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The peripheral actin cortex in cells is essential for secretory vesicle exocytosis, but also acts as a barrier for vesicle release. Wollman and Meyer report that antigen activation triggers cyclical waves of Ca2+ and PtdIns(4,5)P2 that promote N-WASP-mediated oscillations in F-actin polymerization. These permit secretion when F-actin levels are low, but impede exocytosis when F-actin levels are high.
Voinnet and colleagues show that autophagy targets RNAi components DICER and AGO2 for degradation when they are not bound to miRNA. The autophagy receptor NDP52 is required for this homeostatic regulation of the RNAi machinery. The authors also found that autophagy influences the post-translational regulation of DICER mRNA.
Guan and colleagues report that the Hippo pathway effector YAP regulates PI(3)K–mTOR signalling. YAP induces expression of the microRNA miR-29 to block PTEN expression, activating the PI(3)K pathway. Hippo and PI(3)K pathways thus converge to regulate cell growth and proliferation.
Chang and colleagues reveal that the poly(ADP-ribose) polymerase PARP16 participates in the endoplasmic reticulum (ER) stress response. They report that PARP16 is a transmembrane ER protein that PARsylates and activates PERK and IRE1α in response to ER stress.
Malliri and colleagues demonstrate that an apicobasal Rac activity gradient at cell–cell junctions is important for tight-junction assembly and establishment of apicobasal polarity. They show that this gradient is generated by the distinct spatial regulation of the Rac activator Tiam1 by β2-syntrophin and Par-3.
Lemischka and colleagues examine the effects of transient Nanog downregulation on the components of the pluripotent transcriptional regulatory network using single-cell gene expression analysis and modelling approaches. They observe that the initial changes induced by loss of Nanog are stochastic and reversible upon Nanog restoration, owing to the presence of feedback loops in the pluripotency network. Prolonged loss of Nanog compromises these feedback loops and reversion to pluripotency cannot be achieved upon Nanog restoration.
Centrosomes, the microtubule nucleation centre of most cells, consist of two centrioles surrounded by pericentriolar material (PCM). The PCM has been considered as amorphous but, using subdiffraction fluorescence microscopy approaches, Agard and colleagues now reveal the organized structure of the PCM of Drosophila centrosomes.
Kang and colleagues show that the transcription factor Elf5 controls the epithelial–mesenchymal transition (EMT) during development and in metastasis, by repressing the expression of Snail2/Slug, a key EMT-inducing factor.
Centrosomes consist of two centrioles surrounded by pericentriolar material (PCM) that nucleates microtubules. The PCM has been considered as amorphous but, using subdiffraction fluorescence imaging, Pelletier and colleagues now reveal the organized structure of human PCM.
In mammals, polyploidy is only seen in liver hepatocytes and in trophoblast giant cells in the placenta. Leone and colleagues now show that ploidy is controlled in an antagonistic fashion by canonical E2F transcriptional activators and atypical E2F7 and E2F8 repressors, through the control of G2/M-associated genes.
Blanpain and colleagues use inducible genetic lineage tracing to identify and follow the progenitors responsible for the development of the prostate glandular epithelium. They find that multipotent progenitors are initially able to differentiate into the three lineages that make up the prostate, with a later switch to distinct pools of unipotent basal and luminal stem cells.
It is not fully understood how polyploidy is regulated in mammals, as the liver is one of only a few tissues in which it occurs. De Bruin and colleagues demonstrate that gene repression through the E2F8 transcription factor, antagonized by E2F1, is required for polyploidization in mice. They also find that loss of polyploidy does not influence liver differentiation or regeneration.
Wagner and colleagues show that cancer cell survival during liver cancer initiation depends on inhibition of c-Fos-induced apoptosis, through the repression of survivin expression by c-Jun and SIRT6.
Tumbarello, Buss and colleagues report that the motor protein myosin VI has an important role in autophagosome maturation. They show that myosin VI binds to autophagy adaptors to mediate delivery of endocytic cargo and endosomal membrane to autophagosomes, and promote autophagosome–lysosome fusion.
Giannone and colleagues use super-resolution microscopy to analyse the nanoscale dynamic organization of talin and integrins β1 and β3 in focal adhesions.
Fox and colleagues report that VEGF-A stimulation of endothelial cells induces the phosphorylation of profilin by VEGFR2 and Src. This regulation promotes endothelial cell migration and angiogenesis in mice facing pathological conditions such as tissue wounding and ischaemic injury.
Goldman and colleagues report that the transcriptional repressor Insm1a is essential for retinal regeneration following injury in fish. Insm1a suppresses the expression of Ascl1a to promote Müller glial cells’ dedifferentiation at early stages of regeneration, and defines the regeneration zone by negatively regulating the expression of the heparin-binding EGF. It also halts the proliferation of retinal progenitors in the late stages of the process.
During cytokinesis, the intercellular bridge connecting the mother and daughter cell is thinned by a process called secondary ingression before it is eventually severed in an ESCRT-III-dependent manner. Prekeris and colleagues report that FIP3-positive endosomes deliver p50RhoGAP and SCAMP2/3 proteins to the intercellular bridge, which promote actin depolymerization to decrease the bridge diameter and allow ESCRT-III binding.
Notch signalling in the intestinal crypt is modulated to drive commitment to the secretory fate. Clevers and colleagues find that cells expressing the Notch ligand DLL1 are intermediate secretory cells that can revert to Lgr5+ stem cells upon damage.
In a quantitative proteomics approach, Mailand, Choudhary and colleagues characterize ultraviolet-regulated ubiquitylation sites and identify a role for double mono-ubiquitylation of PCNA-associated factor PAF15 in bypassing replication-blocking lesions in DNA.