The role of myosin II in stabilizing actin tethers promoting GLUT4 exocytosis in 3T3-L1 adipocytes

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Jonah B. Nikouyeh (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site:
Yashomati Patel

Abstract: Aberrant insulin signaling results in an impaired ability to clear glucose from the bloodstream, which progresses to type II diabetes mellitus once insulin stimulation no longer results in a significant decrease in blood glucose levels. GLUT4 is the insulin-responsive glucose transporter which, upon insulin stimulation, translocates to the plasma membrane where it is embedded, promoting glucose uptake in muscle and adipose tissue. The potential causes for insufficient glucose uptake are numerous because the insulin signaling pathway has many intermediates and targets, including myosin II. It is known that myosin II is necessary for proper glucose uptake, though the mechanism by which myosin II promotes glucose uptake is unknown. We aim to determine if myosin II is functioning to stabilize the actin tether which is used as a track by secretory GLUT4 vesicles to reach the plasma membrane. GLUT4 vesicle trafficking along the actin tether is accomplished via association of the GLUT4 vesicle with the cargo carrying, actin-based motor proteins, myosin Va and myosin Ic. Here we demonstrate that myosin II is necessary to localize myosin Va and myosin Ic with GLUT4 and F-actin at the plasma membrane. These findings demonstrate that myosin II is necessary to localize these proteins in an insulin-stimulated acto-myosin protein complex which supports GLUT4 translocation to the plasma membrane. These events may be critical regulatory nodes which could yield therapeutic targets helpful in treating those with type II diabetes.

Additional Information

Language: English
Date: 2018
3T3-L1, Diabetes, F-actin, GLUT4, Myosin II
Fat cells

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