Involvement of nitric oxide in cerebroside-induced defense responses and taxol production in Taxus yunnanensis suspension cells.
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.
Wang
Jian Wen
JW
School of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, People's Republic of China.
Zheng
Li Ping
LP
Tan
Ren Xiang
RX
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*
D002554:Cerebrosides; D009569:Nitric Oxide; D017239:Paclitaxel