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PubMed1984

Quantitative analyses of changes in cell shapes during bending of the avian neural plate.

It is widely believed that changes in cell shapes play important roles in the bending or folding of epithelial sheets, but few studies have actually examined cell shapes in such systems. We have determined the percentages of four types of neuroepithelial cells (i.e., spindle, flask, inverted flask, and globular) present during bending of the avian neural plate. Serial transverse plastic sections through seven craniocaudal levels of the neuroepithelium were examined. Four distinct periods of bending were chosen based on the morphology of the neuroepithelium: period I, flat neural plate; period II, midline furrow without elevation of the neural folds; period III, midline furrow with elevation; and period IV, bilateral furrows with convergence of the neural folds. We compared statistically the percentages of different cell types in bending (furrowed) and nonbending regions of the neuroepithelium, as well as changes in cell shapes with time. Our results demonstrate that dramatic changes in cell shapes occur in the midline and bilateral furrows during bending of the neural plate, such that as many as 70% of the neuroepithelial cells in the midline and 55% in the bilateral furrows are wedge shaped by the end of bending. In contrast, less than 35% of the neuroepithelial cells are wedge shaped outside of the three morphological loci of bending. These results support the hypothesis that localized changes in cell morphologies have roles in bending and shaping of the neural plate, but exactly how cells change shapes and what precise roles such changes play in bending remain to be determined.

Animals↗
PubMed2000

Agonist-induced changes in cell shape during regulated secretion in rat pancreatic acini.

The actin cytoskeleton plays an important role in the mediation of exocytosis and the determination of cell shape. Experimentally induced changes in cell shape have been shown to affect stimulated secretion in pancreatic acini. In this study, we have examined whether physiologic agonists induce changes in acinar cell shape to modulate secretion. Computer-enhanced video microscopy, immunofluorescence confocal microscopy, and quantitative Western blotting were used to study cell shape changes and cytoskeletal dynamics in rat pancreatic acini. Amylase assays were performed to study the effect of the actin-myosin cytoskeletal antagonists latrunculin A, BDM, and ML-9 on secretion. We found that pancreatic acini underwent a prominent and reversible shape change in response to the physiologic secretory agonist cholecystokinin. This was accompanied by an apical activation of myosin II as well as a basolateral redistribution of both actin and myosin II. Cytoskeletal antagonists inhibited this shape change and attenuated stimulated amylase secretion. Therefore, in addition to acting as a barrier at the apex, the actin-myosin cytoskeleton may also function to modulate cell shape to further regulate stimulated secretion.

Actins↗
PubMed2003

Caldesmon-dependent switching between capillary endothelial cell growth and apoptosis through modulation of cell shape and contractility.

Caldesmon (CaD), a protein component of the actomyosin filament apparatus, modulates cell shape and cytoskeletal structure when overexpressed. When capillary endothelial cells were infected with an adenoviral vector encoding GFP-CaD under Tet-Off control, progressive inhibition of contractility, loss of actin stress fibers, disassembly of focal adhesions, and cell retraction resulted. This was accompanied by a cell shape (rounding)-dependent increase in apoptosis and concomitant inhibition of cell cycle progression. Cell growth also was inhibited in low expressor cells in which cell tension was suppressed independently of significant changes in cell shape, cytoskeletal structure, or focal adhesions. Thus, changes in both cytoskeletal structure and contractility appear to be central to the mechanism by which extracellular matrix-dependent changes in capillary cell shape influence growth and apoptosis during angiogenesis, and hence the cytoskeleton may represent a potential target for anti-angiogenesis therapy.

Actins↗
PubMed1986

Interaction between membrane proteins PBP3 and rodA is required for normal cell shape and division in Escherichia coli.

In Escherichia coli, the products of several genes are required for septation, and the products of several others are required for the maintenance of the rod shape of the cells. We show here that the combination of certain mutations in a division gene (ftsI) with a specific mutation in one of the shape genes (rodA) could produce cells with normal shape and division, although separately these mutations led to a loss of the capacity to divide (ftsI) or to form normal rod-shaped cells (rodA). In contrast, combinations between other mutant alleles of these genes produced double mutants which had lost the capacity both to divide and to form rod-shaped cells. The mutual phenotypic correction observed within particular pairs of mutant genes suggests that the normal morphogenetic cycle of growth and division may require direct interaction between the two membrane proteins which are the products of these genes.

Bacterial Proteins↗
PubMed1987

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

Neuroepithelial cells change shape from spindle-like to wedge-like within three restricted areas (hinge points) of the bending neural plate. The mechanisms underlying these localized cell shape changes and the specific role that these changes play in bending are unclear. This study was designed to determine whether changes in neuroepithelial cell shape involve basal cellular expansion owing to alteration of the cell cycle. Neurulating chick embryos were treated with colchicine to arrest and accumulate cells in metaphase, and colchicine indices and cell generation times were calculated for the neural plate. During bending of the neural plate, cell generation time in the median hinge point, which contains predominantly wedge-shaped cells, was significantly longer than that in adjacent lateral areas of the neural plate, which contain predominantly spindle-shaped cells. In addition, cell generation time in the flat neural plate, which contains predominantly spindle-shaped cells and has not yet differentiated into the median hinge point and lateral subdivisions, was identical to that in lateral areas of the bending neural plate but was significantly shorter than that in the median hinge point. These results support the hypothesis that changes in neuroepithelial cell shape from spindle-like to wedge-like involve basal cellular expansion owing to alteration of the cell cycle. Additional tests of this hypothesis and studies on the role of localized cell shape changes in neurulation are in progress.

Animals↗
PubMed2003

Induction of L-form-like cell shape change of Bacillus subtilis under microculture conditions.

A remarkable cell shape change was observed in Bacillus subtilis strain 168 under microculture conditions on CI agar medium (Spizizen's minimal medium supplemented with a trace amount of yeast extract and Casamino acids). Cells cultured under a cover glass changed in form from rod-shaped to spherical, large and irregular shapes that closely resembled L-form cells. The cell shape change was observed only with CI medium, not with Spizizen's minimum medium alone or other rich media. The whole-cell protein profile of cells grown under cover glass and cells grown on CI agar plates differed in several respects. Tandem mass analysis of nine gel bands which differed in protein expression between the two conditions showed that proteins related to nitrate respiration and fermentation were expressed in the shape-changed cells grown under cover glass. The cell shape change of CI cultures was repressed when excess KNO3 was added to the medium. Whole-cell protein analysis of the normal rod-shaped cells grown with 0.1% KNO3 and the shape-changed cells grown without KNO3 revealed that the expression of the branched-chain alpha-keto acid dehydrogenase complex (coded by the bfmB gene locus) was elevated in the shape-changed cells. Inactivation of the bfmB locus resulted in the repression of cell shape change, and cells in which bfmB expression was induced by IPTG did show changes in shape. Transmission electron microscopy of ultrathin sections demonstrated that the shape-changed cells had thin walls, and plasmolysis of cells fixed with a solution including 0.1 M sucrose was observed. Clarifying the mechanism of thinning of the cell wall may lead to the development of a new type of cell wall biosynthetic inhibitor.

Bacillus subtilis↗
PubMed1995

Expression of 18.6/CD23 antigen on human lymphoid progenitor cell lines and phorbol 12-myristate 13-acetate (PMA)-induced microglia-shaped cells.

The nature of lymphoid progenitors and factor(s) determining commitment to either the T- or B-lymphocyte pathway are poorly understood in the human system. In this study, we generated a monoclonal antibody (MoAb), 18.6, that recognizes a cell surface antigen on a human lymphoid progenitor cell line (FL4.4). MoAb 18.6 reacted with lymphoid progenitor lines, B lymphoid cell lines, and myelomonocytic cell lines. It did not react with any T cell or erythroid leukemic cell lines. Two color FACS analyses of normal lymphoid tissues showed that MoAb 18.6 reacted with a majority of CD20+ mature B cells and a minority of CD64+ monocytes. Molecules of 3 different sizes with MW of 34, 45, and 68 Kd were precipitated with MoAb 18.6 from the lymphoid progenitor cell line. The 18.6 antigen was not expressed on a fetal liver-derived lymphoid progenitor-like cell line, FL1.4, which has the capacity to differentiate into microglia-shaped cells upon PMA-stimulation. Stimulation of FL1.4 cells with PMA induced expression of the 18.6 antigen within 24 hr and the microglia-shaped cells stained positively with MoAb 18.6. Finally, cloning of a cDNA that encoded the 18.6 antigen revealed that the 18.6 antigen is identical to the CD23 antigen. Taken together, these data suggest that the 18.6/CD23 antigen is expressed on lymphoid precursors at a very early stage of differentiation.

Adult↗
PubMed2005

Regulatory network for cell shape changes during Drosophila ventral furrow formation.

Rapid and sequential cell shape changes take place during the formation of the ventral furrow (VF) at the beginning of Drosophila gastrulation. At the cellular level, this morphogenetic event demands close coordination of the proteins involved in actin cytoskeletal reorganization. In order to construct a regulatory network that describes these cell shape changes, we have used published genetic and molecular data for 18 genes encoding transcriptional regulators and signaling pathway components. Based on the dynamic behavior of this network we explored the hypothesis that the combination of three recognizable phenotypes describing wild type or mutant cell types, during VF invagination, correspond to different activation states of a specific set of these gene products, which are point attractors of the regulatory network. From our results, we recognize missing components in the regulatory network and suggest alternative pathways in the regulation of cell shape changes during VF formation.

Animals↗
PubMed1982

Cell shape and cartilage differentiation of early chick limb bud cells in culture.

The onset of chondrogenesis in te embryonic chick is preceded by a prechondrogenic condensation of the prospective cartilage cells. Similarly, in culture, the chondrogenic phenotype is only expressed by limb mesoderm cells plated at densities above confluence. This has led to the proposal that chondrogenic differentiation requires immediate histogenic interactions prior to overt chondrogenesis (Solursh et al., 1978, In Vitro 14, 51-61; and, 1980, Dev. Biol. 78, 141-150). It is noticeable that in both the in vitro situations cells secreting a cartilaginous matrix are rounded in shape. Recently, Glowacki, Trepman and Folkman (personal communication) have shown a dependence of phenotypic expression by mature chondrocytes on cell shape. Cells maintained in a rounded configuration by culturing on a semi-adhesive substratum (poly(HEMA)) synthesised more sulphur-containing extracellular matrix than cells allowed to flatten on normal tissue culture plastic. We have investigated whether there is a similar shape-dependent relationship in the differentiation of chick embryonic mesoblasts into actively secreting chondroblasts. Our results show that a rounded cell shape is conductive to the synthesis of a sulphated matrix.

Animals↗
PubMed1996

AKR1 encodes a candidate effector of the G beta gamma complex in the Saccharomyces cerevisiae pheromone response pathway and contributes to control of both cell shape and signal transduction.

Mating pheromones of Saccharomyces cerevisiae control both signal transduction events and changes in cell shape. The G beta gamma complex of the pheromone receptor-coupled G protein activates the signal transduction pathway, leading to transcriptional induction and cell cycle arrest, but how pheromone-dependent signalling leads to cell shape changes is unclear. We used a two-hybrid system to search for proteins that interact with the G beta gamma complex and that might be involved in cell shape changes. We identified the ankyrin repeat-containing protein Akr1p and show here that it interacts with the free G beta gamma complex. This interaction may be regulated by pheromone, since Akr1p is excluded from the G alpha beta gamma heterotrimer. Both haploid and diploid cells lacking Akr1p grow slowly and develop deformed buds or projections, suggesting that this protein participates in the control of cell shape. In addition, Akr1p has a negative influence on the pheromone response pathway. Epistasis analysis demonstrates that this negative effect does not act on the G beta gamma complex but instead affects the kinase cascade downstream of G beta gamma, so that the kinase Ste20p and components downstream of Ste20p (e.g., Ste11p and Ste7p) are partially activated in cells lacking Akr1p. Although the elevated signalling is eliminated by deletion of Ste20p (or components downstream of Ste20p), the growth and morphological abnormalities of cells lacking Akr1p are not rescued by deletion of any of the known pheromone response pathway components. We therefore propose that Akr1p negatively affects the activity of a protein that both controls cell shape and contributes to the pheromone response pathway upstream of Ste20p but downstream of G beta gamma. Specifically, because recent evidence suggests that Bem1p, Cdc24p, and Cdc42p can act in the pheromone response pathway, we suggest that Akr1p affects the functions of these proteins, by preventing them from activating mating-specific targets including the pheromone-responsive kinase cascade, until G beta gamma is activated by pheromone.

Base Sequence↗
PubMed1998

Control of cyclin D1, p27(Kip1), and cell cycle progression in human capillary endothelial cells by cell shape and 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 p27(Kip1), 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.

Actins↗
PubMed1978

Phenomenological model relating cell shape to water reabsorption in proximal nephron.

If the complex pattern of intercellular channels in proximal tubule is determined in part by the forces of large transepithelial water flow, the shape of the cells is an indicator of the type and magnitude of the forces required for water movement and the routes of that flow. To test this thesis, morphologic data and volume flow parameters for rabbit proximal tubule are related generally by a mass balance equation. If the intercellular boundaries are assumed to be highly deformable and to respond to changes in hydrostatic pressure, the solution to that equation is a simple relationship between cell shape and the forces required for water movement. The resulting phenomenological model suggests an important new role for peritubular serum proteins and can be used to compute reasonable values for cell wall hydraulic conductivity, intercellular protein diffusion constant, and a channel fluid osmolality not more than 1% greater than that of luminal fluid. It is concluded that quantitative morphologic studies may serve as a powerful means for evaluating and understanding transport phenomena in the nephron.

Biological Transport↗
PubMed1979

Cell shape as an indicator of volume reabsorption in proximal nephron.

If the complex shape of cells and intercellular channels in the renal proximal tubule is determined in part by the forces of large transepithelial water flow, the cell and channel shapes might serve as indicators of the type and magnitude of the forces required for water flow and the routes of that flow. We review here the known morphologic and functional data from the convoluted and straight portions of the rabbit proximal tubule and test the hypothesis of structure-function correlation in that tissue by means of a mass balance equation. If the lateral cell walls are sufficiently deformable to communicate small transmembrane differences in hydrostatic pressure, the resulting phenomenological model suggests an important new role for peritubular serum proteins and can be used to compute reasonable values for cell wall hydraulic conductivity, intercellular protein diffusion constant, and a channel fluid osmolality not more than 1% greater than that of luminal fluid. We conclude that quantitative morphologic studies may serve as a powerful means for evaluating and understanding transport phenomenons in the nephron.

Animals↗
PubMedDate not supplied

Changes in the actin cytoskeleton of cardiac capillary endothelial cells during ischaemia and reperfusion: the effect of phalloidin on cell shape.

A reduction in capillary dimensions has been demonstrated in postischaemic reperfusion in the heart. The aim of this study was to demonstrate that in ischaemia and ischaemia followed by reperfusion, the change in shape of the constituent endothelial cells can be inhibited by phalloidin which stabilises the actin microfilament system. Isolated, perfused rat hearts were made globally ischaemic both with and without reperfusion and in the presence or absence of phalloidin. Changes in ischaemic endothelial cell dimensions were quantified by measuring whole capillary and luminal cross-sectional areas, abluminal and luminal membrane lengths. The distribution of beta-actin within the endothelial cells was determined by immunocytochemistry. In control hearts, beta-actin is distributed throughout the endothelium with a slight increase towards the luminal membrane. In ischaemia, this was more marked and other patterns of actin distribution were also observed. After reperfusion, a 'double ring' of actin could be distinguished. With phalloidin, the actin staining was more regular and the ring pattern was not observed. Morphometry showed that phalloidin was more effective in reducing endothelial cell shape change after reperfusion than after ischaemia alone. We conclude that endothelial cell shape change on reperfusion can be modified by agents which target the contractile proteins.

Actins↗
PubMed1980

Protein synthesis requires cell-surface contact while nuclear events respond to cell shape in anchorage-dependent fibroblasts.

Anchorage-dependent mouse fibroblasts grow only if attached to and spread on a solid substrate. The suspension of cells in methyl-cellulose results in dramatic, coordinated inhibition of the major RNA and protein synthesis systems, and these systems are sequentially restored when cells are replated on a tissue culture dish surface. In the present report the effects on metabolism of cell reattachment are separated from those of subsequent spreading by controlling cell shape. Macromolecular metabolism is first strongly suppressed by long-term suspension culture. The cells are then replated in the presence of a variety of spreading inhibitors. The recovery of protein synthesis, which rapidly follows reattachment, does not require extensive cell spreading. Contact of a limited portion of the plasma membrane with the solid culture dish surface is apparently a sufficient signal by itself. A very different method of controlling cell shape is afforded by changing culture dish surface adhesivity. Suspended cells are replated on dishes precoated with thin layers of the hydrophilic hydrogen poly(2-hydroxyethyl methacrylate). The final mean cell diameter is then varied over wide limits. As before, protein synthesis recovery is unaffected. However, nuclear events such as DNA and rRNA synthesis and mRNA production are profoundly affected by cell shape. Thus, cell surface contact and cell shape give rise to distinctly different regulatory responses.

Animals↗
PubMed1993

Methods for computer assisted analysis of lymphoid cell shape and motility, including Fourier analysis of cell outlines.

Locomotion of lymphocytes and other leukocytes is an essential feature of the immune system, and therefore the evaluation of the locomotor behaviour of a lymphocyte population is part of its functional analysis. Paradoxically, the locomotor status of leukocytes is usually assessed on the basis of static information, by counting the number of spherical versus non-spherical cells. In this paper we describe two methods for the measurement of shape changes in microscopic images of lymphoid cells. First we computed a simple shape change factor, coined incongruence factor, based on the degree of non-overlap of the contours of the cell at the beginning and at the end of a 1 min time interval. Second we have used Fourier analysis of the cell outline: a function describing the undulations of the cell outline is broken down into sinusoidal 'waves' of increasing frequency, each with its corresponding amplitude. The amplitude values for the first ten frequencies produced a satisfactory mathematical description of lymphoid cell shapes, and the change of these amplitudes over a 1 minute time interval produced a quantitative description of the shape alterations of the cells. We have used five approaches to evaluate the shape and shape changes in the following populations of mouse lymphoma cells: a constitutively low-motile T lymphoma cell line (BW5147), a high-motile hybridoma (BW-O-Li1) either on plastic or on a precultured fibroblast-like monolayer, BW-O-Li1 cells after penetration through the monolayer, and BW-O-Li1 cells after treatment with cytochalasin B. We compare the results from direct visual evaluation of cell shape, from computer assisted assessment of sphericity and from Fourier analysis of cell shape at one moment, with the two methods for quantitative shape change analysis. All approaches revealed a clear distinction between spherical low-motile populations, and non-spherical high-motile cells. Moreover, the incongruence factor proved to be a reliable single parameter of active cell deformation. In addition, the Fourier analysis of cell outlines produced useful measures of static shape and of dynamic shape change, at any user-defined level of accuracy.

Animals↗
PubMed2006

p130-angiomotin associates to actin and controls endothelial cell shape.

Angiomotin, an 80 kDa protein expressed in endothelial cells, promotes cell migration and invasion, and stabilizes tube formation in vitro. Angiomotin belongs to a new protein family with two additional members, Amotl-1 and Amotl-2, which are characterized by conserved coiled-coil domains and C-terminal PDZ binding motifs. Here, we report the identification of a 130 kDa splice isoform of angiomotin that is expressed in different cell types including vascular endothelial cells, as well as cytotrophoblasts of the placenta. p130-Angiomotin consists of a cytoplasmic N-terminal extension that mediates its association with F-actin. Transfection of p130-angiomotin into endothelial cells induces actin fiber formation and changes cell shape. The p130-angiomotin protein remained associated with actin after destabilization of actin fibers with cytochalasin B. In contrast to p80-angiomotin, p130-angiomotin does not promote cell migration and did not respond to angiostatin. We propose that p80- and p130-angiomotin play coordinating roles in tube formation by affecting cell migration and cell shape, respectively.

Actins↗
PubMed2003

Anti-membrane-bound transferrin-like protein antibodies induce cell-shape change and chondrocyte differentiation in the presence or absence of concanavalin A.

Membrane-bound transferrin-like protein (MTf), a glycosylphosphatidylinositol-anchored protein, is expressed at high levels in many tumors and in several fetal and adult tissues including cartilage and the intestine, as well as in the amyloid plaques of Alzheimer's disease, although its role remains unknown. MTf is one of the major concanavalin A-binding proteins of the cell surface. In this study, we examined the effects of anti-MTf antibodies and concanavalin A on cell shape and gene expression, using cultures of chondrocytes and MTf-overexpressing ATDC5 and C3H10T1/2 cells. In cultures expressing MTf at high levels, concanavalin A induced cell-shape changes from fibroblastic to spherical cells, whereas no cell-shape changes were observed with wild-type ATDC5 or C3H10T1/2 cells expressing MTf at very low levels. The cell-shape changes were associated with enhanced proteoglycan synthesis and expression of cartilage-characteristic genes, including aggrecan and type II collagen. Some anti-MTf antibodies mimicked this action of concanavalin A, whereas other antibodies blocked the lectin action. The findings suggest that the crosslinking of MTf changes the cell shape and induces chondrogenic differentiation. MTf represents the first identification of a plant lectin receptor involved in cell-shape changes and the differentiation of animal cells.

Animals↗