|Butron, Ana -|
|Chen, Y-C -|
|Rottinghaus, George -|
Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 17, 2009
Publication Date: November 13, 2009
Citation: Butron, A., Chen, Y., Rottinghaus, G., McMullen, M.D. 2009. Genetic Variation at Bx 1 Controls DIMBOA Content in Maize. Theoretical and Applied Genetics. 120:721-734. Interpretive Summary: The European corn borer and related insects cause damage to corn by feeding on leaf and whorl tissue. In corn seedlings natural resistance to this leaf feeding is controlled by a chemical known as DIMBOA. Although the genes involved in the synthesis of DIMBOA are known, the genetic basis of varietal differences in resistance has not been defined. In this study we identify the chromosomal regions controlling DIMBOA synthesis across a diverse set of corn inbred lines. In addition we demonstrated that the largest genetic difference among inbred lines affecting DIMBOA concentration is variation in a gene called bx1, the first step in DIMBOA synthesis. These results are important because they provide corn breeders with the knowledge for marker assisted selection of corn lines with improved insect resistance.
Technical Abstract: The main hydroxamic acid in maize (Zea mays L.) is 2-4-hydroxy-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 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 map the QTLs involved in DIMBOA synthesis across genetically divergent maize inbreds, and to determine if genetic variation at Bx1 controls DIMBOA levels in maize inbreds. A genetic model including eight markers explained approximately 34% of phenotypic variability across eight RIL families. The position of the largest QTL co-localizes with the majority of structural genes of the DIMBOA pathway. Association analysis determined that sequence polymorphisms at Bx1 affects variation of DIMBOA content. After adjusting for population structure, variation for two polymorphisms at Bx1 was significantly associated with DIMBOA content (p <0.001), explaining 12% of phenotypic variability across a population of 282 diverse maize lines. These results suggest that genetic variation for Bx1 is likely behind the QTL detected in the chromosome region 4.01, but specific causal polymorphisms responsible for that variation were not identified.