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Metabolic flux analysis of the phenylpropanoid pathway in elicitor-treated potato tuber tissue.

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The effects of beta-1,3-oligosaccharide elicitor on the metabolism of phenylpropanoids in potato tuber were analyzed quantitatively, by monitoring the time-dependent changes in the levels of seven compounds. The elicitor treatment caused an increase in the pool size of octopamine and tyramine amides

Metabolic flux analysis of the phenylpropanoid pathway in wound-healing potato tuber tissue using stable isotope-labeled tracer and LC-MS spectroscopy.

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The metabolic flux of two phenylpropanoid metabolites, N-p-coumaroyloctopamine (p-CO) and chlorogenic acid (CGA), in the wound-healing potato tuber tissue was quantitatively analyzed by a newly developed method based upon the tracer experiment using stable isotope-labeled compounds and LC-MS. Tuber

Differential effects of environment on potato phenylpropanoid and carotenoid expression.

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BACKGROUND Plant secondary metabolites, including phenylpropanoids and carotenoids, are stress inducible, have important roles in potato physiology and influence the nutritional value of potatoes. The type and magnitude of environmental effects on tuber phytonutrients is unclear, especially under

Postharvest benzothiazole treatment enhances healing in mechanically damaged sweet potato by activating the phenylpropanoid metabolism.

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Sweet potato often suffers mechanical damage during harvest, handling, and transportation. Infections, water loss, and quality changes of sweet potato caused by mechanical damage pose great financial losses. Wound healing is an effective method to alleviate such problems. In this

Nitrogen recycling during phenylpropanoid metabolism in sweet potato tubers.

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In the first step of the phenylpropanoid metabolic pathway, L-phenylalanine (L-Phe) is deaminated to form E-cinnamate, in a conversion catalyzed by phenylalanine ammonia-lyase (PAL; EC 4.3.1.5). The metabolic fate of the ammonium ion (NH4+) produced in this reaction was investigated in sweet potato

Patterns of phenylpropanoids in non-inoculated and potato virus Y-inoculated leaves of transgenic tobacco plants expressing yeast-derived invertase.

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The patterns of secondary metabolites in leaves of yeast invertase-transgenic tobacco plants (Nicotiana tabacum L. cv. Samsun NN) were analyzed. Plants expressing cytosolic yeast-derived invertase (cytInv) or apoplastic (cell wall associated) yeast invertase (cwInv) showed a characteristic

Activation of phenylpropanoid pathway and PR of potato tuber against Fusarium sulphureum by fungal elicitor from Trichothecium roseum.

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The induced resistance of potato tuber (Solanum tuberosum cv. Xindaping) tissue against Fusarium sulphureum by a fungal elicitor from the incompatible pathogen Trichothecium roseum and its possible mechanism were studied. The results showed that the lesion development of the wound-inoculated potato

Creation of a Metabolic Sink for Tryptophan Alters the Phenylpropanoid Pathway and the Susceptibility of Potato to Phytophthora infestans.

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The creation of artificial metabolic sinks in plants by genetic engineering of key branch points may have serious consequences for the metabolic pathways being modified. The introduction into potato of a gene encoding tryptophan decarboxylase (TDC) isolated from Catharanthus roseus drastically

Effects of glucans and eicosapentaenoic acid on differential regulation of phenylpropanoid and mevalonic pathways during potato response to Phytophthora infestans.

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The effects of Phytophthora infestans glucans, eicosapentaenoic acid (EPA) and isolates of this pathogen, on the differential expression of eight genes from the phenylpropanoid and the mevalonate (Ac-MVA) pathways were analyzed in potato by semi-quantitative RT-PCR and qRT-PCR. The application of

Transcription factor StWRKY1 regulates phenylpropanoid metabolites conferring late blight resistance in potato.

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Quantitative resistance is polygenically controlled and durable, but the underlying molecular and biochemical mechanisms are poorly understood. Secondary cell wall thickening is a critical process in quantitative resistance, regulated by transcriptional networks. This paper provides compelling

Transcription factors, sucrose, and sucrose metabolic genes interact to regulate potato phenylpropanoid metabolism.

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Much remains unknown about how transcription factors and sugars regulate phenylpropanoid metabolism in tuber crops like potato (Solanum tuberosum). Based on phylogeny and protein similarity to known regulators of phenylpropanoid metabolism, 15 transcription factors were selected and their expression

Primary Metabolism, Phenylpropanoids and Antioxidant Pathways Are Regulated in Potato as a Response to Potato virus Y Infection.

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Potato production is one of the most important agricultural sectors, and it is challenged by various detrimental factors, including virus infections. To control losses in potato production, knowledge about the virus-plant interactions is crucial. Here, we investigated the molecular processes in

Synthesis and regulation of chlorogenic acid in potato: Rerouting phenylpropanoid flux in HQT-silenced lines.

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Chlorogenic acid (CGA) is the major phenolic sink in potato tubers and can constitute over 90% of total phenylpropanoids. The regulation of CGA biosynthesis in potato and the role of the CGA biosynthetic gene hydroxycinnamoyl CoA:quinate hydroxycinnamoyl transferase (HQT) was characterized. A

Changes in potato phenylpropanoid metabolism during tuber development.

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Phenylpropanoid metabolite and transcript expression during different developmental stages were examined in field grown potatoes. Carbohydrate and shikimic acid metabolism was assessed to determine how tuber primary metabolism influences phenylpropanoid metabolism. Phenylpropanoid concentrations

Nicotiflorin, rutin and chlorogenic acid: phenylpropanoids involved differently in quantitative resistance of potato tubers to biotrophic and necrotrophic pathogens.

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Physiological and molecular mechanisms underlying quantitative resistance of plants to pathogens are still poorly understood, but could depend upon differences in the intensity or timing of general defense responses. This may be the case for the biosynthesis of phenolics which are known to increase

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