On the cover
Cells lacking the protein phosphatase PP6 have misshapen nuclei (blue) due to chromosome segregation errors arising from unchecked Aurora A kinase activity during spindle assembly. Image © 2010 Kang Zeng.
See page 1315.
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Spatially dispersed nucleation and minus end–directed transport of microtubule end disassembly activity can lead to bipolar spindle assembly.
HURP permits MTOC sorting for robust meiotic spindle bipolarity, similar to extra centrosome clustering in cancer cells
Similar to clustering of extra centrosomes in cancer cells, HURP promotes microtubule stability and sorts MTOCs into distinct poles during meiosis.
Arf6-dependent membrane dynamics concentrates active Cdc42 at the leading edge of migrating cells.
Zfp521 regulates osteoblast development during lineage commitment and osteoblast maturation by suppressing Runx2 transcriptional activity.
At low levels of replication stress, Chk1 favors resolving problems at stalled replication forks over initiating origin firing in unreplicated areas of the genome.
Protein phosphatase 6 regulates mitotic spindle formation by controlling the T-loop phosphorylation state of Aurora A bound to its activator TPX2
Loss of PP6 function interferes with spindle formation and chromosome alignment because of amplified Aurora A activity.
The tail of yeast myosin II is localized to the division site by two distinct molecular pathways and sufficient for promoting actomyosin ring assembly, furrow ingression, and guidance in ECM remodeling.
Nessun Dorma, a novel centralspindlin partner, is required for cytokinesis in Drosophila spermatocytes
Nessun Dorma is a component of the ring canal with a polysaccharide-binding domain, which is important for cytokinesis during male meiosis.
The Parkin ubiquitin ligase marks the mitofusins Mfn1 and Mfn2 for proteasome-dependent degradation, promoting disposal of damaged mitochondria by preventing their fusion with healthy organelles.
The relationship between cargo accumulation and clathrin-coated pit initiation and maturation is examined by direct visualization of receptor-engaged clathrin-coated pits.
TRAF6 expression is enhanced during muscle atrophy and induces activation of signal transduction cascades that promote muscle wasting.