Glucose transporter recycling in response to insulin is facilitated by myosin Myo1c

Avirup Bose, Adilson Guilherme, Stacey I. Robida, Sarah M. C. Nicoloro, Qiong L. Zhou, Zhen Y. Jiang, Darcy P. Pomerleau and Michael P. Czech ()
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Avirup Bose: University of Massachusetts Medical School
Adilson Guilherme: University of Massachusetts Medical School
Stacey I. Robida: University of Massachusetts Medical School
Sarah M. C. Nicoloro: University of Massachusetts Medical School
Qiong L. Zhou: University of Massachusetts Medical School
Zhen Y. Jiang: University of Massachusetts Medical School
Darcy P. Pomerleau: University of Massachusetts Medical School
Michael P. Czech: University of Massachusetts Medical School

Nature, 2002, vol. 420, issue 6917, 821-824

Abstract: Abstract Insulin stimulates glucose uptake in muscle and adipocytes by signalling the translocation of GLUT4 glucose transporters from intracellular membranes to the cell surface1,2. The translocation of GLUT4 may involve signalling pathways that are both independent of and dependent on phosphatidylinositol-3-OH kinase (PI(3)K)3,4,5. This translocation also requires the actin cytoskeleton6,7,8, and the rapid movement of GLUT4 along linear tracks may be mediated by molecular motors9. Here we report that the unconventional myosin Myo1c is present in GLUT4-containing vesicles purified from 3T3-L1 adipocytes. Myo1c, which contains a motor domain, three IQ motifs and a carboxy-terminal cargo domain, is highly expressed in primary and cultured adipocytes. Insulin enhances the localization of Myo1c with GLUT4 in cortical tubulovesicular structures associated with actin filaments, and this colocalization is insensitive to wortmannin. Insulin-stimulated translocation of GLUT4 to the adipocyte plasma membrane is augmented by the expression of wild-type Myo1c and inhibited by a dominant-negative cargo domain of Myo1c. A decrease in the expression of endogenous Myo1c mediated by small interfering RNAs inhibits insulin-stimulated uptake of 2-deoxyglucose. Thus, myosin Myo1c functions in a PI(3)K-independent insulin signalling pathway that controls the movement of intracellular GLUT4-containing vesicles to the plasma membrane.

Date: 2002
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DOI: 10.1038/nature01246

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