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A more recent version of this article appeared on July 1, 2003
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Submitted on November 12, 2002
Revised on February 19, 2003
Accepted on March 10, 2003
1 The Henry Wellcome Laboratory of Cell Biology, Division of Biochemistry and Molecular Biology, Davidson Building, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, Scotland
2 School of Biochemistry and Genetics, The Medical School, University of Newcastle, Newcastle-upon-Tyne, NE2 4HH. United Kingdom
3 Institute of Molecular and Cell Biology, 30 Medical Drive,
Singapore 117609, Republic of Singapore
* Corresponding author. E-mail address: G.Gould{at}bio.gla.ac.uk.
Insulin stimulates the movement of glucose transporter-4 (Glut4)-containing vesicles to the plasma membrane of adipose cells. We investigated the role of post-Golgi t-SNAREs in the trafficking of Glut4 in 3T3-L1 adipocytes. Greater than 85% of syntaxin 6 was found in Glut4-containing vesicles, and this tSNARE exhibited insulin-stimulated movement to the plasma membrane. By contrast, the co-localisation of Glut4 with syntaxin's 7, 8 or 12/13 was limited and these molecules did not translocate to the plasma membrane. We used adenovirus to over-express the cytosolic domain of these syntaxin's and studied their effects on Glut4 traffic. Over-expression of the cytosolic domain of syntaxin 6 did not affect insulin-stimulated glucose transport, but increased basal deGlc transport and cell surface Glut4 levels. Moreover, the syntaxin 6 cytosolic domain significantly reduced the rate of Glut4 re-internalisation after insulin withdrawal and perturbed sub-endosomal Glut4 sorting; the corresponding domains of syntaxin's 8 and 12 were without effect. Our data suggest that syntaxin 6 is involved in a membrane trafficking step which sequesters Glut4 away from traffic destined for the plasma membrane. We speculate that this is at the level of traffic of Glut4 into its unique storage compartment, and that syntaxin 16 may be involved.
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