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ARS Home » Midwest Area » Columbia, Missouri » Plant Genetics Research » Research » Publications at this Location » Publication #141068
Title: QUANTITATIVE TRAIT LOCUS ANALYSIS OF C-GLYCOSYL FLAVONE TYPE IN MAIZE SILKS

Author
item CORTES-CRUZ, MOISES - UNIV OF MISSOURI
item Guill, Katherine
item SNOOK, MAURICE - UNIV OF GEORGIA - ATHENS
item McMullen, Michael

Submitted to: Plant and Animal Genome VX Conference Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 1/12/2003
Publication Date: 1/12/2003
Citation: CORTES-CRUZ, M., HOUCHINS, K.E., SNOOK, M.E., MCMULLEN, M.D. QUANTITATIVE TRAIT LOCUS ANALYSIS OF C-GLYCOSYL FLAVONE TYPE IN MAIZE SILKS. PLANT AND ANIMAL GENOME. 2003. ABSTRACT. P. 186.

Interpretive Summary:

Technical Abstract: Resistance to corn earworm (Helicoverpa zea Boddie) has been attributed to high concentrations of C-glycosyl flavones and chlorogenic acid in maize silks. The most common C-glycosyl flavones isolated from maize silks are maysin, apimaysin and methoxymaysin, which are distinguished by their B-ring substitutions. For a better understanding of the genetic mechanisms underlying the synthesis of these compounds, we conducted a quantitative trait locus (QTL) study with two populations: NC7A x Tx501 and Tx501 x Mp708. For chlorogenic acid, maysin and methoxymaysin concentration, a major QTL was located on chromosome 4 near umc1963 for both populations. For apimaysin, in both populations, a major QTL was located at the position of the pr1 locus on chromosome 5. The QTL alleles on chromosome 4 that increased methoxymaysin significantly decreased the synthesis of maysin and chlorogenic acid. This decrease in maysin concentration was four-fold greater than the increase in methoxymaysin. In addition, smaller effects were detected on chromosome 4 for apimaysin as well on chromosome 5 for maysin and methoxymaysin. Our results indicate that the QTL on chromosome 4 responsible for the increase in methoxymaysin synthesis alters the dynamics of both the phenylpropanoid and flavonoid pathways.