In This Issue
People & Ideas
Recruitment of nuclear pore complex (NPC) components during interphase occurs in a different order and with slower kinetics than during postmitotic NPC assembly, suggesting the two processes are regulated by distinct mechanisms.
Palmitoylated Ras proteins traffic through recycling endosomes to the plasma membrane during exocytosis
Palmitoylation directs Ras proteins to the correct intracellular organelles for trafficking and activity.
p400 unwinds chromatin from nucleosomes flanking double-strand breaks to facilitate recruitment of the DNA repair components brca1 and 53BP1.
The polycomb repressor complex ubiquitylates γ-H2AX and other components of the DNA damage response pathway to facilitate genomic repair.
Sds22 defines protein phosphatase 1 location and function at kinetochores and subsequent activity of aurora B in mitosis.
GFP-tagged snRNP components reveal the dynamics and rate for spliceosome assembly in vivo.
Sam68 regulates EMT through alternative splicing–activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene
Expression levels of SF2/ASF are controlled by Sam68 mediated activation of splicing-induced mRNA decay.
Decreasing JunB expression causes muscle atrophy, whereas overexpression induces hypertrophy and blocks atrophy via myostatin inhibition and regulation of atrogin-1 and MuRF expression via FoxO3.
The molecular motors kinesin-1 dynein navigate migrating nuclei around cytoplasmic roadblocks.
The CLIP biosensor reveals the spatiotemporal activity of the Nodal proprotein convertases Furin and Pace4 during embryonic development.
Coa3 and Cox14 form assembly intermediates with newly synthesized Cox1 and are required for association of the Mss51 translational activator with these complexes.
When autophagy is induced, ULK1 phosphorylates AMBRA1, releasing the autophagy core complex from the cytoskeleton and allowing its relocalization to the ER membrane to nucleate autophagosome formation.
Leading cells require LIMK for matrix degradation and invadopodia formation during collective cell migration.
Mutations in otoferlin are linked to human hearing loss. New research defines a function for this C2 domain–containing protein in synaptic vesicle exocytosis in cochlear hair cells.
Electron microscopy reveals that the flat base of the vesicular stomatitis virus is a privileged site for membrane fusion and that the glycoproteins located outside form regular arrays required at late stages of the fusion process.