title: Involvement of nitric oxide in cerebroside-induced defense responses and taxol production in Taxus yunnanensis suspension cells.
abstract: This work was to characterize the generation of nitric oxide (NO) in Taxus yunnanensis cells induced by a fungal-derived cerebroside and the signal role of NO in the elicitation of plant defense responses and taxol production. (2S,2'R,3R,3'E,4E,8E)-1-O-beta-D-glucopyranosyl-2-N-(2'-hydroxy-3'-octadecenoyl)-3-hydroxy-9-methyl-4,8-sphingadienine at 10 microg/ml induced a rapid and dose-dependent NO production in the Taxus cell culture, reaching a maximum within 5 h of the treatment. The NO donor sodium nitroprusside (SNP) potentiated cerebroside-induced H(2)O(2) production and cell death. Inhibition of nitric oxide synthase activity by phenylene-1,3-bis(ethane-2-isothiourea) dihydrobromide or scavenging NO by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide partially blocked the cerebroside-induced H(2)O(2) production and cell death. Moreover, NO enhanced cerebroside-induced activation of phenylalanine ammonium-lyase and accumulation of taxol in cell cultures. These results are suggestive of a role for NO as a new signal component for activating the cerebroside-induced defense responses and secondary metabolism activities of plant cells.
authors: School of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, People's Republic of China.
authors: Jian Wen
authors: JW
authors: Wang
authors: Li Ping
authors: LP
authors: Zheng
authors: Ren Xiang
authors: RX
authors: Tan
mesh_terms: D002460:Cell Line; D002554:Cerebrosides / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology*; D017239:Paclitaxel / Q000096:biosynthesis*; D016897:Respiratory Burst / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D020946:Taxus / Q000166:cytology / Q000378:metabolism*
chemical_list: D002554:Cerebrosides; D009569:Nitric Oxide; D017239:Paclitaxel