Mechanical Basis of Cell Morphogenesis and Volume Control

Abstract

Osmotic differences between the cytoplasm and the surrounding fluid belong to the most important factors in shaping an animal tissue cell. This implies an elastic and contractile fibrillar system attached to the cell membrane which counteracts ionic imbalances and determines cell morphology. Therefore cell volume and cell shape are functionally coupled. Many cell types, epithelial cells in particular, are able to control their volume: ie, swelling (or shrinking) induced by varying the osmolarity of the surrounding fluid is compensated and the previous volume is achieved during a time interval of 10-40 min. This compensation reaction includes the opening of ion channels, activation of the Na/K/2C1 co-transport mechanism, and activities of the cytoskeleton. The changes in ion fluxes have been investigated for various cell types. The main question which is still under debate refers to the signal involved in telling a cell to have reached its appropriate volume. One of the most probable factors is the tension in the cell membrane. By action of tension-sensitive ion channels (K+ , Ca++ -channels) ion fluxes could be modified. Mechanical forces acting on the cell membrane always affect the cortical cytoplasm - membrane complex: In many cell types a fibrillar meshwork is closely connected to the membrane, thus determining its mechanical properties. Destruction of this complex by drugs like cytochalasins alters the mechanics of the cortex and destroys the ability of the cells for volume regulation. If mechanical forces in the cortex are involved in volume control, the loss of this ability would be a reasonable consequence of cytochalasin treatment. Measurement of the forces at the surface of cells during swelling and during the compensation phase is a direct approach to the problem of volume regulation. Scanning acoustic microscopy (SAM) is an elegant method to determine elastic properties on a subcellular level. Measuring the reflection of sound at the surface of a cell gives a good indication of local elasticity (and thus “tension at the surface”). Using the cell line HaCat which was derived from human epidermis, elasticity changes have been followed by SAM during hypotonicity-induced swelling and the subsequent compensatory volume decrease. On the basis of the present results the regulatory volume decrease (RVD) may be achieved by an increase of forces in the cortex by actomyosin-based contractions in addition to altered ion fluxes. Volume increase first results in a destruction of the actin fibrillar system which is immediately restored by stimulated actin polymerisation which strengthens the complex of the plasma membran with the cortical fibrillar layer. The results support the view that tension in the cortex may participate in RVD and be a signal for volume regulation.