Cross-talk between the mechano-gated K2P channel TREK-1 and the actin cytoskeleton

被引：108

作者：

Lauritzen, I ^{[1
]}

Chemin, J ^{[1
]}

Honoré, E ^{[1
]}

Jodar, M ^{[1
]}

Guy, N ^{[1
]}

Lazdunski, M ^{[1
]}

Patel, AJ ^{[1
]}

机构：

[1] Univ Nice, Inst Paul Hamel, Inst Pharmacol Mol & Cellulaire, CNRS,UMR 6097, F-06560 Valbonne, France

来源：

EMBO REPORTS | 2005年 / 6卷 / 07期

关键词：

actin cytoskeleton; K-2P channels; mechano-gating; PKA phosphorylation; KCNK;

D O I：

10.1038/sj.embor.7400449

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

TREK-1 (KCNK2) is a K2P channel that is highly expressed in fetal neurons. This K+ channel is opened by a variety of stimuli, including membrane stretch and cellular lipids. Here, we show that the expression of TREK-1 markedly alters the cytoskeletal network and induces the formation of actin- and ezrin-rich membrane protrusions. The genetic inactivation of TREK-1 significantly alters the growth cone morphology of cultured embryonic striatal neurons. Cytoskeleton remodelling is crucially dependent on the protein kinase A phosphorylation site S333 and the interactive proton sensor E306, but is independent of channel permeation. Conversely, the actin cytoskeleton tonically represses TREK-1 mechano-sensitivity. Thus, the dialogue between TREK-1 and the actin cytoskeleton might influence both synaptogenesis and neuronal electrogenesis.

引用

页码：642 / 648

页数：7

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