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J. Biol. Chem., Vol. 277, Issue 1, 509-515, January 4, 2002
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From the Recruitment of intracellular glucose transporter
4 (GLUT4) to the plasma membrane of fat and muscle cells in response to
insulin requires phosphatidylinositol (PI) 3-kinase as well as a
proposed PI 3-kinase-independent pathway leading to activation of the
small GTPase TC10. Here we show that in cultured adipocytes insulin causes acute cortical localization of the actin-regulatory neural Wiskott-Aldrich syndrome protein (N-WASP) and actin-related
protein-3 (Arp3) as well as cortical F-actin polymerization by a
mechanism that is insensitive to the PI 3-kinase inhibitor wortmannin.
Expression of the dominant inhibitory N-WASP-
A Phosphatidylinositol 3-Kinase-independent Insulin
Signaling Pathway to N-WASP/Arp2/3/F-actin Required for GLUT4
Glucose Transporter Recycling*
,,,¶
Program in Molecular Medicine, University of
Massachusetts Medical School, Worcester, Massachusetts 01605 and the
§ European Molecular Biology Laboratory, Meyerhofstrasse
1, 69117 Heidelberg, Germany
WA protein lacking the
Arp and actin binding regions attenuates the cortical F-actin
rearrangements by insulin in these cells. Remarkably, the N-WASP-WA
protein also inhibits insulin action on GLUT4 translocation, indicating dependence of GLUT4 recycling on N-WASP-directed cortical F-actin assembly. TC10 exhibits sequence similarity to Cdc42 and has
been reported to bind N-WASP. We show the inhibitory TC10 (T31N)
mutant, which abrogates insulin-stimulated GLUT4 translocation and
glucose transport, also inhibits both cortical localization of N-WASP and F-actin formation in response to insulin. These findings reveal that N-WASP likely functions downstream of TC10 in a PI
3-kinase-independent insulin signaling pathway to mobilize cortical
F-actin, which in turn promotes GLUT4 responsiveness to insulin.
*
This work was supported by National Institutes of Health
Grant DK30898 (to M. P. C.).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.
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