Phytoalexin

About: Phytoalexin is a research topic. Over the lifetime, 1161 publications have been published within this topic receiving 63405 citations. The topic is also known as: phytoalexins.

Phenylpropanoid defence responses in transgenic Lotus corniculatus 1. Glutathione elicitation of isoflavan phytoalexins in transformed root cultures

Abstract: When Agrobacterium rhizogenes transformed root cultures of Lotus corniculatus were treated with glutathione, isoflavan phytoalexins accumulated in both tissue and culture medium. This accumulation of phytoalexins was preceded by a transient increase in the activity of phenylalanine ammonia lyase (PAL). Elicitation of PAL occurred throughout the growth curve of Lotus ‘hairy roots’ and in different sectors of transformed root material.

A Review on Sources and Pharmacological Aspects of Sakuranetin.

Abstract: Sakuranetin belongs to the group of methoxylated flavanones. It is widely distributed in Polyomnia fruticosa and rice, where it acts as a phytoalexin. Other natural sources of this compound are, among others, grass trees, shrubs, flowering plants, cheery, and some herbal drugs, where it has been found in the form of glycosides (mainly sakuranin). Sakuranetin has antiproliferative activity against human cell lines typical for B16BL6 melanoma, esophageal squamous cell carcinoma (ESCC) and colon cancer (Colo 320). Moreover, sakuranetin shows antiviral activity towards human rhinovirus 3 and influenza B virus and was reported to have antioxidant, antimicrobial, antiinflammatory, antiparasitic, antimutagenic, and antiallergic properties. The aim of this review is to present the current status of knowledge of pro-health properties of sakuranetin.

Role of a phytoalexin in controlling lesion development in leaves of Viciafaba after infection by Botrytis spp

Abstract: SUMMARY Phytoalexin extracted from infection droplets and diseased tissues behaved as an ether-soluble acid, and was easily separated by solvent partition from other ether-soluble substances. The phytoalexin was formed in leaves by apparently healthy cells in advance of hyphae of either Botrytis fabae or B. cinerea, and in response to physical injury. Concentrations of phytoalexin around deep lesions caused by B. fabae were completely fungistatic. B. fabae caused apparent degradation of phytoalexin in lesions, and removed phytoalexin from solutions in vitro much more readily than did B. cinerea. The lower sensitivity to the phytoalexin, and the possibly related greater ability to metabolize the phytoalexin, are major factors in the greater pathogenicity of B. fabae than of B. cinerea. The same properties largely explain the ability of B. fabae to cause the so-called ‘aggressive’ phase of the chocolate-spot disease under some conditions.

Involvement of de Novo Protein Synthesis, Protein Kinase, Extracellular Ca2+, and Lipoxygenase in Arachidonic Acid Induction of 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Genes and Isoprenoid Accumulation in Potato (Solanum tuberosum L.).

Abstract: A series of inhibitors were tested to determine the participation of de novo protein synthesis, protein kinase activity, extracellular Ca2+, and lipoxygenase activity in arachidonic acid elicitation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) gene expression and sesquiterpene phytoalexin biosynthesis in potato (Solanum tuberosum L. cv Kennebec). Gene-specific probes were used to discriminate effects on the expression of two HMGR genes (hmg1 and hmg2) that respond differentially in tuber tissue following wounding or elicitor treatment. Inhibition of protein synthesis with cycloheximide completely blocked arachidonate-induced hypersensitive necrosis and browning, including HMGR gene induction and phytoalexin accumulation. This suggests that proteins necessary for coupling arachidonic acid reception to HMGR mRNA accumulation are either rapidly turned over or not present constitutively and are induced following elicitor treatment. Staurosporin, a potent inhibitor of protein kinases, and ethyleneglycol-bis([beta]-aminoethyl ether)-N,N[prime]-tetraacetic acid, a Ca2+ chelator, inhibited arachidonate-induction of hmg2 gene expression and phytoalexin accumulation but did not inhibit the wound-induced expression of hmg1. However, staurosporin inhibited arachidonate9s suppression of hmg1 gene expression. Eicosatetraynoic acid, a lipoxygenase inhibitor that suppresses elicitor-induced phytoalexin accumulation, also inhibited arachidonate9s suppression of hmg1 and induction of hmg2. The results indicate that arachidonate9s suppression of hmg1 and activation of hmg2 depend on a common intermediate or set of intermediates whose generation is sensitive to the inhibitors tested.