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The formation of subnuclear domains, such as the paraspeckles where hyperdited mRNAs are stored, is not well understood. The transcription of the paraspeckle non-coding RNA MEN ɛ/β initiates the recruitment of other components to assemble this nuclear body.
In the developing mouse embryo, a region of the dorsal aorta endothelium generates haematopoietic cells, but how the switch to endothelium or haematopoiesis is controlled has been unclear. HoxA3 induces endothelial differentiation through repression of key haematopoietic transcription factors, including Runx1, and is downregulated during haematopoietic differentiation.
Deletion of the E3 ubiquitin ligase Wwp2 in mice is shown to induce malformations in the craniofacial regions. Wwp2 mono-ubiquitylates Goosecoid, a modification found to be essential for Goosecoid effects on the transcription of the cartilage regulatory protein Sox6.
Apoptotic cell corpses are engulfed and removed through an evolutionarily conserved pathway. In Caenorhabditis elegans, inhibition of the Rac GAP SRGP-1 permits sick or dying cells to escape clearance by this pathway.
The genetic locus encompassing TSPYL5 is frequently amplified in breast cancer. TSPYL5 is now shown to repress p53 accumulation by interacting with and inhibiting the p53 de-ubiquitylating enzyme USP7.
A complex containing the Par3/6 polarity proteins and the matrix receptor DDR1 modulates migration by downregulating cortical actomyosin contractility.
A Bicoid gradient drives patterning along the anterior–posterior axis in Drosophila embryos. Degradation of Bicoid by the F-box protein Fsd is shown to be required for the correct gradient profile of bicoid and developmental fate determination.
The role of actin-based motors and the mode of endoplasmic reticulum (ER) transport into spines had remained unclear. Myosin-Va is now shown to act as a point-to-point ER transporter into dendritic spines.
A chaperone complex containing CSPα, Hsc70 and SGT binds to monomeric SNAP-25 and prevents its aggregation and degradation. Loss of CSPα inhibits SNARE complex formation.
JAK2 phosphorylates H3-Y41 residues to exclude the heterochromatin factor HP1α from chromatin. JAK2 is found to be required for maintenance of mouse embryonic stem cells through its action on the Nanog promoter. A mutant form of JAK2 associated with a myeloproliferative disorder allows embryonic stem cells to self renew in absence of cytokines.
The four transcription factors Oct4, Sox2, Klf4 and c-myc induce somatic cells to reprogramme to an early embryonic stem cell state. When expressed in somatic cells under culture conditions that are normally used for stem cells derived from mouse epiblast tissue of post-implantation embryos (EpiSCs), these factors drive reprogramming to a state that closely resembles EpiSCs, highlighting the importance of culture environment in determining the outcome of reprogramming.
The Polycomb group protein EZH2 promotes trimethylation of histone H3K27 and gene silencing. Cdk1 is found to phosphorylate EZH2 to inhibit its methyltransferase activity, affecting EZH2-target genes involved in osteogenic differentiation.
Oscillating activities of actomyosin networks at the apical side of epithelial cells have been linked to morphogenesis in Drosophila. Montell and colleagues show that myosin oscillations on a polarised actin network at basal cell surfaces of follicle epithelial cells are also required for Drosophila egg chamber elongation.
Calcineurin signalling or pressure overload is shown to lead to cardiac hypertrophy through NFAT-mediated increase in miR-199. miR-199 inhibits the Dyrk1a kinase, which leads to further activation of NFAT. Inhibition of miR-199 reverses hypertrophy and fibrosis in mouse models of cardiac failure.
Cyclic AMP is known to affect RAF–MEK–ERK signalling, but the precise mechanism has remained unknown. An interaction between AKAP-Lbc and the scaffolding protein KSR1 is now shown to tie cAMP production to ERK pathway regulation.
IRGM is a human GTPase that triggers autophagy in response to pathogen infection. On Mycobacteria infection, IRGM binds the mitochondrial cardiolipin to induce mitochondrial fission and a general autophagy response. It can also trigger autophagy-independent mitochondria-mediated cell death.
Legs-at-odd-angles (Loa) mutations in cytoplasmic dynein tail have been linked to neurodegeneration in mice although how they affect dynein function has remained unclear. Biochemical, live-cell imaging and modelling techniques now show that loa mutations affect the motor run-length in vitro and in vivo as well as altering motor domain coordination.
The histone H3 variant CENP-A defines centromeric chromatin, but it is not known how it is maintained at these loci. The CENP-A licensing factor HsKNL2, the small GTPases Cdc42 and Rac, and their regulators Ect2 and MgcRacGAP, coordinately promote the stability of newly loaded CENP-A at centromeres.
EFA-6, originally identified as a suppressor of defects associated with dynein muations in early Caenorhabditis elegans embryos, regulates microtubule growth at the embryo cortex through a conserved amino-terminal motif but independently of its ARF6 GTP exchange factor activity.
Two pathways in ubiquitylation are linked, as the RING domain E3 ligase Ubr1, from the N-end rule pathway, is found to bind and cooperate with the HECT domain E3 Ufd4 from the ubiquitin-fusion degradation pathway.