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.
Highlights
Maize is sub-Saharan Africa’s (SSA) most important staple food crop and is cultivated on more than 35 million hectares predominantly under rain-fed conditions and subject to the vagaries of weather (Shiferaw et al.66 Page 2 of 162011)
We found a few new quantitative trait loci (QTL) associated with maize lethal necrosis (MLN) resistance that were not detected by linkage mapping but found only with Joint linkage association mapping (JLAM)
We used four biparental populations to understand the genetic architecture of MLN resistance and validate the earlier findings in CIMMYT-derived sub-tropical maize germplasm
Summary
Maize is sub-Saharan Africa’s (SSA) most important staple food crop and is cultivated on more than 35 million hectares predominantly under rain-fed conditions and subject to the vagaries of weather (Shiferaw et al. Page 2 of 162011). The maize lethal necrosis (MLN) disease emerged as one of the major threats to the maize-based food security in SSA since 2011 (http://mln.cimmyt.org/) This devastating disease was first reported in September 2011 in the South Rift Valley of Kenya and by 2014, MLN was extensively reported in Kenya, Uganda, Tanzania, Rwanda, D.R. Congo, and Ethiopia (Wangai et al 2012; Adams et al 2014; Lukanda et al 2014; Mahuku et al 2015a, b). The MLN disease is caused by co-infection by two viruses—Maize Chlorotic Mottle Virus (MCMV) and Sugarcane Mosaic Virus (SCMV). Field observations indicated that MLN has affected almost all the commercially grown maize varieties in Kenya (De Groote et al 2016), with yield losses ranging from 30 to 100% depending on the stage of disease infection and the environment
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