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Images showing the extent of 'wound healing' after knockdown of 1081 genes in breast epithelial cells. This analysis identified 66 highly validated genes whose knockdown caused either acceleration or impairment of cell migration and involves diverse alterations in cellular processes.article p1027
Talin can activate integrins to bind the extracellular matrix and also connect matrix-engaged integrins to the actin cytoskeleton. New work shows that cell spreading can be dissected into three distinct phases according to their differential requirements for talin function.
The self-perpetuating amyloid isoform, or prion, of the yeast translation termination factor eRF3 modulates programmed translational frameshifting that controls a regulatory circuit determining the polyamine levels in a yeast cell. But it is still unclear whether this effect is adaptive or pathological.
The epithelial–mesenchymal transition (EMT) is a cellular transdifferentiation program that enables epithelial cancer cells to acquire traits of high-grade malignancy, notably invasive and metastatic powers. A new study indicates that it may also function early in tumour progression by preventing oncogene-induced senescence.
Even though less than 2% of the mammalian genome encodes proteins, a significant fraction can be transcribed into non-coding RNAs. An elegant study identifies a function for non-coding RNA transcription in activating neighbouring genes.
A siRNA screen in mammalian epithelial cells uncovers 42 genes not previously implicated in migration or adhesion. Many genes are involved in β-catenin, β1-integrin and actin signaling. Genes that accelerate migration tend to impair adhesion.
Adhesion assembly is needed for cell migration. Horwitz and colleagues report that new adhesions assemble in the lamellipodium in a manner that is independent of myosin II but requires actin polymerization.
Miz1, a Myc-associated transcriptional repressor inhibits cell proliferation. Eilers and colleagues show that the ribosomal protein L23 negatively regulates Miz1 by retaining its activator, nucleophosmin, in the nucleolus.
Talins link integrins to the actin cytoskeleton and are important for cell spreading. Sheetz and colleagues show that talin is dispensable for initial cell spreading but it is required for sustained cell spreading and adhesion.
Namy et al. show that the yeast prion form of the eERF3 translation termination factor boosts antizyme expression, which reduces polyamine synthesis. Changes in polyamine levels account for most of the phenotypic traits conferred by this prion.
The kinase Plk1 regulates multiple processes during mitosis in mammalian cells. Chen and colleagues show that Plk1 also controls a transcriptional network required for orderly cell-cycle progression through Cdk1-dependent phosphorylation of the transcription factor FoxM1
Cellular progression through mitosis is largely controlled by the APC-Cdh1 complex. Zhang and colleagues report that, when the Cdh1 gene is disrupted, cells undergo premature p16-dependent senescence, and that Cdh1-deficient mice show impairment of hippocampus-dependent learning and memory.
Ageing is associated with mitochondrial degeneration. In yeast, reducing cytosolic protein synthesis suppresses age-dependent mitochondrial dysfunction and extends lifespan.
The ubiquitin ligase Mdm2 promotes both proteolytic degradation of the tumour suppressor p53 and its translation. Fahraeus and colleagues report an additional layer of regulation: p53 mRNA binds directly to Mdm2 protein to inhibit ubiquitin ligase activity, promoting its own translation.
A new study shows that coordinated regulation of transcription due to a transcriptional ripple effect is widespread in the mammalian genome. Nishida and colleagues have found that induction of immediate early genes is accompanied by upregulation of genes in the vicinity; this process is dependent on the MAPK pathway and the transcription factor SRF.
Viruses use various mechanisms to hijack cellular processes. Zhou and colleagues now describe a viral histone H3K27 methylase that modifies host histones and represses host target genes.