Inhibitors of animal phospholipase A 2 enzymes are selective inhibitors of auxin-dependent growth. Implications for auxin-induced signal transduction

Abstract

Auxin and elicitors reportedly activate phospolipase A. A number of inhibitors known to inhibit animal phospholipase A 2 were tested for their ability to inhibit hormone and fusicoccin-induced growth. To this end, growth induced by indolyl-3-acetic acid and 2,4-dichlorophenoxyacetic acid in hypocotyl segments of etiolated zucchini (Cucurbita pepo L.) seedlings was determined in the presence of the inhibitors nordihydroguajaretic acid (NDGA), aristolochic acid, 5,8,11,14-eicosatetraynoic acid (ETYA), PB x (a prostaglandin derivative), and oleylethyl phosphocholine. Each chemical proved inhibitory to auxin-induced growth, oleylethyl phosphocholine being the least eective. The eects of the ®rst three inhibitors were investigated in more detail. Growth induced by 10 lM 2,4-dichlorophenoxyacetic acid or 1 lM indolyl-3-acetic acid was inhibited 50% by about 30±50 lM NDGA, by about 25 lM aristolochic acid, and by about 10±20 lM EYTA. Growth inhibition was reversible and became apparent 0.5±1 h after inhibitor addition. Growth induced by 0.5 or 1 lM fusicoccin was much less inhibited by NDGA and by ETYA, whereas aristolochic acid was only slightly less eective on fusicoccin-induced than on auxin-induced growth. These three inhibitors were also tested for their eects on gibberellin-induced growth in light-grown peas (Pisum sativum L.) and on cytokinin-induced expansion growth in excised cotyledons from radish (Raphanus sativum L.) seedlings. In both tests, aristolochic acid had toxic side-eects although gibberellin-induced growth was still apparent. In the gibberellin test, neither NDGA at up to 100 lM nor ETYA at 80 lM was inhibitory to hormone-induced growth. Moreover, 40 lM ETYA was not inhibitory to kinetin-induced growth. We hypothesize that the selectivity of phospholipase A 2 inhibitors for auxin-induced growth implies a dierent signal transduction pathway for each of the dierent signal substances tested, and that auxins might use fatty acid(s) and/or lysophospholipid(s) or their derivatives as the preferred second messengers.

SGR2, a Phospholipase-Like Protein, and ZIG/SGR4, a SNARE, Are Involved in the Shoot Gravitropism of Arabidopsis

“…Cloning of SGR Genes 41 and D have been analyzed (Scherer and Arnold, 1997;Chapman, 1998;Wang, 1999). They are activated by internal or environmental stimuli and produce signal molecules that are associated with several physiological responses (Chapman, 1998).…”

p-Chlorophenoxyisobutyric Acid Impairs Auxin Response in Arabidopsis Root

“…On the other hand, although several classes of compounds such as classical antiauxins, xyloglucan oligosaccharides, anion-channel blockers, and phospholipase A 2 inhibitors have been shown to have an inhibitory effect on auxin action (Jö nsson, 1961;McDougall and Fry, 1989;Scherer and Arnold, 1997;Thomine et al, 1997), they were less studied at molecular level, and their mode of action was not well understood until lately. Recently, Mauro et al (2002) reported that oligogalacturonides inhibit the induction of auxin-responsive genes in tobacco.…”

Ion Channel-Forming Alamethicin Is a Potent Elicitor of Volatile Biosynthesis and Tendril Coiling. Cross Talk between Jasmonate and Salicylate Signaling in Lima Bean

“…Phenidone interferes with the production of fatty acid hydroperoxides (Cucurou et al, 1991), whereas aristolochic acid, a potent inhibitor of phospholipase A 2 , prevents the release of linolenic acid from phospholipids (Rosenthal et al, 1989;Scherer and Arnold, 1997). The efficiency of the block after phenidone, (at 1 mm) or aristolochic acid pretreatment (0.3 mm), was demonstrated by the complete lack of emission of volatile compounds following elicitation with cellulysin shown to act through activation of the octadecanoid pathway (Piel et al, 1998;Koch et al, 1999).…”