Schwarz M, Schroeder J I
Department of Biology and Center for Molecular Genetics, University of California, San Diego, La Jolla 92093-0116, USA.
FEBS Lett. 1998 May 29;428(3):177-82. doi: 10.1016/s0014-5793(98)00526-2.
The plant hormone abscisic acid (ABA) regulates important developmental and stress responses. Recent data show that ABA activates phosphorylation events, but whether dephosphorylation events are post-translationally regulated by ABA or whether these are constitutive remains unknown. Slow anion channels in the plasma membrane of guard cells have been proposed to play an important role during ABA-induced stomatal closing. Anion channels are deactivated by removal of cytosolic ATP. However, when guard cells were treated with ABA and depleted of ATP, anion currents remained active. Subsequent removal of extracellular ABA caused deactivation of currents. Deactivation of currents was reversed by reintroduction of cytosolic MgATP. These data show that anion channels are regulated by ABA even in the absence of cytosolic ATP required for kinase-induced phosphorylation events and that anion channel activity is maintained by ABA under conditions that favor dephosphorylation-induced deactivation. Furthermore, channel activation proceeded at high ATP concentrations with nanomolar cytosolic Ca2+ showing a Ca2+-independent final step in anion channel activation.
植物激素脱落酸（ABA）调控重要的发育过程和应激反应。最近的数据表明ABA能激活磷酸化事件，但去磷酸化事件是否受到ABA的翻译后调控，或者这些事件是否是组成型的，仍然未知。保卫细胞质膜上的慢阴离子通道被认为在ABA诱导的气孔关闭过程中起重要作用。阴离子通道通过去除胞质ATP而失活。然而，当保卫细胞用ABA处理并耗尽ATP时，阴离子电流仍保持活跃。随后去除细胞外ABA导致电流失活。通过重新引入胞质MgATP可使电流失活逆转。这些数据表明，即使在激酶诱导的磷酸化事件所需的胞质ATP不存在的情况下，阴离子通道仍受ABA调控，并且在有利于去磷酸化诱导失活的条件下，阴离子通道活性由ABA维持。此外，在高ATP浓度下，通道激活过程中，纳摩尔浓度的胞质Ca2+显示出阴离子通道激活的最后一步不依赖于Ca2+。
