Auxin and elicitors reportedly activate phospolipase A. A number of inhibitors known to inhibit animal phospholipase A2 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), PBx (a prostaglandin derivative), and oleylethyl phosphocholine. Each chemical proved inhibitory to auxin-induced growth, oleylethyl phosphocholine being the least effective. The effects of the first three inhibitors were investigated in more detail. Growth induced by 10 μM 2,4-dichlorophenoxyacetic acid or 1 μM indolyl-3-acetic acid was inhibited 50% by about 30–50 μM NDGA, by about 25 μM aristolochic acid, and by about 10–20 μM EYTA. Growth inhibition was reversible and became apparent 0.5–1 h after inhibitor addition. Growth induced by 0.5 or 1 μM fusicoccin was much less inhibited by NDGA and by ETYA, whereas aristolochic acid was only slightly less effective on fusicoccin-induced than on auxin-induced growth. These three inhibitors were also tested for their effects 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-effects although gibberellin-induced growth was still apparent. In the gibberellin test, neither NDGA at up to 100 μM nor ETYA at 80 μM was inhibitory to hormone-induced growth. Moreover, 40 μM ETYA was not inhibitory to kinetin-induced growth. We hypothesize that the selectivity of phospholipase A2 inhibitors for auxin-induced growth implies a different signal transduction pathway for each of the different signal substances tested, and that auxins might use fatty acid(s) and/or lysophospholipid(s) or their derivatives as the preferred second messengers.