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Hong et al. reveal that the phospholipid PI(3,5)P2 promotes actin turnover on late endosomes by binding to the branched actin regulator cortactin. Inhibiting PI(3,5)P2 synthesis leads to the accumulation of actin (red) and cortactin (green) on late endosomes (marked by Rab7, blue).
Image © 2015 Hong et al.
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In This Issue
In Focus
Mast cells get all touchy-feely
“Allergy” cells embrace dendritic cells to transfer antigens.
People & Ideas
Nick Lane: Unearthing the first cellular innovations
Lane’s unorthodox career stalks the origins of complex eukaryotic life.
Feature
Review
Report
An organelle-exclusion envelope assists mitosis and underlies distinct molecular crowding in the spindle region
A microtubule-independent membranous “spindle envelope” confines spindle assembly and accounts for faithful chromosome segregation.
Degradation of HK2 by chaperone-mediated autophagy promotes metabolic catastrophe and cell death
Metabolic stress caused by perturbation of receptor tyrosine kinase FLT3 sensitizes cancer cells to autophagy inhibition and leads to excessive activation of chaperone-mediated autophagy, which triggers metabolic catastrophe in cancer cells through the degradation of HK2.
APC is required for muscle stem cell proliferation and skeletal muscle tissue repair
In muscle stem cells, APC dampens canonical Wnt signaling to allow cell cycle progression.
Usp16 regulates kinetochore localization of Plk1 to promote proper chromosome alignment in mitosis
CDK1 and Plk1 sequentially phosphorylate and activate Usp16, which in turn deubiquitinates Plk1 to maintain the kinase’s kinetochore localization and promote proper chromosome alignment in mitosis.
Article
TTBK2 with EB1/3 regulates microtubule dynamics in migrating cells through KIF2A phosphorylation
The microtubule (MT) plus end–tracking protein TTBK2 phosphorylates kinesin-13 family MT depolymerase KIF2A and removes it from MTs, thereby antagonizing KIF2A-induced depolymerization at MT plus ends during cell migration.
PI(3,5)P2 controls endosomal branched actin dynamics by regulating cortactin–actin interactions
The late endosomal lipid PI(3,5)P2 binds to cortactin through the filamentous actin (F-actin) binding domain of cortactin, leading to removal of cortactin from endosomal actin networks and inhibition of cortactin-mediated branched actin nucleation and stabilization.
Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation
PKD regulates the stabilization of the F-actin network within dendritic spines upon chemically induced plasticity changes and is needed for proper hippocampal LTP and spatial memory formation.
Annexin A2–dependent actin bundling promotes secretory granule docking to the plasma membrane and exocytosis
Annexin A2 and the actin cytoskeleton are essential partners in providing lipid platforms for granule recruitment and fusion during exocytosis.
Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair
Clathrin, dynamin, and ARF6 accumulate around wounds in Drosophila embryos in a calcium- and actomyosin-dependent manner and drive polarized E-cadherin endocytosis, which is necessary for actomyosin remodeling during wound repair.
Hsc70 chaperone activity underlies Trio GEF function in axon growth and guidance induced by netrin-1
Hsc70 chaperone activity is required for Rac1 activation by Trio and this function underlies netrin-1/DCC-dependent axon outgrowth and guidance.
The caveolin–cavin system plays a conserved and critical role in mechanoprotection of skeletal muscle
The caveolar membrane microdomain plays an integral role in stabilizing the muscle fiber surface in mice and zebrafish.
Mast cells and dendritic cells form synapses that facilitate antigen transfer for T cell activation
Mast cells (MCs) and dendritic cells (DCs) form synapses that are dependent on MC activation and integrin engagement, and these direct interactions stimulate changes in the secretion profile of select cytokines and facilitate transfer of endosomal contents from activated MCs to DCs.
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