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Feedback inhibition of the general phenylpropanoid and flavonol biosynthetic pathways upon a compromised flavonol-3-O-glycosylation
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Feedback inhibition of the general phenylpropanoid and flavonol biosynthetic pathways upon a compromised flavonol-3-O-glycosylation
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Journal Article
Feedback inhibition of the general phenylpropanoid and flavonol biosynthetic pathways upon a compromised flavonol-3-O-glycosylation
2012
Overview
Flavonols, phenylalanine-derived secondary metabolites, have protective and regulatory functions in plants. InArabidopsis thaliana, they are consecutively glycosylated at their 3-OH and 7-OH groups. UGT78D1 and UGT78D2 are the major flavonol 3-O-glycosyltransferases inArabidopsisleaves. Theugt78d1 ugt78d2double mutant, which was strongly compromised in the initial 3-O-glycosylation, showed a severe and specific repression of flavonol biosynthesis, retaining only one-third of the wild-type level. This metabolic phenotype was associated with a repressed transcription of several flavonol biosynthetic genes including the committed step chalcone synthase [(CHS) or TRANSPARENT TESTA 4 (TT4)]. Furthermore, the committed step of the upstream, general phenylpropanoid pathway, phenylalanine ammonia-lyase (PAL), was down-regulated in its enzyme activity and in the transcription of the flavonol-relatedPAL1andPAL2. However, a complete blocking of flavonoid biosynthesis at CHS released PAL inhibition in att4 ugt78d1 ugt78d2line. PAL activity was even enhanced in theflavonol synthase 1mutant, which compromises the final formation of flavonol aglycones. The dependence of the PAL feedback inhibition on flavonols was confirmed by chemical complementation oftt4 ugt78d1 ugt78d2using naringenin, a downstream flavonoid intermediate, which restored the PAL repression. Although aglycones were not analytically detectable, this study provides genetic evidence for a novel, flavonol-dependent feedback inhibition of the flavonol biosynthetic pathway and PAL. It was conditioned by the compromised flavonol-3-O-conjugation and a decrease in flavonol content, yet dependent on a residual, flavonol synthase 1 (FLS1)-related capacity to form flavonol aglycones. Thus, this regulation would not react to a reduced metabolic flux into flavonol biosynthesis, but it might prevent the accumulation of non-glycosylated, toxic flavonols.
Publisher
Oxford University Press
Subject
/ Biological and medical sciences
/ Fundamental and applied biological sciences. Psychology
/ Gene Expression Regulation, Plant
/ Genes
/ genetics
/ Glycosyltransferases - genetics
/ Glycosyltransferases - metabolism
/ Leaves
/ Lignin
/ mutants
/ naringenin-chalcone synthase
/ Plant physiology and development
/ Plants
/ testa
/ toxicity
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