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At least 19 recordsLinked to original sources
PubMed2002

Intact vinculin protein is required for control of cell shape, cell mechanics, and rac-dependent lamellipodia formation.

Studies were carried out using vinculin-deficient F9 embryonic carcinoma (gamma229) cells to analyze the relationship between structure and function within the focal adhesion protein vinculin, in the context of control of cell shape, cell mechanics, and movement. Atomic force microscopy studies revealed that transfection of the head (aa 1-821) or tail (aa 811-1066) domain of vinculin, alone or together, was unable to fully reverse the decrease in cell stiffness, spreading, and lamellipodia formation caused by vinculin deficiency. In contrast, replacement with intact vinculin completely restored normal cell mechanics and spreading regardless of whether its tyrosine phosphorylation site was deleted. Constitutively active rac also only induced extension of lamellipodia when microinjected into cells that expressed intact vinculin protein. These data indicate that vinculin's ability to physically couple integrins to the cytoskeleton, to mechanically stabilize cell shape, and to support rac-dependent lamellipodia formation all appear to depend on its intact three-dimensional structure.

Animals↗
PubMed1998

Fibroblast growth factor 2 uses PLC-gamma1 for cell proliferation and PI3-kinase for alteration of cell shape and cell proliferation in corneal endothelial cells.

PURPOSE: Fibroblast growth factor 2 (FGF-2) induces endothelial-mesenchymal modulation in corneal endothelial cells, including stimulation of cell proliferation and cell shape change and induction of fibrillar collagen. In the present study, we investigated whether FGF-2 uses distinct signaling pathways for individual biological activities. METHODS: Specific metabolic inhibitors were used to block cell proliferation, while reversion of cellular morphology (modulated with FGF-2) was determined using specific antibodies and inhibitors. Immunocytochemical analysis was performed to identify any changes observed in the cytoskeleton in relation to cell shape. Association of cytoskeleton molecules with phosphatidylinositol 3-kinase was determined using co-precipitation. Cell proliferation was assayed using a colorimetric method for determining the number of viable cells. RESULTS: The fibroblastic morphology induced by FGF-2 reverted to a polygonal shape in cells treated with anti-FGF-2 antibody, anti-phosphatidylinositol 3-kinase antibody, LY294002, and genistein, while anti-phospholipase C gamma1 antibody did not to reverse the modulated cell morphology. Cell proliferation mediated by FGF-2 was blocked by metabolic inhibitors (genistein, LY294002 and wortmannin); genistein inhibited FGF-mediated cell proliferation in a dose-response manner and had a maximum inhibition of 80% at 100 microM, while inhibitors of phosphatidylinositol 3-kinase had less inhibitory effect than did genistein. When cytoskeleton proteins were examined, the characteristic punctated staining profiles of vinculin observed in normal cells were maintained in fibroblastic corneal endothelial cells treated with FGF-2. The inhibitors that cause reversion of cell shape also demonstrated the punctated staining potential. Likewise, the staining profiles of alpha-actinin and smooth muscle alpha-actin were not altered, regardless of cell shape. Filamentous actin and alpha-actinin were co-localized to the cytoskeleton and phosphatidylinositol 3-kinase was associated with the cytoskeleton, regardless of cell shape. CONCLUSIONS: These findings indicate that FGF-2 uses distinct and/or dual signaling pathways for individual biological activities.

Androstadienes↗
PubMed2006

Cell shape and cell division.

The correlation between cell shape elongation and the orientation of the division axis described by early cell biologists is still used as a paradigm in developmental studies. However, analysis of early embryo development and tissue morphogenesis has highlighted the role of the spatial distribution of cortical cues able to guide spindle orientation. In vitro studies of cell division have revealed similar mechanisms. Recent data support the possibility that the orientation of cell division in mammalian cells is dominated by cell adhesion and the associated traction forces developed in interphase. Cell shape is a manifestation of these adhesive and tensional patterns. These patterns control the spatial distribution of cortical signals and thereby guide spindle orientation and daughter cell positioning. From these data, cell division appears to be a continuous transformation ensuring the maintenance of tissue mechanical integrity.

Animals↗
PubMed1978

A scanning electron microscope study of cell shape and cell appendages in the primitive streak region of the rat and chick embryo.

This report provides a scanning electron microscopic account of cell shapes and cell appendages that are observed in the primitive streak region of the rat and chick embryos. Epiblast cells become progressively elongated in the primitive streak region until flask cells predominate medially. The flask cells have a broad basal end directed toward the endoderm. In addition to fine filopodia, broad lamellipodia are found anchoring the flask cells to subjacent cells. The primary mesenchyme cells are at first round in shape and closely packed, but laterally are flattened and more dispersed. The mesenchyme cells are associated with each other by filopodia and lamellipodia and with the epiblast and endoderm by filopodia. On the basis of this description it is suggested that cell movement through the primitive streak occurs by cell extension, attachment by basal lamellipodia, and cell shortening that results in the movement of individual cells in a cell stream.

Animals↗
PubMed1987

Functional differentiation of alveolar type II epithelial cells in vitro: effects of cell shape, cell-matrix interactions and cell-cell interactions.

Alveolar type II epithelial cells rapidly lose characteristics of differentiated function when cultured on plastic dishes. We have attempted to circumvent this problem by culturing type II cells under conditions that might better reproduce their environment in vivo. Cell-matrix interactions were studied by culturing isolated adult rat type II cells on Engelbreth-Holm-Swarm (EHS) tumor basement membrane. Aggregates of type II cells formed on the surface of the matrix during 4 days in culture. Microscopic examination of these aggregates revealed cuboidal cells that retained more characteristics of differentiated type II cells than did cells cultured on plastic. Type II cells cultured on EHS matrix incorporated a higher percentage of acetate into phosphatidylcholine (PC) than did cells on plastic, and a higher percentage of this PC was saturated. Phosphatidylglycerol (PG) synthesis by these cells was no different from that seen in cells on plastic. The effects of cell-cell interactions and cell shape were evaluated by culturing type II cells on feeder layers that in turn were grown on collagen gels. The feeder layer cells included fetal rat lung fibroblasts, adult rat lung fibroblasts, fetal rat skin fibroblasts, bovine aortic endothelial cells, and rat mammary tumor epithelial cells. One-half of the gels remained attached to the culture dish and one-half of the gels were detached after 24 h and allowed to float free in the medium. Type II cells grown in association with any of the attached feeder layers became flattened and lost their differentiated phenotype. These cells incorporated no greater percentage of acetate into PC than did cells on plastic. Saturated PC synthesis was modestly increased. PG synthesis declined in parallel with that seen in cells cultured on plastic. Type II cells cultured on feeder layers that were detached assumed their native cuboidal shape and also exhibited many morphological characteristics of differentiated function. These cells incorporated a significantly greater percentage of acetate into PC compared to cells on either plastic or attached feeder layers. Saturated PC synthesis also increased markedly. These cells, however, incorporated no greater percentage of acetate into PG than did cells on plastic or attached feeder layers. These data suggest an important role for cell shape and cell-matrix interactions and maintenance of type II cell differentiation. The effects of cell-cell interactions, while beneficial, appear to be non-specific.

Animals↗
PubMed1992

Detection of X-ray damage repair by the immediate versus delayed plating technique is dependent on cell shape and cell concentration.

A method commonly used to measure the ability of cells to repair potentially lethal damage (PLD) is to compare immediate plating (IP) and delayed plating (DP) survival. Lower cell survival under IP conditions relative to that after DP conditions has been interpreted to indicate a higher ability of cells to repair potentially lethal damage (PLD) under DP conditions. However, this IP radiosensitization has not been observed in several cell lines and tumor models. IP conditions involve treatment of cells with trypsin and plating them into fresh growth medium. We have investigated the possibility that radiosensitization under IP conditions may be related to both the cell-shape and the nutrient concentration in growth medium (GM, MEM + 15% serum). This idea predicts that the IP and DP survival of spheroids will show a response similar to the IP survival of cells in monolayers and that the IP and DP survival of crowded monolayer cells in high densities will be the same. Chinese hamster V79 cells grown in monolayers (spread cells) and spheroids (clumps of round cells) were used. The IP survival was lower than the DP survival for spread log phase monolayer cells but not for round log phase cells in spheroids. Radiosensitization of cells by fresh (as opposed to spent) growth medium was absent for high density plateau phase cells in monolayers at or above 2 x 10(6) cells/ml. However, PLD repair could be demonstrated in spheroid cells and in high density plateau phase cultures by exposing cells to hyperthermia or hypertonic saline. Comparison of immediate plating versus delayed plating survival detects PLD repair only in well spread low density monolayer cells, but not in round spheroid cells nor in dense monolayer cells at > 10(7) cells/25 cm2 flask/5 ml medium. The absence of a difference between IP and DP cell survival does not mean that PLD repair is absent. Incorrect prediction of tumor response to radiotherapy can occur when PLD repair capacity is assayed as a ratio of DP/IP survival. More than one method must be used to measure the capacity of cells to repair their PLD.

Animals↗
PubMed1990

Protein kinase C activity in erythrocytes in primary hypertension: regulation of cell shape and cation transport.

Protein kinase C activity in the lysate of erythrocytes of patients with essential hypertension (EH) and spontaneously hypertensive rats (SHR) was found to be increased by 1.6-2.0 times as compared with normotensive controls. Membrane cytoskeleton alterations observed in the erythrocytes of patients with EH and SHR were revealed in decreased average erythrocyte volume, increase of cup-shaped cell formation, and increase of basal phosphorylation of band 4.9 protein. In addition, the rate of Na(+)-H+ exchange in erythrocytes of EH patients and SHR was increased by 1.9-fold. In vitro treatment of erythrocytes of healthy donors and Wistar-Kyoto rats (WKY) with protein kinase C activator (12-O-tetradecanoylphorbol-13-acetate) leads to similar changes of cell shape, cell volume, band 4.9 protein phosphorylation and Na(+)-H+ exchange, as well as to an increase of diS-C3-(5) fluorescence. It may be assumed that alterations of these parameters revealed in primary hypertension are caused by increased activity of protein kinase C.

Adult↗
PubMed1978

Morphology of an Escherichia coli mutant with a temperature-dependent round cell shape.

Mutants of Escherichia coli capable of growing in the presence of 10 microgram of mecillinam per ml were selected after intensive mutagenesis. Of these mutants, 1.4% formed normal, rod-shaped cells at 30 degrees C but grew as spherical cells at 42 degrees C. The phenotype of one of these rod(Ts) mutants was 88% cotransducible with lip (14.3 min), and all lip+ rod(Ts) transductants of a lip recipient had the following characteristics: (i) growth was relatively sensitive to mecillinam at 30 degrees C but relatively resistant to mecillinam at 42 degrees C; (ii) penicillin-binding protein 2 was present in membranes of cells grown at 30 degrees C in reduced amounts and was undetectable in the membranes of cells grown at 42 degrees C. The mecillinam resistance, penicillin-binding protein 2 defect, and rod phenotypes all cotransduced with lip with high frequency. Thus the mutation [rodA(Ts)] is most likely in the gene for penicillin-binding protein 2 and causes the organism to grow as a sphere at 42 degrees C, although it grows with normal rodlike morphology at 30 degrees C. At 42 degrees C, cells of this strain were round with many wrinkles on their surfaces, as revealed by scanning electron microscopy. In these round cells, chromosomes were dispersed or distributed peripherally, in contrast to normal rod-shaped cells which had centrally located, more condensed chromosomes. The round cells divided asymmetrically on solid agar, and it seemed that the plane of each successive division was perpendicular to the preceding one. On temperature shift-down in liquid medium many cells with abnormal morphology appeared before normal rod-shaped cells developed. Few abnormal cells were seen when cells were placed on solid medium during temperature shift-down. These pleiotropic effects are presumably caused by one or more mutations in the rodA gene.

Amdinocillin↗
PubMed2004

The RhoGEF Pebble is required for cell shape changes during cell migration triggered by the Drosophila FGF receptor Heartless.

The FGF receptor Heartless (HTL) is required for mesodermal cell migration in the Drosophila gastrula. We show that mesoderm cells undergo different phases of specific cell shape changes during mesoderm migration. During the migratory phase, the cells adhere to the basal surface of the ectoderm and exhibit extensive protrusive activity. HTL is required for the protrusive activity of the mesoderm cells. Moreover, the early phenotype of htl mutants suggests that HTL is required for the adhesion of mesoderm cells to the ectoderm. In a genetic screen we identified pebble (pbl) as a novel gene required for mesoderm migration. pbl encodes a guanyl nucleotide exchange factor (GEF) for RHO1 and is known as an essential regulator of cytokinesis. We show that the function of PBL in cell migration is independent of the function of PBL in cytokinesis. Although RHO1 acts as a substrate for PBL in cytokinesis, compromising RHO1 function in the mesoderm does not block cell migration. These data suggest that the function of PBL in cell migration might be mediated through a pathway distinct from RHO1. This idea is supported by allele-specific differences in the expressivity of the cytokinesis and cell migration phenotypes of different pbl mutants. We show that PBL is autonomously required in the mesoderm for cell migration. Like HTL, PBL is required for early cell shape changes during mesoderm migration. Expression of a constitutively active form of HTL is unable to rescue the early cellular defects in pbl mutants, suggesting that PBL is required for the ability of HTL to trigger these cell shape changes. These results provide evidence for a novel function of the Rho-GEF PBL in HTL-dependent mesodermal cell migration.

Animals↗
PubMed1999

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

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.

Actins↗
PubMed2006

Loss of O-antigen increases cell shape abnormalities in penicillin-binding protein mutants of Escherichia coli.

Escherichia coli mutants lacking multiple penicillin-binding proteins (PBPs) produce aberrantly shaped cells. However, most of these experiments have been performed in E. coli K12 strains, which do not attach a complete O-antigen to their outer membrane lipopolysaccharide. We constructed mutants in different genetic backgrounds and found that the frequency of morphological deformities was higher in strains lacking the O-antigen. Also, complementing O-negative mutants with a heterologous O-antigen from Klebsiella returned a substantial fraction of misshapen cells to a normal morphology. Thus, the O-antigen contributes to cell shape in E. coli, perhaps by reducing the number of ectopic poles, which may be the proximal cause of shape abnormalities.

Binding Sites↗
PubMed2003

The bacterial cytoskeleton: an intermediate filament-like function in cell shape.

Various cell shapes are encountered in the prokaryotic world, but how they are achieved is poorly understood. Intermediate filaments (IFs) of the eukaryotic cytoskeleton play an important role in cell shape in higher organisms. No such filaments have been found in prokaryotes. Here, we describe a bacterial equivalent to IF proteins, named crescentin, whose cytoskeletal function is required for the vibrioid and helical shapes of Caulobacter crescentus. Without crescentin, the cells adopt a straight-rod morphology. Crescentin has characteristic features of IF proteins including the ability to assemble into filaments in vitro without energy or cofactor requirements. In vivo, crescentin forms a helical structure that colocalizes with the inner cell curvatures beneath the cytoplasmic membrane. We propose that IF-like filaments of crescentin assemble into a helical structure, which by applying its geometry to the cell, generates a vibrioid or helical cell shape depending on the length of the cell.

Bacterial Proteins↗
PubMed2003

A study of the electric field distribution in erythrocyte and rod shape cells from direct RF exposure.

This paper shows the importance of using realistic cell shapes with the proper geometry and orientation to study the mechanisms of direct cellular effects from radiofrequency (RF) exposure. For this purpose, the electric field distribution within erythrocyte, rod and ellipsoidal cell models is calculated by using a finite element technique with adaptive meshing. The three cell models are exposed to linearly polarized electromagnetic plane waves of frequencies 900 and 2450 MHz. The results show that the amplification of the electric field within the membrane of the erythrocyte shape cell is more significant than that observed in other cell geometries. The results obtained show the dependence of the induced electric field distribution on frequency, electrical properties of membrane and cytoplasm and the orientation of the cell with respect to the applied field. The analysis of the transition of an erythrocyte shape to an ellipsoidal one shows that a uniformly shelled ellipsoid model is a rough approximation if a precise simulation of bioeffects in cells is desired.

Animals↗
PubMed2002

Directional control of lamellipodia extension by constraining cell shape and orienting cell tractional forces.

Directed cell migration is critical for tissue morphogenesis and wound healing, but the mechanism of directional control is poorly understood. Here we show that the direction in which cells extend their leading edge can be controlled by constraining cell shape using micrometer-sized extracellular matrix (ECM) islands. When cultured on square ECM islands in the presence of motility factors, cells preferentially extended lamellipodia, filopodia, and microspikes from their corners. Square cells reoriented their stress fibers and focal adhesions so that tractional forces were concentrated in these corner regions. When cell tension was dissipated, lamellipodia extension ceased. Mechanical interactions between cells and ECM that modulate cytoskeletal tension may therefore play a key role in the control of directional cell motility.

3T3 Cells↗
PubMed1995

Cell shape, cytoskeletal mechanics, and cell cycle control in angiogenesis.

Capillary endothelial cells can be switched between growth and differentiation by altering cell-extracellular matrix interactions and thereby, modulating cell shape. Studies were carried out to determine when cell shape exerts its growth-regulatory influence during cell cycle progression and to explore the role of cytoskeletal structure and mechanics in this control mechanism. When G0-synchronized cells were cultured in basic fibroblast growth factor (FGF)-containing defined medium on dishes coated with increasing densities of fibronectin or a synthetic integrin ligand (RGD-containing peptide), cell spreading, nuclear extension, and DNA synthesis all increased in parallel. To determine the minimum time cells must be adherent and spread on extracellular matrix (ECM) to gain entry into S phase, cells were removed with trypsin or induced to retract using cytochalasin D at different times after plating. Both approaches revealed that cells must remain extended for approximately 12-15 h and hence, most of G1, in order to enter S phase. After this restriction point was passed, normally 'anchorage-dependent' endothelial cells turned on DNA synthesis even when round and in suspension. The importance of actin-containing microfilaments in shape-dependent growth control was confirmed by culturing cells in the presence of cytochalasin D (25-1000 ng ml-1): dose-dependent inhibition of cell spreading, nuclear extension, and DNA synthesis resulted. In contrast, induction of microtubule disassembly using nocodazole had little effect on cell or nuclear spreading and only partially inhibited DNA synthesis. Interestingly, combination of nocodazole with a suboptimal dose of cytochalasin D (100 ng ml-1) resulted in potent inhibition of both spreading and growth, suggesting that microtubules are redundant structural elements which can provide critical load-bearing functions when microfilaments are partially compromised. Similar synergism between nocodazole and cytochalasin D was observed when cytoskeletal stiffness was measured directly in living cells using magnetic twisting cytometry. These results emphasize the importance of matrix-dependent changes in cell and nuclear shape as well as higher order structural interactions between different cytoskeletal filament systems for control of capillary cell growth during angiogenesis.

Actin Cytoskeleton↗
PubMed1997

Expression of OCI-5/glypican 3 during intestinal morphogenesis: regulation by cell shape in intestinal epithelial cells.

OCI-5, the rat homologue of human glypican 3 (GPC3), is believed to be involved in morphogenesis and growth control during development. The finding that GPC3 is mutated in patients with the Simpson-Golabi-Behmel overgrowth syndrome is consistent with this idea. In this report, using RNA in situ hybridization, expression of OCI-5 in the developing intestine is detected in both endoderm- and mesenchyme-derived cells in a phased manner related to age and proximal/distal position. To investigate the mechanism of its regulation during intestinal development, OCI-5 expression was studied in the primitive rat intestinal epithelial cell line IEC-18. The expression of the OCI-5 transcript is increased in IEC-18 cells at confluence, in low calcium media, and during spheroid culture, all conditions which result in the cells acquiring a more rounded cell shape. In contrast, cytoskeletal disruption with colchicine causes cells to flatten and spread and abolishes both the confluence- and the low calcium-dependent induction of OCI-5. Treatment with vanadate, a phosphatase inhibitor, causes cells to acquire a spindle-shaped morphology and prevents OCI-5 induction in all situations. Nuclear run-on analysis demonstrates that the rate of OCI-5 transcription is increased at confluence, in low calcium media, and during spheroid culture of IEC-18, and decreased by treatment of cells with colchicine. Together, these data suggest that OCI-5 expression is regulated in IEC-18 by cell shape. The pattern of expression of OCI-5 in the developing intestine is consistent with it playing a role in epithelial-mesenchymal interactions during intestinal morphogenesis, when cell shape changes are likely to occur.

Animals↗
PubMedDate not supplied

Vanadate affects nuclear division and induces aberrantly-shaped cells during subsequent cytokinesis in Tetrahymena.

Sodium orthovanadate at 0.1-5.0 mM affected cell proliferation of Tetrahymena in a dose-dependent manner. At 1 h the cell increment was 76-12% of the control (100%), but after lag periods in 1-5 mM the growth rate remained at 76% of control in 0.1 mM vanadate and at 64-61% of control in 0.2-5.0 mM vanadate. Endocytosis was affected in both a time- and dose-dependent manner; an increasing number of cells did not form vacuoles. Cell motility increased initially in 0.1 mM vanadate but decreased later as it did in 0.5-2.0 mM vanadate where the proportion of immobile cells increased with time. Cell divisions occurred at all concentrations but macronuclear elongation was disturbed and subsequent cytokinesis resulted in daughter cells containing the entire G2 macronucleus, a large or small portion of it, or no nucleus at all. Moreover, odd cell shapes appeared with time. The size of the cell and nucleus increased but there was great variation with disturbed cytoplasm/nucleus ratios. Treated cells had dilated rough endoplasmic reticulum that included dense material, presumed to be vanadate, which was not seen in control cells. Scant amounts of dense material were found in dense granules, small vacuoles, and abundantly in contractile vacuoles. It is argued that interference with proper microtubular function is the main effect of vanadate.

Animals↗