Signal transduction pathway for oxidative burst and taxol production was studied in suspension cultures of Taxus chinensis var. mairei induced by oligosaccharide from Fusarium oxysprum. Suspension cells exhibited an oxidative burst approximately 4h after challenge with oligosaccharide. The secondary metabolism including accumulation of extracellular phenolics and taxol production were enhanced, while the alkalization of the outer medium and activity of phenylalanine ammonia lyase (PAL) was promoted significantly. Pretreatment with the tyrosine (Tyr) kinase inhibitor herbimycin A abolished the oxidative burst and the subsequent induction of taxol production within 15 min after addition of elicitor. Suramin, a G-protein inhibitor, inhibited the oxidative burst if added up to 30 min after oligosaccharide treatment. The oxidative burst was also induced by the ion channel generator amphotericin B. In contrast, the ion channel blocker anthracene-9-carboxylate acid and Ca2+ channel blocker nifedipine inhibited the oxidative burst within 45 min after treatment. Oligosaccharide rapidly induced Tyr pbosphrylation of receptor, which was inhibited by herbimycin A and anthracene-9-carboxylate acid. These responses were also inhibited by phospholipase C-neomycin. The response Lime of oligosaccharide to phospholipase C pathway was ca at 60 min. These data suggested that the activation of ion channels and phospholipase C follow Tyr kinase and G-protein in the signal pathway leading to the oxidative burst.