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拟南芥保卫细胞微管骨架的重排参与NO诱导的气孔关闭 被引量:6

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摘要 以GFP:α-tubulin-6转基因拟南芥为材料,利用药理学实验及激光扫描共聚焦显微技术研究了微管骨架在NO诱导气孔关闭过程中的动态变化及其可能的调控机制.结果表明:(ⅰ)微管特异性抑制剂长春花碱和NO供体SNP均能诱导气孔关闭,并且长春花碱能加强SNP对气孔开度的抑制作用,而微管稳定剂紫杉醇则部分抑制了NO对气孔关闭的诱导作用;(ⅱ)开放气孔保卫细胞中,大量周质微管从保卫细胞的背壁向腹壁呈辐射状整齐规则地排布,并且几乎所有微管纤维都与保卫细胞腹壁成90°垂直;(ⅲ)同一条件下保卫细胞经外源NO供体SNP光下处理30min,保卫细胞内整齐的辐射状微管逐步散乱,微管部分解聚,纤维数量减少,部分交错扭曲,排布方式也由与腹壁垂直转变为倾斜,说明微管骨架可能参与了NO诱导的气孔关闭;(ⅳ)进一步研究发现,胞内Ca2+螯合剂BAPTA-AM可以大幅度削弱由NO诱导的气孔关闭作用,而对长春花碱诱导的气孔关闭无明显影响;开放气孔的保卫细胞经SNP处理后,再施加BAPTA-AM,散乱的微管骨架排布随处理时间延长逐步趋于正常,到30min时基本恢复成辐射状,与对照相比无明显区别,表明在NO对微管排布的调节机制中有Ca2+参与.综合以上结果推测,在NO调控的气孔运动中,NO可能是通过调节胞内Ca2+来促进微管骨架系统的重排,进而影响气孔的开关运动.
出处 《科学通报》 EI CAS CSCD 北大核心 2008年第3期293-298,共6页 Chinese Science Bulletin
基金 北京市科技新星计划(批准号:2003B34) 国家自然科学基金(批准号:30600318,30400228)资助项目
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参考文献23

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