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Northern corn leaf blight (NCLB), caused by Setosphaeria turcica, is a major fungal disease affecting maize production in sub-Saharan Africa. Utilizing host plant resistance to mitigate yield losses associated with NCLB can serve as a costeffective strategy. In this study, we conducted a high-resolution genome-wide association study (GWAS) in an association mapping panel and linkage mapping with three doubled haploid (DH) and three F3 populations of tropical maize. These populations were phenotyped for NCLB resistance across six hotspot environments in Kenya. Across environments and genotypes, NCLB scores ranged from 2.12 to 5.17 (on a scale of 1-9). NCLB disease severity scores exhibited significant genotypic variance and moderate-to-high heritability. From the six biparental populations, 23 quantitative trait loci (QTLs) were identified, each explaining between 2.7% and 15.8% of the observed phenotypic variance. Collectively, the detected QTLs explained 34.28%, 51.37%, 41.12%, 12.46%, 12.11%, and 14.66% of the total phenotypic variance in DH populations 1, 2, and 3 and F3 populations 4, 5, and 6, respectively. GWAS, using 337,110 highquality single nucleotide polymorphisms (SNPs), identified 15 marker-trait associations and several putative candidate genes linked to NCLB resistance in maize. Joint linkage association mapping (JLAM) identified 37 QTLs for NCLB resistance. Using linkage mapping, JLAM, and GWAS, several QTLs were identified within the genomic region spanning 4 to 15 Mbp on chromosome 2. This genomic region represents a promising target for enhancing NCLB resistance via marker-assisted breeding. Genome-wide predictions revealed moderate correlations with mean values of 0.45, 0.44, 0.55, and 0.42 for within GWAS panel, DH pop1, DH pop2, and DH pop3, respectively. Prediction by incorporating marker-by-environment interactions did not show much improvement. Overall, our findings indicate that NCLB resistance is quantitative in nature and is controlled by few major-effect and many minor-effect QTLs. We conclude that genomic regions consistently detected across mapping approaches and populations should be prioritized for improving NCLB resistance, while genome-wide prediction results can help incorporate both major- and minor-effect genes. This study contributes to a deeper understanding of the genetic and molecular mechanisms driving maize resistance to NCLB. [ABSTRACT FROM AUTHOR]

Maize lethal necrosis (MLN) is a viral disease with a devastating effect on maize production. Developing and deploying improved varieties with resistance to the disease is important to effectively control MLN; however, little is known about the causal genes and molecular mechanism(s) underlying MLN resistance. Screening thousands of maize inbred lines revealed KS23-5 and KS23-6 as two of the most promising donors of MLN resistance alleles. KS23-5 and KS23-6 lines were earlier developed at the University of Hawaii, United States, on the basis of a source population constituted using germplasm from Kasetsart University, Thailand. Both linkage mapping and association mapping approaches were used to discover and validate genomic regions associated with MLN resistance. Selective genotyping of resistant and susceptible individuals within large F2 populations coupled with genome-wide association study identified a major-effect QTL (qMLN06_157) on chromosome 6 for MLN disease severity score and area under the disease progress curve values in all three F2 populations involving one of the KS23 lines as a parent. The major-effect QTL (qMLN06_157) is recessively inherited and explained 55%–70% of the phenotypic variation with an approximately 6 Mb confidence interval. Linkage mapping in three F3 populations and three F2 populations involving KS23-5 or KS23-6 as one of the parents confirmed the presence of this major-effect QTL on chromosome 6, demonstrating the efficacy of the KS23 allele at qMLN06.157 in varying populations. This QTL could not be identified in population that was not derived using KS23 lines. Validation of this QTL in six F2 populations with 20 SNPs closely linked with qMLN06.157 was further confirmed its consistent expression across populations and its recessive nature of inheritance. On the basis of the consistent and effective resistance afforded by the KS23 allele at qMLN06.157, the QTL can be used in both marker-assisted forward breeding and marker-assisted backcrossing schemes to improve MLN resistance of breeding populations and key lines for eastern Africa.

Background: Quality control (QC) analysis is an important component in maize breeding and seed systems. Genotyping by next-generation sequencing (GBS) is an emerging method of SNP genotyping, which is being increasingly adopted for discovery applications, but its suitability for QC analysis has not been explored. The objectives of our study were 1) to evaluate the level of genetic purity and identity among two to nine seed sources of 16 inbred lines using 191 Kompetitive Allele Specific PCR (KASP) and 257,268 GBS markers, and 2) compare the correlation between the KASP-based low and the GBS-based high marker density on QC analysis. Results: Genetic purity within each seed source varied from 49 to 100 % for KASP and from 74 to 100 % for GBS. All except one of the inbred lines obtained from CIMMYT showed 98 to 100 % homogeneity irrespective of the marker type. On the contrary, only 16 and 21 % of the samples obtained from EIAR and partners showed ≥95 % purity for KASP and GBS, respectively. The genetic distance among multiple sources of the same line designation varied from 0.000 to 0.295 for KASP and from 0.004 to 0.230 for GBS. Five lines from CIMMYT showed ≤ 0.05 distance among multiple sources of the same line designation; the remaining eleven inbred lines, including two from CIMMYT and nine from Ethiopia showed higher than expected genetic distances for two or more seed sources. The correlation between the 191 KASP and 257,268 GBS markers was 0.88 for purity and 0.93 for identity. A reduction in the number of GBS markers to 1,343 decreased the correlation coefficient only by 0.03. Conclusions: Our results clearly showed high discrepancy both in genetic purity and identity by the origin of the seed sources (institutions) irrespective of the type of genotyping platform and number of markers used for analyses. Although there were some numerical differences between KASP and GBS, the overall conclusions reached from both methods was basically similar, which clearly suggests that smaller subset of preselected and high quality markers are sufficient for QC analysis that can easily be done using low marker density genotyping platforms, such as KASP. Results from this study would be highly relevant for plant breeders and seed system specialists. [ABSTRACT FROM AUTHOR]

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_157qMLN8_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. [ABSTRACT FROM AUTHOR]