On the cover
Quinones et al. find that competition between pro- and anti-endocytic BAR domain proteins directs cell migration by regulating the trafficking and activity of guidance cue receptors. Border cells (top) don't migrate toward the ovary (bottom) in Drosophila egg chambers lacking the endocytic inhibitor Missing-In-Metastasis. The egg chambers are stained for F-actin (red), phosphotyrosine (green), and DNA (blue).
See page 353.
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PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy
Defective mitochondrial quality control is shown to be a mechanism for neurodegeneration in some forms of Parkinson's disease.
A screen in oligodendrocytes establishes a Rab family member and its GAPs as regulators of exosome secretion by controlling endocytic vesicle docking with the plasma membrane.
A biosensor for cyclin B–Cdk1 activity shows that it uses an unconventional yet simple mechanism for nuclear accumulation.
Hsp90–Sgt1 and Skp1 target human Mis12 complexes to ensure efficient formation of kinetochore–microtubule binding sites
The Hsp90–Sgt1 chaperone and the ubiquitin ligase subunit Skp1 regulate the assembly and turnover of the kinetochore complex Mis12.
A proline-rich region in the Drosophila Pat1 homologue works with the protein's C-terminal domain to recruit decapping and deadenylase complexes to target mRNAs.
The S. cerevisiae Slt2p MAPK cascade picks out peroxisomes for autophagy-mediated degradation (pexophagy) but is not involved in turnover of other cellular components.
In the absence of moesin, RhoA slips out of its normal role as a GTPase to activate the JNK MAPK pathway and spur apoptosis.
The Notch intracellular domain and β-catenin team up with RBP-J to regulate gene transcription and promote the development of arterial endothelial cells.
αE-catenin has cell–cell contact–dependent and –independent functions in regulating actin and membrane dynamics.
The I-BAR domain–containing protein, missing-in-metastasis, directs cell motility by opposing the endocytic activity of the endophilin–CD2AP–cortactin complex.
Loss of β3 integrin enhances turnover of focal adhesions and cell migration speed due to increased β1 integrin–talin interactions.