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Astral microtubules emanating from the spindle poles engage force-generating proteins such as dynein at the cell cortex to regulate spindle positioning. McAinsh and colleagues show that the microtubule-associated proteins MAP4 and CLASP1 control the interactions of astral microtubules at the cell cortex to ensure correct spindle positioning.
The STAT3 transcription factor maintains pluripotency by preventing differentiation. A Brg1-containing chromatin-remodelling complex, esBAF, is shown to direct STAT3 to its targets across the pluripotent genome. Deletion of Brg1 leads to binding of the polycomb complex and subsequent silencing of LIF/STAT targets. Unexpectedly, Brg1 also helps the polycomb complex silence Hox genes thereby further contributing to pluripotency.
N-WASP activates Arp2/3-mediated actin nucleation. N-WASP is now shown to stabilize and organize the actin cytoskeleton at cell–cell junctions through its interaction with the actin-binding protein WIRE.
The ubiquitin ligase APC/C is required for the metaphase-to-anaphase transition in mitosis. Downstream of Cdk1, CUEDC2 is shown to activate the APC/C by mediating the release of the checkpoint protein Mad2 from APC/C.
Planar cell polarity (PCP) directs the orientation of mammalian epithelial cells in the skin but it is unclear how polarity is preserved during division. A dileucine motif in the atypical cadherin Celsr1 is shown to trigger the endocytosis of PCP components in mitosis to ensure that they are distributed equally to daughter cells and recycled back to the plasma membrane after division.
Wnt secretion is facilitated by retrograde trafficking of the Wnt receptor Wntless. Korswagen and colleagues now show that endosome-to-Golgi trafficking of Wntless depends on an alternative retromer pathway that contains SNX3 in place of the canonical retromer sorting nexins.
How regulatory elements spatially interact with their target DNA sequences is unclear. The β-globin locus control region (LCR) is found to take part in interchromosomal interactions with a few genes controlled by shared transcription factors, and to transcriptionally upregulate β-globin mRNA in a subset of cells.
The Ras GEF Ras-GRF2 is found to inhibit the activity of the Cdc42 Rho GTPase independently of its Ras-activating function. Binding of Ras-GRF2 to Cdc42 prevents its activation by Cdc42 GEFs suppressing Cdc42-mediated cell migration, invasion and transformation.
Inhibition of the repressor function of the Wnt3a effector β-catenin–TCF3 is shown to be required to maintain pluripotency in cooperation with the activating role of the second Wnt effector β-catenin–TCF1. Both Tcf3 and Tcf1 are involved in the recruitment of β-catenin to Oct4 binding sites in embryonic stem cell chromatin.
Canonical Wnt signalling and its transcriptional effector β-catenin have been implicated in embryonic stem cell (ESC) function. Self-renewal is now shown to be maintained in β-catenin-deficient mouse ESCs, whereas mesendodermal and neuronal differentiation are impaired. A β-catenin variant that cannot function in transcription but re-establishes cadherin-mediated cell-adhesion rescues these differentiation defects.
In most eukaryotes, the centromere is defined by epigenetic marks such as the histone H3 variant CENH3/CENP-A/CID. Ectopic induction of kinetochores in Drosophila S2 cells by CID overexpression leads to kinetochore assembly specifically in silent intergenic regions bordering heterochomratin, demonstrating a role for these domains in centromere identity.
The cell division axis is determined by the position of the mitotic spindle. How geometrical cues influence spindle orientation is analysed in cells cultured on micropatterns. These experiments show that the mitotic spindle rotates to align with the forces produced by retraction fibres and suggest that forces may be transmitted through a sub-cortical actin structure.
Myosin and actin are known to reshape the plasma membrane during endocytosis. Myosin 1b regulates the actin-dependent formation of tubules at the trans-Golgi network. As such, it has a critical role in initiating post-Golgi carrier formation.
A genome-wide RNAi synthetic lethal screen unravels the role of p53 in small nucleolar RNPs (snoRNPs) through a genetic interaction with UNRIP, which has been previously shown to interact with the snoRNP chaperone SMN. p53 regulates the levels of Nolc1, which affects snoRNP stability, whereas UNRIP contributes to nuclear SMN import, revealing a synergistic requirement for both in snoRNP assembly.
Sensory cilia assembly has been proposed to occur through the kinesin-2-driven delivery of precursors to the axoneme tip by intraflagellar transport (IFT). Microscopy analysis and mathematical modelling provide evidence that tubulin subunits are transported to their sites of incorporation into microtubules at axonemal tips by IFT.
Activating mutations in the receptor tyrosine kinase Met can promote tumorigenesis. These Met mutants are now shown to undergo altered endocytic trafficking, and the retention of active Met at endosomes correlates with increased tumour formation and metastasis.
A combination of genetic fate mapping and imaging reveals that the distal visceral endoderm of mouse embryo arises following the migration of Lefty1-expressing primitive endoderm progenitor already present in the implanting blastocyst.
In human embryonic stem cells, the histone demethylase LSD1 is found to occupy the promoters of a subset of developmental genes that bear methylation marks on the lysine residues 4 and 27 of histone 3, and are co-occupied by OCT4 and NANOG. LSD1 participates in the silencing of these genes by controlling the levels of methylation at their regulatory regions on lysine 4 of histone 3.
Semaphorin 3A (Sema3A) is a key guidance cue for neuronal growth. Sema3A is now shown to facilitate the conversion of axons to dendrites by stimulating signalling through CaV2.3 calcium channels.
Live-cell imaging of the spatiotemporal kinetics of PKA activation during cell migration reveals that PKA regulates the protrusion and retraction cycle of the leading edge. Protrusion formation correlates with RhoA and PKA activation. PKA subsequently phosphorylates RhoA to increase its interaction with RhoGDI and terminate RhoA activity at the leading edge.