Actomyosin contractility controls cell surface area of oligodendrocytes
1 Max-Planck-Institute for Experimental Medicine, Hermann-Rein-Str. 3, Göttingen, Germany
2 Department of Neurology, Robert-Koch-Str. 40, University of Göttingen, Göttingen, Germany
3 Deptartment of Cellular Machines, Biotechnology Center, University of Technology, Tatzberg 47-51, Dresden, Germany
BMC Cell Biology 2009, 10:71 doi:10.1186/1471-2121-10-71Published: 25 September 2009
To form myelin oligodendrocytes expand and wrap their plasma membrane multiple times around an axon. How is this expansion controlled?
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.
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.