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作 者:XUE ShaoWu YANG Pin HE YiKun
机构地区:[1]College of Life Science, Capital Normal University, Beijing 100037, China [2]Institute of Molecular Science, Chemical Biology and Molecular Engineering Laboratory of Ministry of Education, Shanxi University, Taiyuan, 030006 China
出 处:《Chinese Science Bulletin》2008年第14期2156-2159,共4页
基 金:Supported by the National Natural Science Foundation of China (Grant No. 20701028)
摘 要:We explore nitric oxide (NO) effect on K+in channels in Arabidopsis guard cells. We observed NO inhib- ited K+in currents when Ca2+ chelator EGTA (Ethylene glycol-bis(2-aminoethylether)-N,N,N′,N′-tetraacetic acid) was not added in the pipette solution; K+in currents were not sensitive to NO when cytosolic Ca2+ was chelated by EGTA. NO inhibited the Arabidopsis stomatal opening, but when EGTA was added in the bath solution, inhibition effect of NO on stomatal opening vanished. Thus, it implies that NO ele- vates cytosolic Ca2+ by activating plasma membrane Ca2+ channels firstly, then inactivates K+in chan- nels, resulting in stomatal opening suppressed subsequently.We explore nitric oxide (NO) effect on K^+in, channels in Arabidopsis guard cells. We observed NO inhibited K^+in, currents when Ca^2+ chelator EGTA (Ethylene glycol-bis(2-aminoethylether)-N,N,N′,N;tetraacetic acid) was not added in the pipette solution; K^+in currents were not sensitive to NO when cytosolic Ca^2+ was chelated by EGTA. NO inhibited the Arabidopsis stomatal opening, but when EGTA was added in the bath solution, inhibition effect of NO on stomatal opening vanished. Thus, it implies that NO elevates cytosolic Ca^2+ by activating plasma membrane Ca^2+ channels firstly, then inactivates K^+in, chartnels, resulting in stomatal opening suppressed subsequently.
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