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作 者:Katrin Held Franqois Pascaud Christian Eckert Pawel Gajdanowicz Kenji Hashimoto Claire Corratge-Faillie Jan Niklas Offenborn Benoit Lacombe Ingo Dreyer Jean-Baptiste Thibaud Jorg Kudla
机构地区:[1]Institut fur Biologie und Biotechnologie der Pflanzen, Universitgit Miinster, 48149 Minster, Germany [2]Biochimie et Physiologie Moleculaire des Plantes (UMR 5004 CNRS-INRA-SupAgro-UM2), Campus INRA-SupAgro, Place Viala, F34060 Montpellier Cedex 1, France [3]InstitutJ~r Biochemie und Biologie, Universitgit Potsdam, Karl-Liebkeneht-Str. 24/25, 14476 Potsdam-Golm, Germany
出 处:《Cell Research》2011年第7期1116-1130,共15页细胞研究(英文版)
摘 要:Potassium (K^+) channel function is fundamental to many physiological processes. However, components and mech- anisms regulating the activity of plant K^+channels remain poorly understood. Here, we show that the calcium (Ca^2+) sensor CBL4 together with the interacting protein kinase CIPK6 modulates the activity and plasma membrane (PM) targeting of the K^+channel AKT2 from Arabidopsis thaliana by mediating translocation of AKT2 to the PM in plant cells and enhancing AKT2 activity in oocytes. Accordingly, akt2, cbl4 and cipk6 mutants share similar developmental and delayed flowering phenotypes. Moreover, the isolated regulatory C-terminal domain of CIPK6 is sufficient for mediating CBL4- and Ca^2+-dependent channel translocation from the endoplasmic reticulum membrane to the PM by a novel targeting pathway that is dependent on dual lipid modifications of CBL4 by myristoylation and palmitoylation. Thus, we describe a critical mechanism of ion-channel regulation where a Ca^2+ sensor modulates K^+ channel activity by promoting a kinase interaction-dependent but phosphorylation-independent translocation of the channel to the PM.
关 键 词:calcium sensor protein kinase potassium channel signal transduction
分 类 号:Q73[生物学—分子生物学] Q949.326.1
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