Genetic variation at bx1 controls DIMBOA content in maize |
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Authors: | Ana Butrón Y C Chen G E Rottinghaus M D McMullen |
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Institution: | 1. Misión Biológica de Galicia (CSIC), Apdo. 28, 36080, Pontevedra, Spain 2. Veterinary Medical Diagnostic Laboratory, University of Missouri, Columbia, 65211, MO, USA 3. Plant Genetics Research Unit, USDA-Agricultural Research Service and the Division of Plant Sciences, University of Missouri, Curtis Hall 302, Columbia, 65211, MO, USA
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Abstract: | The main hydroxamic acid in maize (Zea mays L.) is 2-4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA). DIMBOA confers resistance to leaf-feeding by several corn borers.
Most genes involved in the DIMBOA metabolic pathway are located on the short arm of chromosome 4, and quantitative trait loci
(QTLs) involved in maize resistance to leaf-feeding by corn borers have been localized to that region. However, the low resolution
of QTL linkage mapping does not allow convincing proof that genetic variation at bx loci was responsible for the variability for resistance. This study addressed the following objectives: to determine the
QTLs involved in DIMBOA synthesis across genetically divergent maize inbreds using eight RIL families from the nested association
mapping population, to check the stability of QTLs for DIMBOA content across years by evaluating two of those RIL families
in 2 years, and to test the involvement of bx1 by performing association mapping with a panel of 281 diverse inbred lines. QTLs were stable across different environments.
A genetic model including eight markers explained approximately 34% of phenotypic variability across eight RIL families and
the position of the largest QTL co-localizes with the majority of structural genes of the DIMBOA pathway. Candidate association
analysis determined that sequence polymorphisms at bx1 greatly affects variation of DIMBOA content in a diverse panel of maize inbreds, but the specific causal polymorphism or
polymorphisms responsible for the QTL detected in the region 4.01 were not identified. This result may be because the causal
polymorphism(s) were not sequenced, identity is masked by linkage disequilibrium, adjustments for population structure reduce
significance of causal polymorphisms or multiple causal polymorphisms affecting bx1 segregate among inbred lines. |
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