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Actomyosin contractility controls cell surface area of oligodendrocytes

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Abstract Background To form myelin oligodendrocytes expand and wrap their plasma membrane multiple times around an axon. How is this expansion controlled? Results Here we show that cell surface area depends on actomyosin contractility and is regulated by physical properties of the supporting matrix. Moreover, we find that chondroitin sulfate proteoglycans (CSPG), molecules associated with non-permissive growth properties within the central nervous system (CNS), block cell surface spreading. Most importantly, the inhibitory effects of CSPG on plasma membrane extension were completely prevented by treatment with inhibitors of actomyosin contractility and by RNAi mediated knockdown of myosin II. In addition, we found that reductions of plasma membrane area were accompanied by changes in the rate of fluid-phase endocytosis. Conclusion In summary, our results establish a novel connection between endocytosis, cell surface extension and actomyosin contractility. These findings open up new possibilities of how to promote the morphological differentiation of oligodendrocytes in a non-permissive growth environment. See related minireview by Bauer and ffrench-Constant: http://www.jbiol.com/content/8/8/78
Title: Actomyosin contractility controls cell surface area of oligodendrocytes
Description:
Abstract Background To form myelin oligodendrocytes expand and wrap their plasma membrane multiple times around an axon.
How is this expansion controlled? Results Here we show that cell surface area depends on actomyosin contractility and is regulated by physical properties of the supporting matrix.
Moreover, we find that chondroitin sulfate proteoglycans (CSPG), molecules associated with non-permissive growth properties within the central nervous system (CNS), block cell surface spreading.
Most importantly, the inhibitory effects of CSPG on plasma membrane extension were completely prevented by treatment with inhibitors of actomyosin contractility and by RNAi mediated knockdown of myosin II.
In addition, we found that reductions of plasma membrane area were accompanied by changes in the rate of fluid-phase endocytosis.
Conclusion In summary, our results establish a novel connection between endocytosis, cell surface extension and actomyosin contractility.
These findings open up new possibilities of how to promote the morphological differentiation of oligodendrocytes in a non-permissive growth environment.
See related minireview by Bauer and ffrench-Constant: http://www.
jbiol.
com/content/8/8/78.

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