We have observed that homozygosity for intensifier (in) markedly enhances the amount of UDP glucose-flavonoid glucosyl transferase (UFGT) activity in mature endosperms of three maize genotypes (A1, A2, Bz1, Bz2, C1, C2, R, Vp; a1, A2, Bz1, Bz2, C1, C2, R, Vp; and A1, A2, Bz1, bz2, C1, C2, R, Vp) that are competent to produce the enzyme. Dooner and Nelson have previously demonstrated normal UFGT levels in a1 and bz2 mutants (Biochemical Genetics 15:509-519, 1977). The specific activities of UFGT for the different genotypes are given in Table 1. All comparisons were made in a W22 background and for ears grown in Madison during the summer of 1981. Similar results were obtained for a1, in vs. a1, In, or bz2, in vs. bz2, In genotypes grown in 1980. Enzyme levels were higher for in genotypes on the basis of specific activity (both as µmoles isoquercitrin formed per hr per mg protein and nmoles isoquercitrin formed per hr per endosperm). Furthermore, the difference in enzyme activity of In versus in genotypes is not due to the presence of an inhibitor in the In stocks. When the extracts from In and in endosperms were mixed, the UFGT activities were additive.
The effect of intensifier on UFGT levels was verified in comparisons within ears between bz2, In/In/in and bz2, in/in/in kernels (Table 1). The amount of UFGT was higher for in/in/in kernels as compared to In/In/in kernels. However, there is no apparent dosage effect for in on UFGT activity; this is in contrast to the results of Reddy and Peterson (Can. J. Genet. Cyt. 20:337-347, 1978), who reported that heterozygotes for intensifier had pigment levels intermediate between those of the two homozygous conditions.
Coe concluded that genetic evidence favors placing intensifier prior to A1 in the anthocyanin synthetic pathway (In, A1, Bz1, A2, Pr; Am. Naturalist 91: 381-85, 1957). The increased synthesis of an enzyme (UFGT) later in the biosynthetic sequence than intensifier may result from induction of Bz1 due to increased flow of intermediates through that pathway or may be caused by some other regulatory mechanism controlled by intensifier and acting on the genes for anthocyanin biosynthetic enzymes. It is not, however, due to the synthesis of an inhibitor in In stocks.
The dominant alleles C and R are also required for anthocyanin formation in the aleurone. Recessive mutations at C and R and the dominant C-I mutation result in much reduced levels of UFGT (Dooner and Nelson, Biochemical Genetics 15:509-519, 1977). They concluded that products of C and R are required for the induction of UFGT. In contrast, it is the recessive allele of intensifier that elevates UFGT activity. If, as Dooner and Nelson have speculated, UFGT may be precursor-inducible, these results suggest that homozygosity for in may divert greater quantities of intermediates through the last steps of the anthocyanin biosynthetic pathway at the expense of other flavonoid compounds.
Anita S. Klein and Oliver Nelson
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