PKC decodes Ca2+

M ovements of a swift kinase keep up with quick calcium bursts, based on fi ndings of Reither et al. (page 521). Cellular Ca 2+ signals come in many fl avors—from long-lasting global increases to waves to brief local plumes. Each fl avor is translated into a specifi c cellular response by Ca 2+ sensors, including calmodulin and conventional PKCs (cPKCs). Upon Ca 2+ binding, PKCα—a common cPKC—translocates to the plasma membrane, the location of most of its targets, including ion channels and transporters. The bulkiness of PKCα might suggest that its diffusion constants should be too low for rapidly following the fast and brief Ca 2+ signals. Many researchers thus suspected that tiny calmodulin must be the main translator of these signals. But the new fi ndings reveal that PKCα is fl eet footed. The authors found that PKCα's membrane translocation mim-ics—in both space and time—the full range of the cellular Ca 2+ signals. Just fractions of a second after a Ca 2+ burst, PKCα was found at the membrane, where it lingered either for mere milliseconds or for longer stretches of several seconds. The short-lived membrane residence solely depended on cytosolic Ca 2+. The more intimate interactions required PKCα's binding to the membrane lipid diacylglycerol (DAG). Since this binding is required for full activation of the kinase, the authors suspect that the shorter interactions might not necessarily lead to downstream signaling events. Copies of PKCα that encounter Ca 2+ in the center of the cell are unlikely ever to make it to the plasma membrane, as the Ca 2+-PKCα complex is short lived. The authors thus suggest that PKCα activation depends solely on sub–plasma membrane Ca 2+ signals. Perinuclear signals probably trigger an entirely different set of downstream events—perhaps via calmodulin, which has many cytoplasmic substrates. Ca 2+ waves are read out as waves of PKCí µí»‚ translocation to the plasma membrane (shown). Abnormal mitosis in cells adhering on an inactive integrin í µí»ƒ results in binucleated cells. Integrins for mitosis I ntegrins are widely known for their adhesive and migratory functions. On page 491, Reverte et al. reveal that integrins are also needed for the microtubule assembly that makes cell division possible. For many cell types, division does not occur unless the cells are stuck to a matrix. The blockade to division was fi rst linked to integrins when it was discovered that cells do not enter …