Discovery and validation of genomic regions associated with resistance to maize lethal necrosis in four biparental populations

Abstract

In sub-Saharan Africa, maize is the key determinant of food security for smallholder farmers. The sudden outbreak of maize lethal necrosis (MLN) disease is seriously threatening the maize production in the region. Understanding the genetic basis of MLN resistance is crucial. In this study, we used four biparental populations applied linkage mapping and joint linkage mapping approaches to identify and validate the MLN resistance-associated genomic regions. All populations were genotyped with low to high density markers and phenotyped in multiple environments against MLN under artificial inoculation. Phenotypic variation for MLN resistance was significant and heritability was moderate to high in all four populations for both early and late stages of disease infection. Linkage mapping revealed three major quantitative trait loci (QTL) on chromosomes 3, 6, and 9 that were consistently detected in at least two of the four populations. Phenotypic variance explained by a single QTL in each population ranged from 3.9% in population 1 to 43.8% in population 2. Joint linkage association mapping across three populations with three biometric models together revealed 16 and 10 main effect QTL for MLN-early and MLN-late, respectively. The QTL identified on chromosomes 3, 5, 6, and 9 were consistent with the QTL identified by linkage mapping. Ridge regression best linear unbiased prediction with five-fold cross-validation revealed high accuracy for prediction across populations for both MLN-early and MLN-late. Overall, the study discovered and validated the presence of major effect QTL on chromosomes 3, 6, and 9 which can be potential candidates for marker-assisted breeding to improve the MLN resistance.Electronic supplementary materialThe online version of this article (10.1007/s11032-018-0829-7) contains supplementary material, which is available to authorized users.

Genome-Wide Analyses and Prediction of Resistance to MLN in Large Tropical Maize Germplasm

“…Results in this study showed that the genetic variance for both the traits were significant and the heritability was moderate to high. This information was consistent with previous studies on MLN resistance which observed significant genetic variances and moderate to high heritability [2,15,26,31]. Higher estimates of heritabilities depict the ability of the traits for improvement of the maize germplasm for MLN resistance.…”

“…Nevertheless, the SNP identified on chromosome 6, S6_148513637 is falling very close to the consistent QTL qMLN6-158 reported for both MCMV [26], and MLN [31]. Interestingly, a QTL for SCMV resistance is very close region from diversity panel [36].…”

“…SNP S4_199711804 is another significantly associated SNP found in this study is falling within the confidence interval of major effect QTL, qMLN4-235 reported for MLN [26]. Among 10 SNPs found on chromosome 3, S3_55239348, S3_56468811 were coincided with the QTL reported for both MCMV and MLN [26], whereas SNPs S3_136082606, S3_147938951, S3_149313702, were coincided with QTL reported for MLN in four biparental populations [31]. Four SNPs, S3_161574458, S3_161574468, S3_161574470, and S3_161574471 are overlapping with the QTL reported for MLN in three DH populations [26].…”

“…Among the 32 SNPs identified together for MLN disease severity and AUDPC values, most were overlapped with SNPs reported in earlier three studies where multiple populations were used with linkage mapping, joint linkage association mapping (JLAM), and GWAS approaches [15,26,31]. SNP S4_199711804 is another significantly associated SNP found in this study is falling within the confidence interval of major effect QTL, qMLN4-235 reported for MLN [26].…”

“…The genetic architecture of MLN has been reported in biparental and association panels [15,26,31]. The present study showed that GWAS analyses is powerful for revealing marker-trait associations for both MLN-DS and AUDPC using high marker density.…”