On the cover
Li et al. reveal that Sentin (green) localizes to the tips of growing microtubules (red) by binding to EB1, thereby promoting plus-end dynamics in Drosophila cells. Image courtesy of Wenjing Li.
See page 973.
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The microtubule plus end regulator EB1 brings Sentin and possibly a microtubule polymerase to microtubule plus ends to promote microtubule dynamics.
Direct regulation of Treslin by cyclin-dependent kinase is essential for the onset of DNA replication
Phosphorylation of human Treslin by Cdk is essential for its association with TopBP1 and for the initiation of DNA replication in S phase.
Direct interaction between the catalytic domain of Epac1 and the nuclear pore component RanBP2 blocks Epac1 catalytic activity and downstream cAMP signaling.
Aurora A is abnormally expressed and activated in cells lining cysts associated with polycystic kidney disease and can phosphorylate and inactivate polycystin 2.
The cortical protein Lte1 promotes mitotic exit by inhibiting the spindle position checkpoint kinase Kin4
Lte1 directly inhibits Kin4 activity and restricts its binding to the mother spindle pole body, which allows proper mitotic exit of cells with a correctly aligned spindle.
Hyperactivated Aurora B kinase is a primary mediator of Bub1 overexpression-induced aneuploidy and tumorigenesis in mice.
Polarized fluorescence microscopy reveals that septins across diverse species assemble into similar higher-order structures consisting of dynamic, paired filaments.
SLAIN2’s interactions with multiple different microtubule plus end–tracking proteins stimulate processive microtubule polymerization and ensure proper microtubule organization.
Cbp3–Cbp6 interacts with the yeast mitochondrial ribosomal tunnel exit and promotes cytochrome b synthesis and assembly
A complex specifically required for the biogenesis of the respiratory chain component cytochrome b binds to the tunnel exit of yeast mitochondrial ribosomes to coordinate protein synthesis and assembly.
Type XII collagen–null mice have fragile bones with disorganized collagen fiber arrangement, decreased bone matrix formation, and delayed osteoblast differentiation.