On the cover
Thomson et al. reveal that cyclin-dependent kinases (Cdks) control the pattern of DNA duplication in S phase by activating clustered sites of DNA replication (red) in mammalian nuclei (blue). Inhibiting (center) or boosting (bottom) Cdk activity alters the number of these sites, known as replication factories.
See page 209.
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In This Issue
People & Ideas
Polo-like kinase 4 kinase activity limits centrosome overduplication by autoregulating its own stability
Plk4 phosphorylates itself in trans to prevent accumulation and self-limit kinase activity, which may be important for regulating centriole duplication.
Wee1B, Myt1, and Cdc25 function in distinct compartments of the mouse oocyte to control meiotic resumption
Keeping Wee1B in the nucleus is important to maintain meiotic arrest, but its timely export is also required for meiosis to resume.
Replication factory activation can be decoupled from the replication timing program by modulating Cdk levels
Cdk activity can differentially regulate the number of active replication factories, replication rates, and the rate of progression through the timing program during S phase.
Soluble ERAD substrates strictly require the Hrd1 E3 ligase for degradation compared with membrane-anchored peptides that may also use other E3 ligases.
Two peripheral GRASP membrane proteins work together to keep the Golgi from falling apart.
FYCO1 is a Rab7 effector that binds to LC3 and PI3P to mediate microtubule plus end–directed vesicle transport
FYCO1 recognition of LC3 on autophagosomes facilitates microtubule-mediated cytosolic transport of this degradative organelle.
RhoA is activated from internalized Nogo-A to promote growth cone collapse and inhibit neurite outgrowth.
Analysis of the relationship between actin network velocity and traction forces at the substrate shows that force transmission mechanisms vary with distinct regions of the cell.