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Cell Motility and the Cytoskeleton is an international journal published twelve times a year specializing in the rapid publication of articles concerning all phenomena related to cell motility including structural biochemical biophysical and theoretical approaches. In addition to extended reports of original research the journal will also publish invited review articles mini-reviews views and reviews brief rapid communications and book and film reviews. Topics of interest will include molecular architecture; supramolecular structure; cell shape; interactions of motile systems (e.g. tubulin- and actin-based systems); interactions of cytoskeletal proteins; non-motile roles of motile or cytoskeletal proteins; biochemical biophysical and molecular aspects of cytoskeletal proteins and related controlor binding-proteins; genetics and molecular biological approaches to the study of motility and/or the cytoskeleton; the pathology of motile behavior and the cytoskeleton; nuclear-cytoplasmic transport and interchange; membrane structure and receptor transport; action of drugs on motility and the cytoskeleton; prokaryotic flagellar motility; prokaryotic gliding motility; changes in organelle shape (axostyles costae); microtubule gliding and particle transport; axonal transport; reticulopodial movement in foraminifera radiolaria; targeted intracellular particle transport; actin-based particle transport; bulk cytoplasmic streaming (in protists plant animal and fungal cells); amoeboid motility; movement of tissue cells in vitro or in vivo; endo- and exocytosis; spreading of platelets tissue cells; morphogenetic movements; the role of motile and cytoskeletal proteins in development; the nuclear matrix; intranuclear movements; mitotic movements (e.g. kinetochore centrosomes and particles); cytokinesis; muscular contraction; cytoplasmic contractility; spasmoneme and myoneme contraction; eukaryotic flagellar and ciliary movement; the centriole centrosome and flagellar rootlet derivatives. Original research articles should report complete findings and include only as much introductory review and bibliographic material as is necessary to explain the research and its relevance to the literature. Authors wishing to contribute review articles mini-reviews rapid communications or book and film reviews should contact the Editor-in-Chief or the Associate Editor for views and reviews. Mini-reviews should not contain an exhaustive review of an area but rather a focused brief treatment of a contemporary development or issue in a single area. All contributions to these categories will be prioritized for acceptance by Editorial Board review.
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The ability to survive mitosis in the presence of microtubule poisons differs significantly between human nontransformed (RPE-1) and cancer (U2OS, HeLa) cells.
被引量：47 发表：2009
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Linked regulation of motility and integrin function in activated migrating neutrophils revealed by interference in remodelling of the cytoskeleton.
Neutrophils migrate rapidly by co-ordinating regulation of their beta2-integrin adhesion with turnover of filamentous F-actin. The seven-protein Arp2/3 complex regulates actin polymerisation upon activation by proteins of the WASP-family. To investigate links between actin polymerisation, adhesion, and migration, we used a novel osmotic-shock method to load neutrophils with peptides: (1). WASP-WA and Scar-WA (which incorporate the actin- and Arp2/3-binding regions of WASP and Scar1), to compete with endogenous WASP-family members; (2). proline rich motifs (PRM) from the ActA protein of L. monocytogenes or from vinculin, which bind vasodilator-stimulated phosphoprotein (VASP), a regulator of cytoskeleton assembly. In a flow system, rolling-adherent neutrophils were stimulated with formyl tri-peptide. This caused rapid immobilisation, followed by migration with increasing velocity, supported by activated beta2-integrin CD11b/CD18. Loading ActA PRM (but not vinculin PRM) caused concentration-dependent reduction in migration velocity. At the highest concentration, unstimulated neutrophils had elevated F-actin and were rigid, but could not change their F-actin content or shape upon stimulation. Scar-WA also caused marked reduction in migration rate, but WASP-WA had a lesser effect. Scar-WA did not modify activation-dependent formation of F-actin or change in shape. However, a reduction in rate of downregulation of integrin adhesion appeared to contribute to impaired migration. These studies show that interference in cytoskeletal reorganisation that follows activation in neutrophils, can impair regulation of integrin function as well as motility. They also suggest a role of the Arp2/3 complex and WASP-family in co-ordinating actin polymerisation and integrin function in migrating neutrophils.
被引量：9 发表：2003
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Keratinocyte motility induced by TGF-beta1 is accompanied by dramatic changes in cellular interactions with laminin 5.
Transforming growth factor-beta1 (TGF-beta1) has the ability to induce epithelial cell migration while stopping proliferation. In this study, we show that, concomitant to promoting migration of normal human keratinocytes in vitro, TGF-beta1 induced a marked decrease in their adhesion capacity to processed alpha3-containing laminin 5-coated surfaces. Indeed, the expression levels of alpha3 and alpha6 integrin subunit mRNA and protein, as well as the cell surface alpha3beta1 and alpha6beta4 integrins, were down-regulated. Recent studies showed that keratinocytes over express and deposit laminin 5 during migration and we have shown that laminin 5 found in the matrix of TGF-beta1 induced migrating keratinocytes is present in its unprocessed form [Décline and Rousselle, 2001: J. Cell Sci. 114:811-823]. We show here that TGF-beta1 treatment of the cells promoted a significant increase in their adhesion to the alpha3 chain carboxy-terminal LG4/5 subdomain and that this interaction is likely to be mediated by a heparan sulfate proteoglycan type of receptor. Our results indicate that alpha6beta4 and alpha3beta1 integrin interactions with laminin 5 are diminished during migration while a specific interaction occurs between an additional cellular receptor and the alpha3 LG4/5 module present on unprocessed laminin 5.
被引量：14 发表：2003
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Chondramides, novel cyclodepsipeptides from myxobacteria, influence cell development and induce actin filament polymerization in the green alga Micrasterias.
The effects of chondramides A-D, new actin targeting cyclodepsipeptides from the myxobacterium Chondromyces crocatus, are probed on the unicellular green alga Micrasterias denticulata, a model organism for studies on cytomorphogenesis. All four chondramides readily enter the cells and cause severe shape malformations when applied during growth. However, the four derivatives have different lowest effective concentrations. Chondramide A: 20 microM, chondramide B: 15 microM, chondramide C: 5 microM chondramide D: 10 microM. At the ultrastructural level, chondramide C, the most effective drug, causes the appearance of abnormal, dense F-actin bundles, and a substantial increase in ER, which covers large parts of the developing semicell. Also the secondary cell wall is malformed by the drug. When chondramide C effects are investigated by means of indirect immunofluorescence, alterations of the F-actin system are also visible. Instead of the cortical F-actin network of untreated controls, distinct parts of the cell are covered by abundant F-actin aggregations. Phalloidin staining of chondramide C treated cells results in a decreased fluorescence in a time-dependent manner due to binding competitions between these drugs. F-actin polymerizing and bundling capacities of chondramides A-D are presented in Micrasterias for the first time, and may in future make this substances a useful tool for cell biological research.
被引量：13 发表：2001
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Depletion of a Drosophila homolog of yeast Sup35p disrupts spindle assembly, chromosome segregation, and cytokinesis during male meiosis.
被引量：18 发表：1998
