sinapic acid ester/arabidopsis

Sinapoylmalate is one of the major phenylpropanoid metabolites that is accumulated in the vegetative tissue of Arabidopsis thaliana. A thin-layer chromatography-based mutant screen identified two allelic mutant lines that accumulated sinapoylglucose in their leaves in place of sinapoylmalate. Both

The FAH1 and F3H genes encode ferulate-5-hydroxylase and flavanone-3-hydroxylase, which are enzymes in the pathways leading to the synthesis of sinapic acid esters and flavonoids, respectively. Nucleotide variation at these genes was surveyed by sequencing a sample of 20 worldwide Arabidopsis

Nitrate reductase (NR) activity is necessary for the synthesis of nitric oxide (NO), a key signaling molecule in plants. Here, we investigated the effect of NR deficiency on NO production and phenylpropanoid metabolism of Arabidopsis thaliana leaves. HPLC-mass spectrometry analysis showed that the

Sinapic acid and its esters have broad functions in different stages of seed germination and plant development and are thought to play a role in protecting against ultraviolet irradiation. To better understand the interactions between sinapic acid esters and seed germination processes in response to

Phenylalanine ammonia-lyase (PAL, EC 4.3.1.5) catalyzes the first step in the phenylpropanoid pathway, and is considered an important regulation point between primary and secondary metabolism. In the present work we analyzed expression of the PAL genes in leaves of Arabidopsis thaliana rosette-stage

Increases in the terrestrial levels of ultraviolet-B (UV-B) radiation (280 to 320 nm) due to diminished stratospheric ozone have prompted an investigation of the protective mechanisms that contribute to UV-B tolerance in plants. In response to UV-B stress, flowering plants produce a variety of

Mutants of Arabidopsis deficient in a major leaf phenylpropanoid ester, 2-O-sinapoyl-L-malate, were identified by thin-layer chromatographic screening of methanolic leaf extracts from several thousand mutagenized plants. Mutations at a locus designated SIN1 also eliminate accumulation of the sinapic