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.
Effects of La3+ and Eu3+ on outward potassium channels(K+out) in Vicia guard cells have been studied by patch clamping technique.Extracellular La3+ inhibited K+out currents with a half-inhibition concentration(IC50) of 81 μmol·L-1.Interestingly,intracellular La3+ activated K+out currents at a free concentration of 1.13 × 10-14 mol·L-1,and inhibited K+out currents at a free concentration of 5.86 × 10-14 mol·L-1.Extracellular Eu3+ also activated K+out currents at concentrations of 10 μmol·L-1 and 50 μmol·L-1,and inhibited K+out currents at concentrations of more than 1 mmol·L-1.The effects of La3+ and Eu3+ on K+out currents may contribute to regulation of the plant water status,which may be one of the mechanisms of the biological effect of rare earth elements.
XUE ShaoWu & YANG Pin Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education,Institute of Molecular Science,Shanxi University,Taiyuan 030006,China
