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J. Biol. Chem., Vol. 278, Issue 18, 16262-16270, May 2, 2003
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From the ¶ Programme in Structural Biology, Research
Institute, Hospital for Sick Children, Toronto, Ontario M5G 2X8, and
Departments of The ClC-2 chloride channel has been
implicated in essential physiological functions. Analyses of ClC-2
knock-out mice suggest that ClC-2 expression in retinal pigment
epithelia and Sertoli cells normally supports the viability of
photoreceptor cells and male germ cells, respectively. Further, other
studies suggest that ClC-2 expression in neurons may modify inhibitory
synaptic transmission via the
Evidence for a Functional Interaction between the ClC-2 Chloride
Channel and the Retrograde Motor Dynein Complex*
§,
,**
Physiology and Pathology,
University of Toronto, Toronto, Ontario M5S 1A8, Canada
-aminobutyric acid, type A
receptor. However, complete understanding of the physiological
functions of ClC-2 requires elucidation of the molecular basis for its
regulation. Using cell imaging and biochemical and electrophysiological
techniques, we show that expression of ClC-2 at the cell surface may be
regulated via an interaction with the dynein motor complex. Mass
spectrometry and Western blot analysis of eluate from a ClC-2 affinity
matrix showed that heavy and intermediate chains of dynein bind ClC-2 in vitro. The dynein intermediate chain
co-immunoprecipitates with ClC-2 from hippocampal membranes suggesting
that they also interact in vivo. Disruption of dynein motor
function perturbs ClC-2 localization and increases the functional
expression of ClC-2 in the plasma membranes of COS7 cells. Thus, cell
surface expression of ClC-2 may be regulated by dynein motor activity. This work is the first to demonstrate an in vivo
interaction between an ion channel and the dynein motor complex.
*
This work was supported in part by a National Institutes of
HealthGrant DK49096 (to C. E. B.) and by the Heart and Stroke Foundation of Canada.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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