Phosphoinositides and calcium regulate cellular actin assembly and disassembly, coordinating changes in the mechanical properties of the cell cortex during cell locomotion.
Cell locomotion and changes in cell structure initiated by binding of extracellular ligands to transmembrane receptors are generally accompanied by a transient increase in cytoplasmic Ca2+ concentration, Ca2+, and by synthesis and hydrolysis of phosphorylated phosphatidylinositol lipids, or polyphosphoinositides (PPls). These two potential signals to cyto skeleton are not necessarily immediate consequence of receptor stimu lation, but are themselves modulated by upstream signals that include GTPases, protein kinases, ion channels, and probably other agents (reviewed in 118). Cell motility and changes in morphology also require spatially and temporally coordinated changes in mechanical properties of cell cortex, and these changes are brought about by transitions between gel (solid) and sol (liquid) states of cytoskeleton (32, 119, 120). A link between Ca2+ and phospholipids, on one hand, and changes in cell rigidity, on other, was apparent enough to suggest nearly 40 years ago (52) that the rigidity of cortex depends on fact that it contains
Paul A. Janmey (Sat,) reported a review. Phosphoinositides and calcium regulate cellular actin assembly and disassembly, coordinating changes in the mechanical properties of the cell cortex during cell locomotion.