Faculty Opinions recommendation of Cell shape and contractility regulate ciliogenesis in cell cycle-arrested cells.

2010 ◽  
Author(s):  
Reika Watanabe
Keyword(s):  
Cell Cycle ◽  
Cell Shape

scholarly journals Integrin binding and cell spreading on extracellular matrix act at different points in the cell cycle to promote hepatocyte growth.

1994 ◽  
Vol 5 (9) ◽  
pp. 967-975 ◽  
Author(s):  
L K Hansen ◽  
D J Mooney ◽  
J P Vacanti ◽  
D E Ingber
Keyword(s):  
Cell Cycle ◽  
Extracellular Matrix ◽  
Cell Shape ◽  
Time Course ◽  
Cell Spreading ◽  
S Phase ◽  
Similar Time ◽  
Cell Shape Changes ◽  
Hepatocyte Growth ◽  
Shape Changes

This study was undertaken to determine the importance of integrin binding and cell shape changes in the control of cell-cycle progression by extracellular matrix (ECM). Primary rat hepatocytes were cultured on ECM-coated dishes in serum-free medium with saturating amounts of growth factors (epidermal growth factor and insulin). Integrin binding and cell spreading were promoted in parallel by plating cells on dishes coated with fibronectin (FN). Integrin binding was separated from cell shape changes by culturing cells on dishes coated with a synthetic arg-gly-asp (RGD)-peptide that acts as an integrin ligand but does not support hepatocyte extension. Expression of early (junB) and late (ras) growth response genes and DNA synthesis were measured to determine whether these substrata induce G0-synchronized hepatocytes to reenter the growth cycle. Cells plated on FN exhibited transient increases in junB and ras gene expression (within 2 and 8 h after plating, respectively) and synchronous entry into S phase. Induction of junB and ras was observed over a similar time course in cells on RGD-coated dishes, however, these round cells did not enter S phase. The possibility that round cells on RGD were blocked in mid to late G1 was confirmed by the finding that when trypsinized and replated onto FN-coated dishes after 30 h of culture, they required a similar time (12-15 h) to reenter S phase as cells that had been spread and allowed to progress through G1 on FN. We have previously shown that hepatocytes remain viable and maintain high levels of liver-specific functions when cultured on these RGD-coated dishes. Thus, these results suggest that ECM acts at two different points in the cell cycle to regulate hepatocyte growth: first, by activating the G0/G1 transition via integrin binding and second, by promoting the G1/S phase transition and switching off the default differentiation program through mechanisms related to cell spreading.

Cell cycle and neuroepithelial cell shape during bending of the chick neural plate

1987 ◽  
Vol 218 (2) ◽  
pp. 196-206 ◽  
Author(s):  
Jodi L. Smith ◽  
Gary C. Schoenwolf
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Neural Plate ◽  
Neuroepithelial Cell

scholarly journals Interplay between septin organization, cell cycle and cell shape in yeast

2005 ◽  
Vol 118 (8) ◽  
pp. 1617-1628 ◽  
Author(s):  
A. S. Gladfelter ◽  
L. Kozubowski ◽  
T. R. Zyla ◽  
D. J. Lew
Keyword(s):  
Cell Cycle ◽  
Cell Shape

scholarly journals Cell shape and contractility regulate ciliogenesis in cell cycle–arrested cells

2010 ◽  
Vol 191 (2) ◽  
pp. 303-312 ◽  
Author(s):  
Amandine Pitaval ◽  
Qingzong Tseng ◽  
Michel Bornens ◽  
Manuel Théry
Keyword(s):  
Cell Cycle ◽  
Primary Cilium ◽  
Network Architecture ◽  
Cell Shape ◽  
Individual Cell ◽  
Dorsal Surface ◽  
Ventral Surface ◽  
Control Individual ◽  
Cell Cycle Exit ◽  
Actin Network

In most lineages, cell cycle exit is correlated with the growth of a primary cilium. We analyzed cell cycle exit and ciliogenesis in human retinal cells and found that, contrary to the classical view, not all cells exiting the cell division cycle generate a primary cilium. Using adhesive micropatterns to control individual cell spreading, we demonstrate that cell spatial confinement is a major regulator of ciliogenesis. When spatially confined, cells assemble a contractile actin network along their ventral surface and a protrusive network along their dorsal surface. The nucleus–centrosome axis in confined cells is oriented toward the dorsal surface where the primary cilium is formed. In contrast, highly spread cells assemble mostly contractile actin bundles. The nucleus–centrosome axis of spread cells is oriented toward the ventral surface, where contractility prevented primary cilium growth. These results indicate that cell geometrical confinement affects cell polarity via the modulation of actin network architecture and thereby regulates basal body positioning and primary cilium growth.

scholarly journals A Complex of Two Centrosomal Proteins, CAP350 and FOP, Cooperates with EB1 in Microtubule Anchoring

2006 ◽  
Vol 17 (2) ◽  
pp. 634-644 ◽  
Author(s):  
Xiumin Yan ◽  
Robert Habedanck ◽  
Erich A. Nigg
Keyword(s):  
Cell Cycle ◽  
Mammalian Cells ◽  
Cell Shape ◽  
Terminal Domain ◽  
Centrosomal Proteins

The anchoring of microtubules (MTs) to subcellular structures is critical for cell shape, polarity, and motility. In mammalian cells, the centrosome is a prominent MT anchoring structure. A number of proteins, including ninein, p150Glued, and EB1, have been implicated in centrosomal MT anchoring, but the process is far from understood. Here we show that CAP350 and FOP (FGFR1 oncogene partner) form a centrosomal complex required for MT anchoring. We show that the C-terminal domain of CAP350 interacts directly with FOP and that both proteins localize to the centrosome throughout the cell cycle. FOP also binds to EB1 and is required for localizing EB1 to the centrosome. Depletion of either CAP350, FOP, or EB1 by siRNA causes loss of MT anchoring and profound disorganization of the MT network. These results have implications for the mechanisms underlying MT anchoring at the centrosome and they attribute a key MT anchoring function to two novel centrosomal proteins, CAP350 and FOP.

Abstract 475: Human Saphenous Vein Progenitor Cells Are Susceptible to Mechanical Stimulation. Novel Insights in Pathologic Programming of Saphenous Vein Bypass Graft Disease

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Gloria Garoffolo ◽  
Rosa Vono ◽  
Matteo Carrara ◽  
Rosaria Santoro ◽  
Stefano Zoli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Progenitor Cells ◽  
Saphenous Vein ◽  
Cell Shape ◽  
Bypass Graft ◽  
Uniaxial Strain ◽  
Cell Orientation ◽  
Human Saphenous Vein ◽  
Time Points

Background: Implantation of saphenous vein (SV) grafts into coronary position determines structural vessel wall remodeling and intimal hyperplasia. The role of the altered wall mechanics and cell-based mechanosensing has been recently implicated in the priming of this pathologic process. We investigated the effects of cyclic uniaxial strain on human saphenous vein progenitor cells (SVPs), a cell type endowed with pericyte stem cell characteristics resident in the adventitia. Methods: CD34 + CD31 - SVPs were isolated with immuno-magnetic sorting (MACS) from SVs of patients (age 58±12.6, Mean±SD) undergoing saphenectomy. Cells were subject to uniaxial strain (10% elongation; 1Hz) for 24 and 72 hrs using the FlexCell system. Cell orientation, immunofluorescence and western analyses were performed to assess the effects of strain on cell orientation/shape, cell cycle and activity of the YAP/Hippo-dependent mechanotransduction machinery. RNA-sequencing from control vs. strained SVPs was performed at both time points using RNA from cells of 5 independent donors. Results: Results indicated an increase in the expression of the cell cycle-associated markers Ki67 and pHH3 in mechanically stimulated vs. control SVPs at 24 hrs, followed by a significant reduction at 72 hrs of stimulation. Variations in cell shape was observed as verified by a significant change in the nuclei orientation in the strain field as well as in the cell shape index/spread areas at both time points. Immunofluorescence revealed a significant increase in cells showing a nuclear localization of the YAP transcription factor at 72hrs. In line with these findings Western analyses indicated a significant decrease in the ratio between phosphorylated/total YAP and its upstream kinase LATS in mechanically stimulated vs. control SVPs, suggesting an inhibition of the HIPPO kinase pathway by mechanosensing. RNASeq gene expression analyses showed a coherent modification of gene expression pathways and the upregulation of a specific HIPPO/YAP/TEAD gene expression signature in SVPs mechanically stimulated for 72hrs. Conclusions: These findings demonstrate the direct susceptibility of human SVPs to pathologic strain and identifies this cell population as mechano-perceptors in the vein wall.

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 Cell cycle–dependent active stress drives epithelia remodeling

2021 ◽  
Vol 118 (10) ◽  
pp. e1917853118
Author(s):  
John Devany ◽  
Daniel M. Sussman ◽  
Takaki Yamamoto ◽  
M. Lisa Manning ◽  
Margaret L. Gardel
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Epithelial Tissue ◽  
Experimental Conditions ◽  
Active Stress ◽  
Cell Cycle Inhibition ◽  
Cell Shapes ◽  
Cycle Dependent ◽  
Cell Cycle Dynamics ◽  
Shape Changes

Epithelia have distinct cellular architectures which are established in development, reestablished after wounding, and maintained during tissue homeostasis despite cell turnover and mechanical perturbations. In turn, cell shape also controls tissue function as a regulator of cell differentiation, proliferation, and motility. Here, we investigate cell shape changes in a model epithelial monolayer. After the onset of confluence, cells continue to proliferate and change shape over time, eventually leading to a final architecture characterized by arrested motion and more regular cell shapes. Such monolayer remodeling is robust, with qualitatively similar evolution in cell shape and dynamics observed across disparate perturbations. Here, we quantify differences in monolayer remodeling guided by the active vertex model to identify underlying order parameters controlling epithelial architecture. When monolayers are formed atop an extracellular matrix with varied stiffness, we find the cell density at which motion arrests varies significantly, but the cell shape remains constant, consistent with the onset of tissue rigidity. In contrast, pharmacological perturbations can significantly alter the cell shape at which tissue dynamics are arrested, consistent with varied amounts of active stress within the tissue. Across all experimental conditions, the final cell shape is well correlated to the cell proliferation rate, and cell cycle inhibition immediately arrests cell motility. Finally, we demonstrate cell cycle variation in junctional tension as a source of active stress within the monolayer. Thus, the architecture and mechanics of epithelial tissue can arise from an interplay between cell mechanics and stresses arising from cell cycle dynamics.

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