Translating Biochemistry to Breeding for High Carotenoid Traits in Maize

Combined use of association mapping and linkage analysis is highly effective in the identification of loci governing quantitatively inherited traits. In this strategy, the underlying genetic basis and function of QTL can be tested through a hypothesis driven approach that draws upon biochemical information from model species. Results from the linkage mapping experiment can then be reconsidered in the context of a larger biochemical system. Understanding of the genetic architecture controlling carotenoid concentrations in maize endosperm has been enhanced by this strategy through the identification of two QTL, LCYε and CrtR-B1 (Harjes, 2008; Yan, 2008) that significantly affect the synthesis and conversion of carotenoids within the pathway. Previous QTL analyses indicated that a locus in bin 9.07 significantly affected carotenoid traits in multiple populations. On the basis of the QTL effect and location, we proposed that genetically controlled degradation processes could be the contributing factor and tested ZmCCD1, a maize homolog of the carotenoid cleavage dioxygenase family. A polymorphism in the promoter of ZmCCD1 was found to associate with changes in total carotenoid concentration as well as lutein. The allelic series discovered in this process was used to design allele-specific markers for use in a linkage mapping analysis of carotenoid QTL in the A619 x SC55 F2:3 population. Results indicate that the position of a significant and large effect for lutein and total carotenoid concentrations lies at the ZmCCD1 map location, and reveals that the allele associated with a strong degradation effect is dominant. Interactions of ZmCCD1 with known loci LCYε and CrtR-B1 are evaluated in the context of statistical epistasis and kernel development.