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liquiritigenin/medicago
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5 risultati
Medicago truncatula ABCG10 is a transporter of 4-coumarate and liquiritigenin in the medicarpin biosynthetic pathway.
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The ABCG10 protein of the model legume Medicago truncatula is required for efficient de novo production of the phenylpropanoid-derived phytoalexin medicarpin. Silencing the expression of MtABCG10 results, inter alia, in a lower accumulation of medicarpin and its precursors. In this study, we
Flavonoids enantiomer distribution in different parts of goldenrod (Solidago virgaurea L.), lucerne (Medicago sativa L.) and phacelia (Phacelia tanacetifolia Benth.).
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Plant material is a rich source of valuable compounds such as flavanones. Their different forms influence bioavailability and biological activity, causing problems with the selection of plant material for specific purposes. The purpose of this research was to determine selected flavanone
Phytoestrogenic compounds in alfalfa sprout (Medicago sativa) beyond coumestrol.
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Coumestrol has long been known as the phytoestrogenic compound in alfalfa. However, it has been demonstrated that the ethyl acetate extract of alfalfa sprout (AEA) attenuated the disease severity and increased survival and life span of autoimmune-prone MRL-lpr/lpr mice. Coumestrol, on the contrary,
Ethylene Signaling Is Important for Isoflavonoid-Mediated Resistance to Rhizoctonia solani in Roots of Medicago truncatula.
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The root-infecting necrotrophic fungal pathogen Rhizoctoniasolani causes significant disease to all the world's major food crops. As a model for pathogenesis of legumes, we have examined the interaction of R. solani AG8 with Medicago truncatula. RNAseq analysis of the moderately resistant M.
Silencing the flavonoid pathway in Medicago truncatula inhibits root nodule formation and prevents auxin transport regulation by rhizobia.
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Legumes form symbioses with rhizobia, which initiate the development of a new plant organ, the nodule. Flavonoids have long been hypothesized to regulate nodule development through their action as auxin transport inhibitors, but genetic proof has been missing. To test this hypothesis, we used RNA
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