On the cover
Super-resolution structured illumination microscopy of a spermatocyte chromosome spread reveals rings of KASH5 (green) at the tips of homologous chromosome pairs stained for the axial element protein SCP3 (red). Horn et al. demonstrate that KASH5 is part of a mammalian LINC complex that spans the nuclear envelope to connect meiotic chromosomes with cytoplasmic dynein, allowing the chromosomes to cluster together and form homologous pairs.
Image © 2013 Horn et al.
See page 1023.
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Cell biology in neuroscience
Single-cell analyses in budding yeast reveal that neighboring replicons are assembled stochastically and stay associated to maintain stable replication factories.
PLP inhibits the activity of interphase centrosomes to ensure their proper segregation in stem cells
PLP levels are regulated by Centrobin and act to suppress mother centrosome maturation by blocking the localization of Polo kinase.
A complex of KASH5 and Sun1 is required for meiotic homologous chromosome pairing through the coupling of telomere attachment sites to cytoplasmic dynein and microtubules.
Cyclin B1 mRNA translation is temporally controlled through formation and disassembly of RNA granules
Temporally regulated formation of RNA granules containing cyclin B1 transcript is critical for the precise timing of translational activation.
Live cell imaging, high-resolution microscopy, and computational modeling show that dynamic formin-filamin-actin asters self-organize into an actomyosin contractile network that may maintain mechanical coherence of cytoplasm.
Vaccinia virus actin–based motility relies on integration of the N-WASP–ARP2/3 and Rac1–FHOD1 pathways.
Rather than acting directly on Cdc42, Bem1 works in concert with the Cdc42 binding partner Rdi1 to relocalize Cdc42 to the cytosol during symmetry breaking in the absence of an intact actin cytoskeleton.
Folliculin localizes to lysosomes and directly interacts with Rag GTPases, promoting mTORC1 activation, when amino acids are abundant.
Polyglutamine-expanded huntingtin specifically targeted to synapses binds to synapsin-1, inhibits its phosphorylation, and causes defects in neurotransmitter release and age-dependent defects in neurological function.