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J. Biol. Chem., Vol. 280, Issue 13, 12181-12189, April 1, 2005

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Chloride Conductance Is Required for the Protein Kinase A and Rac1-dependent Phosphorylation of Moesin at Thr-558 by KCl in PC12 Cells^*

Songhee Jeon, Sohee Kim, Eunhee Kim, Ji Eun Lee, Sung Joon Kim¶, Yong-Sung Juhnn||, Yong Sik Kim**, Chang-Dae Bae, and Joobae Park

From the Departments of Molecular Cell Biology and Physiology, Samsung Biomedical Research Institute, and Center for Neuronal Cell Excitability Research, Sungkyunkwan University School of Medicine, Suwon 440-746 and the ^||Department of Biochemistry and Molecular Biology and ^**Department of Psychiatry and Institute for Human Behavioral Medicine, Seoul National University College of Medicine, Seoul 110-744, Korea

Moesin is a member of the ERM family, a family of cross-linkers between the plasma membrane and the actin cytoskeleton, which are known to be activated by phosphorylation. Previously, we reported the RhoA and Rho kinase-dependent phosphorylation of moesin at Thr-558 in hippocampal neuronal cells by glutamate. Here we studied the induction of moesin phosphorylation by KCl (60 mM) in PC12 cells. Moesin phosphorylation at Thr-558 was increased after 2 min of KCl treatment, peaked at 5 min, and returned to the basal level by 60 min. KCl also activated Rac1, but not RhoA, in PC12 cells, and KCl-induced moesin phosphorylation was suppressed in dominant negative Rac1 (N17 Rac1)-expressed cells. The inhibition of protein kinase A (PKA), known as an upstream kinase of Rac1, abolished Rac1 activation and moesin phosphorylation by KCl. Interestingly, the phosphorylation of moesin by KCl was independent of KCl-induced membrane depolarization and calcium influx but was dependent on KCl-induced chloride conductance. 60 mM KCl induced chloride conductance in PC12 cells, and pretreatment with Cl^– channel blocker abolished Rac1 activation and moesin phosphorylation by KCl. These results suggest that the phosphorylation of moesin at Thr-558 in PC12 cells by KCl treatment is PKA- and Rac1-dependent and that KCl-induced chloride conductance is involved in the activation of this signaling system.

Received for publication, July 21, 2004 , and in revised form, January 3, 2005.

^* This work was supported by the Grants from KOSEF (R13-2002-012-00000-0) and Samsung Biomedical Research Institute. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains Supplemental Fig. S1.

^¶ Present address: Dept. of Physiology, Seoul National University College of Medicine, Seoul 110-744, Korea.

To whom correspondence should be addressed. Tel.: 82-31-299-6130; Fax: 82-31-299-6149; E-mail: jbpark{at}med.skku.ac.kr.

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