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Etienne-Manneville and colleagues demonstrate that the adherens junctions of adjacent migrating cultured cells exhibit retrograde flow along the lateral cell sides. They show that the rearward treadmilling of junctions is followed by N-cadherin endocytosis at the cell rear and anterograde trafficking to support formation of new junctional complexes at the cell front.
De Camilli and colleagues reveal that reducing cholesterol or sphingomyelin causes formation of tubular structures resembling early endocytic intermediates at the plasma membrane. These structures recruit sphingosine kinase 1 (SPHK1). Depleting SPHK1 inhibits endocytic recycling, revealing a link between sphingosine metabolism and endocytosis.
Gomis and colleagues report on the mechanisms driving colon cancer metastasis. They show that whereas ERK2 activity promotes colon cancer metastasis to the liver, reduced p38 signalling upregulates the PTHLH cytokine to allow liver metastatic cell extravasation and colonization of the lung.
Gundersen and colleagues report that the FHOD1 formin is involved in nuclear positioning, by physically linking nesprin-2G, a protein of the outer nuclear membrane, to actin cables, to allow the formation of the transmembrane actin-associated nuclear (TAN) lines that are needed to move the nucleus.
Clathrin-independent endocytosis removes membrane receptors and other proteins from the cell surface, yet the mechanisms controlling this process remain unclear. Galectin-3 is now shown to regulate the biogenesis of a subpopulation of clathrin-independent carriers (CLICs). Galectin-3 binds to glycosylated cargo proteins and interacts with membrane glycosphingolipids to induce membrane deformation and CLIC formation.
Cadherin-containing cell–cell junctions respond to intercellular tension by increasing their size, strength and complexity. The mechanical regulation of cadherin adhesions is now shown to involve myosin-dependent tension in the cortical actomyosin cytoskeleton. This reduces actin turnover to decrease the mobility of cadherin molecules and increase their concentration at junctions.
Despite the widespread occurrence of aneuploidy in cancer cells, the molecular causes for chromosomal instability are not well established. Cyclin B2 is now shown to control a pathway — involving the centrosomal kinases aurora A and Plk1 and the tumour suppressor p53 — the alteration of which causes defective centrosome separation, aneuploidy and tumour development.
Pluripotent embryonic stem cells (ESCs) can be derived from blastocyst-stage mouse embryos. However, the exact in vivo counterpart of ESCs has remained elusive. A combination of expression profiling and stem cell derivation identifies epiblast cells from late-stage blastocysts as the source, and functional equivalent, of ESCs.
The degradation of dysfunctional proteins and organelles by autophagy is important for cell viability. Dikic and co-authors discuss how cargo selection is achieved during selective autophagy and how the processes involved in cargo delivery are related to membrane trafficking pathways.
Puisieux et al. discuss endothelial to mesenchymal transition (EMT)-inducing transcription factors in tumorigenesis. They explore how EMT contributes not only to tumour progression through its roles in invasion and metastasis, but also to malignant transformation and early tumour development by impinging on tumour suppressive pathways and cell differentiation states.
It has been unclear at which stage of mouse development embryonic stem cells can be derived. Nichols and colleagues use single-cell cultures to demonstrate that derivation of cells able to proliferate without ERK signalling (a characteristic of ESCs) is limited to the early pre-implantation epiblast and is favoured by culture on a laminin substrate.
The Par polarity proteins are involved in regulating asymmetric division in stem cells in the fly. Macara and colleagues identify a PAR3 homologue that is expressed in multipotent stem cells in terminal end buds of the murine mammary gland, and is necessary for stem cell maintenance through its effect on Lkb1 kinase activity.
Thiery, Viasnoff and colleagues study the roles of myosin contractility and actin dynamics in regulating the recruitment of E-cadherin at adherens junctions, using an assay that allows live 3D imaging of the intercellular contact of a suspended cell doublet.
Wittmann and colleagues demonstrate that the turnover of mature focal adhesions is regulated by CLASP proteins. They show that CLASP recruitment to focal adhesions is involved in localized exocytosis and extracellular matrix degradation, suggesting that local matrix metalloprotease secretion might promote focal adhesion disassembly.
