scholarly journals A Genomic Multiprocess Survey of Machineries that Control and Link Cell Shape, Microtubule Organization, and Cell-Cycle Progression

2014 ◽  
Vol 31 (2) ◽  
pp. 227-239 ◽  
Author(s):  
Veronika Graml ◽  
Xenia Studera ◽  
Jonathan L.D. Lawson ◽  
Anatole Chessel ◽  
Marco Geymonat ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Cell Cycle Progression ◽  
Microtubule Organization ◽  
Cycle Progression

The amino-terminal matrix assembly domain of fibronectin stabilizes cell shape and prevents cell cycle progression

1999 ◽  
Vol 112 (19) ◽  
pp. 3225-3235 ◽  
Author(s):  
R.A. Christopher ◽  
S.R. Judge ◽  
P.A. Vincent ◽  
P.J. Higgins ◽  
P.J. McKeown-Longo
Keyword(s):  
Cell Cycle ◽  
Extracellular Matrix ◽  
Cell Shape ◽  
Cellular Response ◽  
Cell Cycle Progression ◽  
Cytochalasin D ◽  
Matrix Assembly ◽  
Cycle Progression ◽  
Amino Terminal ◽  
Fibronectin Matrix

Adhesion to the extracellular matrix modulates the cellular response to growth factors and is critical for cell cycle progression. The present study was designed to address the relationship between fibronectin matrix assembly and cell shape or shape dependent cellular processes. The binding of fibronectin's amino-terminal matrix assembly domain to adherent cells represents the initial step in the assembly of exogenous fibronectin into the extracellular matrix. When added to monolayers of pulmonary artery endothelial cells, the 70 kDa fragment of fibronectin (which contains the matrix assembly domain) stabilized both the extracellular fibronectin matrix as well as the actin cytoskeleton against cytochalasin D-mediated structural reorganization. This activity appeared to require specific fibronectin sequences as fibronectin fragments containing the cell adhesion domain as well as purified vitronectin were ineffective inhibitors of cytochalasin D-induced cytoarchitectural restructuring. Such pronounced morphologic consequences associated with exposure to the 70 kDa fragment suggested that this region of the fibronectin molecule may affect specific growth traits known to be influenced by cell shape. To assess this possibility, the 70 kDa fragment was added to scrape-wounded monolayers of bovine microvessel endothelium and the effects on two shape-dependent processes (i.e. migration and proliferation) were measured as a function of time after injury and location from the wound. The addition of amino-terminal fragments of fibronectin to the monolayer significantly inhibited (by >50%) wound closure. Staining of wounded monolayers with BrdU, moreover, indicated that either the 70 kDa or 25 kDa amino-terminal fragments of fibronectin, but not the 40 kDa collagen binding fragment, also inhibited cell cycle progression. These results suggest that the binding of fibronectin's amino-terminal region to endothelial cell layers inhibits cell cycle progression by stabilizing cell shape.

scholarly journals A genome-wide resource of cell cycle and cell shape genes of fission yeast

Open Biology ◽  
2013 ◽  
Vol 3 (5) ◽  
pp. 130053 ◽  
Author(s):  
Jacqueline Hayles ◽  
Valerie Wood ◽  
Linda Jeffery ◽  
Kwang-Lae Hoe ◽  
Dong-Uk Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Cell Shape ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Gene Deletions ◽  
Genome Wide ◽  
A Genome ◽  
Protein Encoding ◽  
Encoding Genes

To identify near complete sets of genes required for the cell cycle and cell shape, we have visually screened a genome-wide gene deletion library of 4843 fission yeast deletion mutants (95.7% of total protein encoding genes) for their effects on these processes. A total of 513 genes have been identified as being required for cell cycle progression, 276 of which have not been previously described as cell cycle genes. Deletions of a further 333 genes lead to specific alterations in cell shape and another 524 genes result in generally misshapen cells. Here, we provide the first eukaryotic resource of gene deletions, which describes a near genome-wide set of genes required for the cell cycle and cell shape.

The centrosomal/basal body protein OFD1 is required for microtubule organization and cell cycle progression

2020 ◽  
Vol 64 ◽  
pp. 101369 ◽  
Author(s):  
Mariaevelina Alfieri ◽  
Daniela Iaconis ◽  
Roberta Tammaro ◽  
Lucia Perone ◽  
Gaetano Calì ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Basal Body ◽  
Cell Cycle Progression ◽  
Microtubule Organization ◽  
Cycle Progression ◽  
Body Protein

scholarly journals Cell Shape-dependent Control of Ca2+Influx and Cell Cycle Progression in Swiss 3T3 Fibroblasts

2007 ◽  
Vol 282 (44) ◽  
pp. 32112-32120 ◽  
Author(s):  
Stephen R. Pennington ◽  
Brian J. Foster ◽  
Shaun R. Hawley ◽  
Rosalind E. Jenkins ◽  
Olga Zolle ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
3T3 Fibroblasts ◽  
Swiss 3T3 ◽  
Swiss 3T3 Fibroblasts

scholarly journals Control of Cyclin D1, p27Kip1, and Cell Cycle Progression in Human Capillary Endothelial Cells by Cell Shape and Cytoskeletal Tension

1998 ◽  
Vol 9 (11) ◽  
pp. 3179-3193 ◽  
Author(s):  
Sui Huang ◽  
Christopher S. Chen ◽  
Donald E. Ingber
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Shape ◽  
Cell Cycle Progression ◽  
Growth Control ◽  
S Phase ◽  
Cycle Progression ◽  
Cytoskeletal Structure ◽  
Capillary Endothelial Cells ◽  
Cytoskeletal Tension

The extracellular matrix (ECM) plays an essential role in the regulation of cell proliferation during angiogenesis. Cell adhesion to ECM is mediated by binding of cell surface integrin receptors, which both activate intracellular signaling cascades and mediate tension-dependent changes in cell shape and cytoskeletal structure. Although the growth control field has focused on early integrin and growth factor signaling events, recent studies suggest that cell shape may play an equally critical role in control of cell cycle progression. Studies were carried out to determine when cell shape exerts its regulatory effects during the cell cycle and to analyze the molecular basis for shape-dependent growth control. The shape of human capillary endothelial cells was controlled by culturing cells on microfabricated substrates containing ECM-coated adhesive islands with defined shape and size on the micrometer scale or on plastic dishes coated with defined ECM molecular coating densities. Cells that were prevented from spreading in medium containing soluble growth factors exhibited normal activation of the mitogen-activated kinase (erk1/erk2) growth signaling pathway. However, in contrast to spread cells, these cells failed to progress through G1 and enter S phase. This shape-dependent block in cell cycle progression correlated with a failure to increase cyclin D1 protein levels, down-regulate the cell cycle inhibitor p27Kip1, and phosphorylate the retinoblastoma protein in late G1. A similar block in cell cycle progression was induced before this same shape-sensitive restriction point by disrupting the actin network using cytochalasin or by inhibiting cytoskeletal tension generation using an inhibitor of actomyosin interactions. In contrast, neither modifications of cell shape, cytoskeletal structure, nor mechanical tension had any effect on S phase entry when added at later times. These findings demonstrate that although early growth factor and integrin signaling events are required for growth, they alone are not sufficient. Subsequent cell cycle progression and, hence, cell proliferation are controlled by tension-dependent changes in cell shape and cytoskeletal structure that act by subjugating the molecular machinery that regulates the G1/S transition.

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