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.

Protein phosphatase inhibitors activate anti‐fungal defence responses of soybean cotyledons and cell cultures

Abstract: Summary The application of a variety of structurally different protein phosphatase inhibitors (okadaic acid, acanthifolicin, microcystins, nodularin, tautomycin, calyculin A, cantharidin and endothall) to cut surfaces of soybean cotyledons (Glycine max L.) resulted in the production of isoflavonoid phytoalexins (plant defence compounds). Daidzein was the predominant isoflavonoid produced by soybean cotyledons in response to protein phosphatase inhibitors. In contrast, several isoflavonoid phytoalexins were seen after application of either an elicitor β-glucan fraction isolated from yeast extract or hepta-(1→3, 1→6)-β-glucoside which is the most potent elicitor-active component isolated from the soybean pathogen Phytophthora megasperma f. sp. glycinea. Isoflavonoid production in response to either protein phosphatase inhibitors or elicitors reached a maximum after 20–24 h. The addition of protein phosphatase inhibitors to a soybean cell suspension culture induced the expression of phenylalanine ammonia-lyase (PAL), the first enzyme in the isoflavonoid biosynthetic pathway. Induction of PAL activity was blocked by protein synthesis inhibitors, cycloheximide or anisomysin, and largely prevented by a protein kinase inhibitor, K252a. Another common response of plant cells to fungal elicitation, alkalinization of the soybean cell culture media, was induced within minutes in response to protein phosphatase inhibitors and was largely prevented by K252a. These studies suggest a direct role for phosphorylation in activation of plasma membrane ion flux(es), whereas the longer-term effects of protein phosphatase inhibitors on isoflavonoid production and PAL expression could be due to either direct effects of increased protein phosphorylation, or the secondary consequences of other phosphorylation-induced cellular changes. They also indicate that protein phosphatase inhibitors are likely to be of general use in investigating mechanisms of plant responses to environmental stimuli.

Ultraviolet Illumination Induces Scoparone Production in Kumquat and Orange Fruit and Improves Decay Resistance

Abstract: Additional index words. postharvest, phytoalexin, Fortunella margarita, Citrus sinensis Abstract. Ultraviolet (UV) illumination (254 nm) induced production of the phytoalexin scoparone in flavedo of kumquat (Fortunella margarita Lour. Swingle cv. Nagami) and orange (Citrus sinensis (L.) Osbeck cvs. Shamouti and Valencia). Trace amounts of scoparone (<2.0 µg·g -1 fresh weight of flavedo) were detected in nontreated fruits. Phytoalexin accumulation in kumquat reached a peak of 530 µg·g -1 11 days after illumination, hut the amount declined rapidly, returning to a trace level 1 month after treatment.. Production of scoparone in illuminated fruits was enhanced by increasing the UV dose from 1.5 × 10 3 to 9.0 × 10 3 J·m -2 for orange and from 0.2 × 10 3 to 1.5 × 10 3 J·m -2 for kumquat and by raising the storage temperature from 2 to 17C. Phytoalexin accumulation correlated with an increase in antifungal activity of flavedo extracts. UV-illuminated kumquat fruit inoculated with Penicillium digitatum Sacc. 2 days after treatment had a lower incidence of decay than the control. Illumination of previously inoculated fruit failed to prevent decay. Kumquat fruit stored at 17C showed signs of UV-induced peel damage. Chemical name used: 6,7-dimethoxycoumarin (scoparone). Phytoalexins, the low-molecular antimicrobial substances of various chemical structures, are elicited in plant tissues by either biotic (pathogen challenge) or abiotic (wounding, chemicals, irradiation, etc.) (Bailey and Mansfield, 1982) stresses. Short- wave ultraviolet light (UV) is known as a nonspecific phyto- alexin elicitor. Since 1971, when Hadwiger and Schwochau described the induction of the isoflavonoid phytoalexin pisatin in UV-treated pea pods, many studies on diverse plants have been devoted to this subject (Beier and Oertli, 1983; Bridge and

Maize death acids, 9-lipoxygenase–derived cyclopente(a)nones, display activity as cytotoxic phytoalexins and transcriptional mediators

Abstract: Plant damage promotes the interaction of lipoxygenases (LOXs) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides, and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed "jasmonates." As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA, and a series of related 14- and 12-carbon metabolites, collectively termed "death acids." 10-OPEA accumulation becomes wound inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death, which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Unlike jasmonates, functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.