机械刺激诱导的烟草悬浮细胞一氧化氮产生途径及其与Ca^(2+)和钙调素的关系  

Pathways of Mechanical Stimulation-Induced Nitric Oxide Production and Their Relationship with Ca^(2+) and Calmodulin in Tobacco (Nicotiana tobacum L.) Suspension Culture Cells

作　　者：柯学[1,2] 李忠光[2,3,4] 刘娴[2,3,4] 龚明[2,3,4] 

机构地区：[1]中国农业大学水利与土木工程学院,北京100083 [2]云南师范大学生命科学学院,昆明650092 [3]云南师范大学生物能源持续开发利用教育部工程研究中心,昆明650092 [4]云南师范大学云南省生物质能与环境生物技术重点实验室,昆明650092

出　　处：《植物生理学报》2011年第1期85-90,共6页Plant Physiology Journal

基　　金：国家自然科学基金(30460016);云南省教育厅基金(07Z11860,09Y0145)

摘　　要：通过提高摇床转速对烟草细胞施加机械刺激(MS)可诱导其胞内一氧化氮(NO)的快速产生和一氧化氮合酶(NOS)活性的提高,这种MS诱导的NO产生可被NO清除剂cPTIO和NOS抑制剂L-NMMA显著抑制。此外,Ca2+螯合剂EGTA、质膜Ca2+通道阻断剂La3+、胞内Ca2+通道拮抗剂钌红,以及钙调素抑制剂CPZ和TFP预处理均不同程度地抑制了机械刺激诱导的烟草细胞NO的产生,而机械刺激过程中钙调素活性显著上升并与NOS活性和NO含量的变化相一致。这些结果暗示着(类)NOS酶催化的精氨酸依赖途径可能是机械刺激诱发烟草细胞NO产生的主要途径,Ca2+/CaM可能通过调节(类)NOS活性来调控NO的产生。Application of mechanical stimulation （MS） on tobacco （Nicotiana tobacum） suspension culture cells led to rapid production of intracellular nitric oxide （NO） and increased activity of nitric oxide synthase （NOS）, but this MS-induced NO production could be significantly inhibited by the NO scavenger cPTIO and NOS inhibitor L-NMMA. In addition, the Ca2＋ specific chelator EGTA, plasma membrane Ca2＋ channel blocker La3＋, intracellular Ca2＋ channel antagonist ruthenium red, and the calmodulin inhibitors chlorpromazine and trifluoperazine pretreatments all led to the inhibition of the MS-induced NO production to some extent; on the other hand, the MS treatment raised calmodulin activity in the tobacco cells, being consistent with the change of NO content and NOS activity. All this results suggested that the arginine-dependent pathway catalyzed by NOS-like enzyme could be main source for this MS-induced NO production and Ca2＋/calmodulin was involved in the regulation of the NO production by control of NOS activity.

关 键 词：机械刺激 一氧化氮 一氧化氮合酶 钙 钙调素 烟草细胞 

分 类 号：S572[农业科学—烟草工业]