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Tissue remodelling events create gaps in the basement membrane and have been previously accounted for by the degradation or reduced synthesis of basement membrane components. Live-cell imaging shows that basement membrane sliding enlarges the opening of the uterus during Caenorhabditis elegans development and that integrins-based adhesion negatively regulates sliding.
Very little is known about how chromatin-modifying enzymes are regulated in response to signalling cascades. A jmjc demethylase, PHF2, is found to be activated by PKA-mediated phosphorylation, which promotes its association with the DNA-binding protein ARID5B. PHF2 then induces demethylation of ARID5B, and the PHF2–ARID5B complex modifies histone at its target promoters.
The polarized distribution of E-cadherin observed in Drosophila embryos during epithelial cell intercalation is shown to be controlled by polarized clathrin- and dynamin-mediated endocytosis. This process depends on the activity of diaphanous and myosin II, which regulate the lateral clustering of E-cadherin.
How do exocytic vesicles disengage from the exocyst complex? Phosphorylation of the RalA GTPase effector Sec5, rather than RalA inactivation per se, is now shown to mediate dissociation of the Sec5–RalA complex.
Cdk5-mediated phosphorylation of endophilin B1 is shown to be required for autophagy induction in starved neurons, by promoting endophilin B1 dimerization and recruitment of the autophagy regulator UVRAG. This effect leads to neuronal loss in models of Parkinson’s disease.
ARFGAP1 regulates COPI coat formation and participates in COPI-dependent trafficking. ARFGAP1 is now shown to interact with the clathrin adaptor complex AP-2 through a region distinct from its COP1-interacting domain, and to regulate transport of AP-2 cargo proteins.
A systematic comparison shows that differential DNA methylation accounts for some of the differences in somatic gene expression between induced pluripotent stem cells (iPSCs) and embryonic stem cells. The somatic genes that have persistent expression in iPSCs tend to be isolated from other genes that undergo silencing during reprogramming. This may explain the observed delay in recruitment of the DNA methylation machinery and in the genes being silenced.
In meiosis, HORMAD1 promotes alignment of homologues chromosomes and formation of the synaptonemal complex and is required for efficient accumulation of checkpoint and repair proteins on unsynapsed DNA.
TFG-1 is identified as a regulator of COPII coat assembly that interacts with SEC-16 to control protein exit from the endoplasmic reticulum. TFG–kinase fusion proteins have been detected in some cancers and might promote oncogenesis by prematurely phosphorylating target substrates as they exit the endoplasmic reticulum.
Mitochondria are found to fuse at the onset of autophagy. This event, which is regulated by a cyclic AMP–PKA (protein kinase A) signalling pathway, increases ATP synthase activity to prevent starvation-induced cell death.
Upregulation of microRNA-143 occurs in livers of obese mice. Transgenic overexpression of miR-143 in mice leads to insulin resistance through downregulation of the oxysterol-binding protein-related protein ORP8, impairing Akt activation in response to insulin.
Actin condenses at the lamellipodium of migrating cells to form arc-like bundles parallel to the leading edge. During the retraction phase of the edge movement, these arcs are shown to be displaced towards the rear of the lamella, and their movement slows down when they join focal adhesions. Actin arcs thus provide a spatiotemporal connection between the lamellipodium and the lamella.
The activity of protein kinase A (PKA) is regulated by association and dissociation of its regulatory (R) subunits. The E3 ubiquitin ligase praja2 is now shown to ubiquitylate and stimulate the degradation of the R subunits in response to elevated cAMP levels.
Human high-density lipoprotein (HDL) is found to transport endogenous miRNAs in plasma and to deliver them to recipient cells where they can silence mRNA reporter targets. HDL miRNAs isolated from atherogenic mice models or human atherosclerotic subjects induce changes in gene expression different from the ones seen with control HDL–miRNA populations.
As focal adhesions mature in response to mechanical tension and contractility, their protein composition changes. A proteomics analysis of focal adhesions following changes in myosin II activity highlights a role for the Rac guanine exchange factor β-Pix in promoting cell migration and nascent focal adhesion turnover, thereby preventing their maturation.
Ciliogenesis starts as cells enter quiescence and primary cilium resorption precedes mitosis. The centrosomal protein Nde1 is shown to regulate cilia length during the cell cycle. Loss of Nde1 in zebrafish leads to developmental patterning defects reflecting impaired control of cilium formation.
Ciliogenesis starts as cells enter quiescence and primary cilium resorption precedes mitosis. Phosphorylation of Tctex1 is found to accelerate cilium disassembly and S-phase entry in ciliated cells, providing a molecular link between ciliogenesis and the cell cycle. Phospho-Tctex1 action requires an intact actin cytoskeleton and may be relevant for fate determination of cortical neural progenitors.
ESCRT complexes mediate membrane scission. Cell lines that stably express fluorescently labelled ESCRT components reveal the distinct dynamics involved in the recruitment of specific ESCRT components to virus-like particles during retroviral release.
The microtubule-severing protein Katanin is now shown to possess microtubule depolymerising activity. Purified recombinant Katanin exerts both activities in vitro. In migrating cells from Drosophila, Katanin localizes at the leading edge where it negatively regulates cell motility.
A conditional knockout of the transcription factor SRF in the mouse skin shows that SRF-mediated modulation of actin regulator transcription during development is essential for normal cortical network formation and correct spindle orientation in mitosis.