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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.
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.
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.
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.
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.
The Nek2 kinase directs the separation of duplicated centrosomes. Now the Hippo pathway components hSav1 and Mst2 are shown to regulate the function of Nek2 at the centrosome. This pathway cooperates with the kinesin Eg5 to mediate centrosome separation.
Normal migrating cells exhibit contact inhibition of locomotion (CIL) when meeting a neighbouring cell, but metastatic cancer cells lose this inhibition. Interactions btween ephrin and ephrin receptors are now shown to underlie CIL in migrating cells.
Uncapped telomeres activate a p53-mediated DNA damage response to elicit cellular senescence. In turn, p53 negatively modulates telomere capping by promoting ubiquitin-mediated degradation of the TRF2 shelterin component.
Epithelial cell transcytosis of polymeric IgA by its receptor requires polarized membrane trafficking. A signalling cascade involving the tyrosine kinase YES, EGFR, ERK and the Rab11 effector FIP5 is now shown to regulate this process.
Endothelial cells form a vascular niche that supports haematopoietic stem cell function. Akt activation in endothelial cells upregulates angiocrine factors to promote long-term haematopoietic stem cell repopulation capacity while co-activation of Akt and MAPK shift the balance towards maintenance and differentiation of their progenitors.
Polarized-membrane trafficking supports the delivery of polarity proteins to discrete plasma-membrane domains, although the interplay between trafficking and polarity pathways is not fully understood. The small GTPases Rab8 and Rab11a direct the apical localization and activation of Cdc42 and Par3, which is essential for lumen formation.
Notch and vascular endothelial growth factor receptor (VEGFR) coordinates endothelial cells behaviour during angiogenesis sprouting although exactly how is uncertain. Endothelial cells dynamically compete for the leading position in a sprout through relative levels of Vegfr1 and Vegfr2 in a Notch dependent manner.
The ubiquitin ligase RACO-1 is found to be a co-factor for the AP-1 transcription factor c-Jun, and its depletion reduces AP-1 target gene expression, proliferation and tumour formation. RACO-1 is stabilised by growth factors through the MEK/ERK pathway, which promotes K63 linked ubiquitylation, opposing the K48-linked proteolytic auto-ubiquitylation of RACO-1.
In yeast, the MAPK-responsive protein Dig1 regulates Ste12 transcription factor activity in response to pheromone. Dig1 is now shown to prevent long-range interchromosomal interactions between Ste12-target genes, dampening transcriptional 'noise'.
SCFFbw7 mediates the ubiquitylation and degradation of Myc. Now, Myc is also shown to be stabilized by ubquitylation through SCFβ-TrCP. During recovery from S phase arrest, SCFβ-TrCP mediates the addition of a polyubiquitin chain on the Myc amino terminus that is functionally distinct from that formed by Fbw7.
The conserved vertebrate transcriptional repressor Tel regulates angiogenesis by directly controlling endothelial sprouting through modulation of Notch ligand Dll4 and vessel branching through other angiogenesis factors such as sprouty and VE-cadherin