摘要
观察了Ca2 + 、Ca2 + 的螯合剂和Ca2 + 通道抑制剂对NO调控的蚕豆气孔运动的影响。结果表明 ,NO的供体 1～ 10 0 μmol/LSNP (sodiumnitroprusside ,硝普纳 )可诱导气孔关闭 ;除去表皮条缓冲液中的Ca2 + 后 ,NO不再影响气孔的运动 ;Ca2 + 的螯合剂EGTA和BAPTA几乎可以完全抑制NO诱导的气孔关闭作用 ;胞内钙通道抑制剂钌红 (rutheniumred)和L型Ca2 + 通道阻断剂硝苯吡啶 (nifedipine)能够减弱SNP诱导气孔运动的关闭趋势 ;加入Ca2 + 通道抑制剂LaCl3 ,则外源NO失去其诱导气孔关闭的作用。说明在NO调控的气孔运动中 ,在NO信号途径的下游可能涉及来自胞内和胞外Ca2 + 的参与 ,并且胞外Ca2 + 更为重要。
The effects of Ca 2+ in the regulation of stomatal movement induced by nitric oxide (NO) were studied. NO from 1-100 μmol/L induced stomatal closuring of Vicia faba L.(Fig.1). The induction of stomatal closure by NO was changed by exogenous Ca 2+ (Fig.2). Chelation of intracellular Ca 2+ with 1,2-bis (O-aminophenoxy)ethane-N,N,N′,N′-tetraacetate (BAPTA) or extracellular Ca 2+ chelation with thylene glycol-bis(β-aminoethy ether) N, N, N, N-tetracetic acid (EGTA) almost completely abolished the stomatal closure induced by NO (Fig.3). Ruthenium red, an inhibitor of internal Ca 2+ (including vacuole) could reduce the stomatal closure induced by NO (Fig.4). When Ca 2+ channels in plasma membrane were blocked by LaCl 3 or nifedipine(NIF), the effect of NO on stomatal closure was suppressed differently (Fig.5). These results suggeste that Ca 2+ play a key role in NO regulation of stomatal movement. Influx of Ca 2+ into cytoplasm passing through Ca 2+ channels is important for NO downstream signaling.
出处
《植物生理与分子生物学学报》
CAS
CSCD
2003年第4期342-346,共5页
Journal Of Plant Physiology and Molecular Biology
基金
国家重点基础研究专项经费 (No .G19990 1170 0 )资助
关键词
CA^2+
一氧化氮
气孔运动
信号转导
蚕豆
Ca 2+
nitric oxide
stomatal movement
signal transduction
Vicia faba L.
