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The insulin- and growth factor-stimulated protein kinases protein kinase B (PKB)/Akt and p70 S6 ribosomal kinase (S6K) are crucial regulators of cell growth. Recent advances, supported by work in this issue of Nature Cell Biology, have indicated that the tumour suppressor tuberous sclerosis complex-2 (TSC2) functions as an antagonist of S6K activation, an inhibition that is relieved by PKB-mediated phosphorylation of TSC2. In contrast to some previous models, these findings indicate that PKB functions upstream of S6K.
Some thirty years ago, a model was proposed to explain patterning of the vertebrate limb along its proximal–distal axis. This model was based on the ability of cells to measure time to assess their position. Two recent publications in Nature present data that may be difficult to reconcile with the early model. One report proposes that the limb is already specified in minute form in the early limb bud, whereas the other focuses on fibroblast growth factor (FGF) signalling from the apical ridge.
Recent studies of border cells in the Drosophila melanogaster ovary have identified a novel mechanism that is involved in cell migration. Binding of the minus-end-directed motor, Myosin VI, to the cell adhesion molecule, DE-Cadherin, stabilizes the cadherin–catenin complex. This interaction might promote the formation of long cellular extensions (LCEs) at the leading edge of migrating border cells.
Using sophisticated fluorescence microscopy, polymerization of single actin filaments can now be observed directly. Recent experiments show that the ends of actin filaments grow and shorten more rapidly than would be predicted from measured rate constants for monomer association and dissociation. This suggests that actin filaments may undergo a type of dynamic instability, similar to microtubules, or even use a previously uncharacterized mechanism to drive filament turnover.