Abstract
Aprotein that pushes forward the cell cycle coordinates division with the ensuing growth of the cell surface, according to work from Derek McCusker, Douglas Kellogg (University of California, Santa Cruz, CA), and colleagues. Figure 1 Vesicles delivering new surface materials in the growing bud are missing (right) when Cdk1 activity is blocked. It's well accepted that progress through the cell cycle depends on cell growth. In contrast, says Kellogg, “general thinking held that growth is continuous and independent of the cell cycle.” But McCusker et al. now show that Cdk1, which triggers the G1 to S phase transition in budding yeast, also directly promotes the bud's growth. Bud growth quickly stalled upon blocking Cdk1 activity. The stall stemmed from a loss of polarized secretion. Normal cells placed secretory components such as vesicle tethering proteins and a myosin motor at the growing bud tip, but these proteins were rapidly delocalized when Cdk1 was inhibited. The group then sought targets of Cdk1 that regulated cell surface growth. Several proteins that depended on Cdk1 for phosphorylation during bud growth were found in a complex that included a guanine nucleotide exchange factor and an activating protein for the Cdc42 GTPase, which is required for polarized cell growth. How phosphorylation of proteins in this complex leads to new bud membrane addition is not yet clear. The complex might orient the actin cytoskeleton in the right direction for secretion, although at least one affected secretory protein did not require actin for its polarization. Reference: McCusker, D., et al. 2007. Nat. Cell Biol. doi: 10.1038/ncb1568 [PubMed] [Cross Ref]
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