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Epigenetic centromere specification directs aurora B accumulation but is insufficient to efficiently correct mitotic errors
Aurora B activity is inhibited when centromeric repeat sequences are absent, although kinetochores can still assemble.
This virus takes a less-travelled cytoskeletal road both to reach its replication site in the nucleus and to get back to the plasma membrane to escape the host cell.
Dividing cells can sense DNA damage and initiate a primary response, but repair isn’t completed until the cells enter G1.
The phosphatase Cdc14 exerts negative feedback on its upstream regulators to limit its release from the nucleolus to once per cell cycle.
Correlative light and electron microscopy provides support for the linear amalgamation of yeast prion proteins.
Type I PIPK-α regulates directed cell migration by modulating Rac1 plasma membrane targeting and activation
PIPKI-α does a job other PIPKI isoforms cannot; it recruits Rac1 to the plasma membrane upon integrin activation, spatially regulating the actin-organizing GTPase during migration.
The soluble ligand Wnt5b repels cells expressing the Ryk (related to tyrosine kinase) receptor, establishing directional motility during gastrulation.