On the cover
Yan et al. reveal that the deubiquitinating enzyme complex BRISC regulates the localization and function of the spindle assembly factor NuMA. NuMA (green) forms a ring-like structure at the single spindle pole of a control cell treated with the Eg5 inhibitor STLC (bottom left), but is disorganized in cells lacking the BRISC subunits BRCC36 (top left) or ABRO1 (top right). Cells are also labeled for microtubules (red) and DNA (blue).
Image © 2015 Yan et al.
See page 209.
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An analysis of individual secretory vesicles during yeast exocytosis explores how Sec4-GTP hydrolysis, Myo2p motors, an SM protein, and exocyst components contribute to the timing of vesicle tethering and fusion.
BLM helicase facilitates telomere replication by resolving G-quadruplex structures that can form in the G-rich repeats during leading strand synthesis.
The deubiquitinating enzyme complex BRISC is required for proper mitotic spindle assembly in mammalian cells
The microtubule-associated protein BRISC regulates the interaction of NuMA with dynein and importin-β by removing K63-linked polyubiquitin chains from NuMA, thereby promoting proper bipolar spindle assembly.
ROCK1 forms the stable actomyosin filament bundles that initiate front–back and dendritic spine polarity, while ROCK2 regulates contractile force, Rac1 activity, and cofilin-mediated actin remodeling at the leading edge of migratory cells and the spine head of neurons.
The Ras-like small G-protein MglA is an integral part of the gliding motility complex at bacterial focal adhesions and stimulates the assembly of the motility complex by directly connecting it to the MreB actin cytoskeleton.
IQGAP1 mediates CXCR4 cell surface expression and signaling by regulating EEA-1+ endosome interactions with microtubules during CXCR4 trafficking and recycling.
Ypt1 directly recruits the kinase Hrr25 to COPII vesicles to activate it in two different pathways: ER to Golgi and the catabolic macroautophagy pathway induced in response to cell stress.
Analysis of the interplay of protein biogenesis factors at the ribosome exit site reveals new role for NAC
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Myosin 1b functions as an effector of EphB2/ephrinB signaling and controls cell morphology and cell repulsion.