 lines. To confirm whether these two QTL are reproducible under different field conditions, the 56 BC3F2 lines including their parents were evaluated in replicated trials for two seasons under artificial MLN inoculations in Naivasha, Kenya in 2018. Strong association of genotype with phenotype was detected. Consequently, 19 superior BC3F2 lines with favorable alleles and showing improved levels of resistance to MLN under artificial field inoculation were identified. These elite lines represent superior genetic resources for improvement of maize hybrids for resistance to MLN. However, 20 BC3F2 lines were fixed for both KASP markers but were susceptible to MLN under field conditions, which could suggest weak linkage between the KASP markers and target genes. The validated two major QTL can be utilized to speed up the breeding process but additional loci need to be identified between the KASP markers and the resistance genes to strengthen the linkage.

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.