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At least 379 records · Page 21Linked to original sources
PubMed2002

Cdc42 antagonizes inductive action of cAMP on cell shape, via effects of the myotonic dystrophy kinase-related Cdc42-binding kinase (MRCK) on myosin light chain phosphorylation.

Rho GTPases play pivotal roles in regulating cell morphology. We previously showed that RhoA acts via ROKalpha to counteract the effects of the classical second messenger cyclic AMP on cell shape changes. Here we show that active Cdc42V12 also competes against the cAMP-induced stellate morphology in SH-EP cells. This Cdc42 effect is not mediated by the RhoA/ ROK pathway but rather the related MRCKalpha, a myotonic dystrophy kinase-related Cdc42-binding kinase. Co-expression of a dominant inhibitory MRCKalpha mutant with Cdc42V12 blocks the ability of the GTPase to counteract cAMP, suggesting that MRCK acts downstream of Cdc42 in this process. Cdc42V12 enhances the phosphorylation of myosin light chain (MLC) at the cell periphery and sustains focal adhesion complexes, while MLC kinase inhibitors destroy focal adhesion complexes and impair the Cdc42V12 protective effect. The data suggest that the maintenance of focal adhesion complexes via the regulation of myosin II activity underlies the ability of Cdc42 to protect against the effect of elevated cAMP.

ADP Ribose Transferases↗
PubMed1988

Electric field-directed cell shape changes, displacement, and cytoskeletal reorganization are calcium dependent.

C3H/10T1/2 mouse embryo fibroblasts were stimulated by a steady electric field ranging up to 10 V/cm. Some cells elongated and aligned perpendicular to the field direction. A preferential positional shift toward the cathode was observed which was inhibited by the calcium channel blocker D-600 and the calmodulin antagonist trifluoperazine. Rhodaminephalloidin labeling of actin filaments revealed a field-induced disorganization of the stress fiber pattern, which was reduced when stimulation was conducted in calcium-depleted buffer or in buffer containing calcium antagonist CoCl2, calcium channel blocker D-600, or calmodulin antagonist trifluoperazine. Treatment with calcium ionophore A23187 had similar effects, except that the presence of D-600 did not reduce the stress fiber disruption. The calcium-sensitive photoprotein aequorin was used to monitor changes in intracellular-free calcium. Electric stimulation caused an increase of calcium to the micromolar range. This increase was inhibited by calcium-depleted buffer or by CoCl2, and was reduced by D-600. A calcium-dependent mechanism is proposed to explain the observed field-directed cell shape changes, preferential orientation, and displacement.

Actin Cytoskeleton↗
PubMed1987

Mutations affecting penicillin-binding proteins 2a, 2b and 3 in Bacillus subtilis alter cell shape and peptidoglycan metabolism.

Bacillus subtilis mutants with altered penicillin-binding proteins (PBPs), or altered expression of PBPs, were isolated by screening for changes in susceptibility to beta-lactam antibiotics. Mutations affecting only PBPs 2a, 2b and 3 were isolated. Cell shape and peptidoglycan metabolism were examined in representative mutants. Cells of a PBP 2a mutant (UB8521) were usually twisted whereas PBP 2b (UB8524) and 3 (UB8525) mutants produced helices, particularly after growth at 41 degrees C. The PBP 2a mutant (UB8521) had a higher peptidoglycan synthetic activity than its parent strain whereas the opposite applied to the PBP 2b mutant UB8524. The PBP 3 mutant (UB8525) had a similar peptidoglycan synthetic activity to that of the parent strain when grown at 37 degrees C, but 40% higher activity after growth at 41 degrees C. The PBP 2a mutant (UB8521) exhibited the same wall thickening activity as the parent, but the PBP 2b and 3 mutants (UB8524 and UB8525) were partially defective in this respect. The changes in the susceptibility of PBP 2a, 2b and 3 mutants to beta-lactam antibiotics imply that these PBPs are killing targets, consistent with the fact that these PBPs are also important for shape determination and peptidoglycan synthesis.

Acyltransferases↗
PubMed2003

Inhibition of p38 mitogen-activated protein kinase interferes with cell shape changes and gene expression associated with Schwann cell myelination.

In the present study we demonstrate that p38, a member of the mitogen-activated protein kinase (MAPK) family, is essential for ascorbate- and laminin-induced myelination in Schwann cell-dorsal root ganglion neuron cocultures. The inhibitory effect of the specific p38 blockers, PD 169316 and SB 203580, on ascorbate-induced myelination was exerted during the early stages (1-2 days) of ascorbate treatment. Inhibition of p38 was further shown to prevent the alignment of Schwann cells along axons in laminin-treated cocultures. The addition of laminin to Schwann cell-dorsal root ganglion neuron cocultures stimulated phosphorylation of p38, thereby demonstrating a link between laminin-induced myelination and p38 activation. Similarly, the small heat shock protein, Hsp27, which is phosphorylated by MAPKAPK2, a downstream substrate of p38, was phosphorylated in response to the addition of laminin to the cocultures. The p38 inhibitors did not affect the proliferation or survival of Schwann cells in the cocultures as assessed by BrdU incorporation and total cell counts. However, p38 inhibition interfered with an early stage in myelination, thereby preventing ascorbate-induced increases in the levels of mRNAs encoding MBP, MAG, and P(0) and reducing laminin deposition. These results indicate that activation of p38 by a signaling pathway(s) involving laminin and appropriate integrin receptor(s) is required for the alignment of Schwann cells with axons that precedes myelination.

Animals↗
PubMed1985

Cell surface and cytokinetic structures in cell shape determination of mouse fibroblasts. Events involved in cell rounding induced by removal of loosely bound macromolecular moieties from the cell surface.

Cell rounding was induced in synchronised mouse embryo fibroblasts without the use of drugs by a new method based on removal from the cell surface of loosely bound macromolecular moieties. The cells were examined by scanning and transmission electron microscopy and also by specific fluorescence methods during experimentally induced progression from the spread to a rounded form to assess changes in the cell surface and in the arrangement of cytoskeletal elements. Early events were a loss of order in the subcortical microfilament network and the formation of surface blebs. This was followed by disintegration of stress fibres and body retraction. Microtubules and intermediate filaments maintained their integrity but moved inwards towards the rounded perinuclear part of the cells. The relationship between surface alterations, organisation of the cytoskeleton and cell conformation is discussed.

Animals↗
PubMed1992

Microfilaments, cell shape changes, and the formation of primary mesenchyme in sea urchin embryos.

Primary mesenchyme formation in sea urchin embryos occurs when a subset of epithelial cells of the blastula move from the epithelial layer into the blastocoel. The role of microfilaments in producing the cell shape changes that characterize this process, referred to as ingression, was investigated in this study. f-Actin was localized by confocal microscopy using labeled phalloidin. The distribution of f-actin was observed before, during, and after ingression and was correlated with cellular movements. Prior to the onset of ingression, staining became intense in the apical region of putative primary mesenchyme and disappeared following the completion of mesenchyme formation. The apical end of these cells constricted coincidentally with the appearance of the intensified staining, indicating that f-actin may be involved in this constriction. In addition, papaverine, a smooth muscle cell relaxant that interferes with microfilament-based contraction, and that was shown in this study to inhibit cytokinesis, diminished apical constriction and delayed ingression. Despite this interference with apical constriction, the basal surface of ingressing cells protruded into the blastocoel. It is suggested that apical constriction, while not necessary for ingression, does contribute to the efficient production of mesenchyme and that protrusion of the basal surface results from changes that occur independent of apical constriction.

Actin Cytoskeleton↗
PubMed2004

An extracellular driving force of cell-shape changes.

The cellular capacity to internalise objects, involving attachment, engulfment and uptake, exists in virtually all organisms. Many uptake reactions are associated with cell signalling. However, the mechanical forces that form endocytotic vesicles are not known. We propose a 'leverage-mediated' uptake mechanism involving lateral cross-linking processes on the cell surface that can generate the configurational energy to create an inverse curvature of the membrane.

Animals↗
PubMed1989

Red blood cell aggregation and sedimentation: the role of the cell shape.

The influence of erythrocyte shape changes on the sedimentation rate was studied in vitro and in vivo. In vitro the highest sedimentation rate was observed with a slight degree of stomatocytosis (morphological index-0.3; i.e. one red cell out of three being a stomatocyte I). With increasing degrees of stomatocytosis the sedimentation rate gradually decreased. Echinocytosis reduced the aggregation and sedimentation very drastically; the sedimentation rate was virtually zero when echinocytosis I or higher degrees were present. The influence of abnormal cell shapes occurring in vivo was studied in patients with an abnormal blood smear. It was found that a severely abnormal red cell morphology reduced the sedimentation rate in a standardized, fibrinogen-rich plasma to about half. These results indicate that the shape plays a crucial role in the aggregation and sedimentation of red cells and they may contribute to the understanding of the interaction of red cells with other cells such as endothelium.

Blood Sedimentation↗
PubMed2000

Fork head prevents apoptosis and promotes cell shape change during formation of the Drosophila salivary glands.

The secretory tubes of the Drosophila salivary glands are formed by the regulated, sequential internalization of the primordia. Secretory cell invagination occurs by a change in cell shape that includes basal nuclear migration and apical membrane constriction. In embryos mutant for fork head (fkh), which encodes a transcription factor homologous to mammalian hepatocyte nuclear factor 3beta (HNF-3beta), the secretory primordia are not internalized and secretory tubes do not form. Here, we show that secretory cells of fkh mutant embryos undergo extensive apoptotic cell death following the elevated expression of the apoptotic activator genes, reaper and head involution defective. We rescue the secretory cell death in the fkh mutants and show that the rescued cells still do not invaginate. The rescued fkh secretory cells undergo basal nuclear migration in the same spatial and temporal pattern as in wild-type secretory cells, but do not constrict their apical surface membranes. Our findings suggest at least two roles for fkh in formation of the embryonic salivary glands: an early role in promoting survival of the secretory cells, and a later role in secretory cell invagination, specifically in the constriction of the apical surface membrane.

Animals↗
PubMed1992

Modulation of endothelial cell shape by SPARC does not involve chelation of extracellular Ca2+ and Mg2+.

SPARC (secreted protein, acidic and rich in cysteine) is an extracellular, Ca(2+)-binding protein that inhibits the spreading of newly plated cells and elicits a rounded morphology in spread cells. In this study, I investigated whether the rounding effect of SPARC depends on the ability of the protein to chelate Ca2+ at the cell surface. Bovine aortic endothelial cells were plated in the presence of different concentrations of SPARC and Ca2+; control experiments were performed with 1 mM EGTA and with Mg2+. Quantitative estimates of cell rounding were calculated according to a rounding index. SPARC, at concentrations between 0.15 and 0.58 microM, elicited rounding (or prevented spreading) of cells cultured for 16-38 h in 0.5-2.0 mM Ca2+. Addition of 0.5-2.0 mM Mg2+ to cells previously rounded in the presence of SPARC did not abrogate the effect of SPARC. When the levels of extracellular Ca2+ were adjusted with 1 mM EGTA to maximum values ranging from 7.1 to 320 microM, cells displayed a rounded morphology in the presence of exogenous SPARC. Although the rounding induced by 1 mM EGTA was essentially reversed by the inclusion of 2 mM Ca2+, cultures containing these reagents together with SPARC maintained the rounded phenotype. These results do not support a mechanism that involves the abstraction of Ca2+ from proteins at the cell surface or the provision of Ca2+ from native extracellular SPARC to cells. Therefore, SPARC does not appear to act as a local chelator of extracellular Ca2+ and Mg2+ and presumably exerts its function as a modulator of cell shape via a different pathway.

Animals↗
PubMed1979

Palate morphogenesis. III. Changes in cell shape and orientation during shelf elevation.

The process of palate shelf elevation has been analyzed by light microscopy in mouse embryos cultured in vitro. The observations presented correlate changes in cell shape and orientation in the palate with the morphogenetic movement of the shelf. These studies suggest that in addition to any physical-chemical force elevating the shelf an active contraction of specific palate cells could also aid the process. Contribution to elevation could be derived from masses of contracting cells from the previously described non-muscle contractile systems in posterior (region 2) and mid-anterior (region 3) palate as well as other peripheral mesenchymal cells. Finally, elongation and contraction of the tongue side epithelial cells may also play a role in palate elevation.

Animals↗
PubMed1975

Form and pattern in ciliated protozoa: analysis of a genic mutant with altered cell shape in Tetrahymena pyriformis, Syngen 1.

A single cell isolated from the sexual progeny of mutagenized parents gave rise to a clone of cells with an abnormal, conical shape. Breeding analysis revealed that this shape results from the action of a single recessive gene, co (conical). Homozygous mutant cells are shorter and wider than wild type cells, and have their widest point at a more posterior position. Nonetheless, cortical parameters such as number of ciliary rows, number of ciliary units within these rows, and positions of contractile vacuole pores remain essentially unchanged in conical cells, suggesting a considerable degree of mutual independence of pattern and form. Shape changes prior to cell division bring about some convergence in form of dividing conical and wild type cells. However, in conical cells the new oral apparatus and fission line form well posterior to the cell equator, so the opisthes are invariably smaller than proters. Macronuclei nonetheless undergo constriction at the normal central location, and the characteristic inequality in the DNA content of the two macronuclear division products is not increased by the conical condition. Generation times are, on the average, nearly the same in the two wild type daughter cells and in conical proters, while the small conical opisthes have generation times averaging one-third longer. This prolongation explains why population doubling times are always somewhat longer in cultures of conical cells than in parallel cultures of wild type cells. The unusually long generation times of conical opisthes allows for the compensation of initial size differences. Observations on shape changes in conjugating cells of various genotypic combinations suggest that the wild type gene product is not freely exchangeable across the conjugation bridge. The implications of the conical phenotype for problems of cellular patterning and positioning of organelle systems are considered in the discussion.

Alleles↗
PubMed1975

Desaggregation of human red blood cells by various surface-active agents as related to changes of cell shape and hemolysis.

The effect of several surface-active substances (Na-oleate, Na-desoxycholate, Triton X 100, Pluronic F 38, Pluronic F 68, Pluronic F 108) on dextran-induced red cell aggregation (RCA) and red cell shape was investigated. Sedimentation measurements and photometric determinations of RCA indicated a desaggregating effect of oleate, Triton, F 38 and F 68. Shape changes were found in the presence of oleate and desoxycholate (crenation) and Triton (cup formation); in addition, these substances induced pronounced hemolysis. No hemolysis and no shape changes were found with any of the Pluronic polyols.

Blood Sedimentation↗
PubMed1979

[Spindle-shaped cell blue naevus with lymph nodes "metastases" (author's transl)].

"Metastases" in lymph nodes are not only found from cellular blue naevi but also from their spindle-shaped cell fascicular type. These "metastases" are mostly situated in the fibrous capsule, very rarely in the parenchyma of the lymph nodes. Individually the cells resembled those of the cutaneous tumour. Their occurence in the peripheral sinuses should be verified. Epitheloid vessel-wall cells (glomus-type cells), sometimes pigmented and occasionally found in large cell aggregates, can be noted in the capsule of the lymph nodes. By several authors, these cells are considered to be benign naevus cells. The histopathogenesis and the clinical importance of the "metastases" from blue naevus are discussed.

Aged↗
PubMed1985

A calcium requirement for electric field-induced cell shape changes and preferential orientation.

C3H/10T1/2 mouse embryo fibroblasts stimulated by a steady electric field (10 V/cm) for 30 min exhibited lamellar retraction on the sides facing the electrodes. Some cells elongated and preferentially oriented with their long axis perpendicular to the field direction. Depletion of external calcium or blockage of calcium influx with lanthanum or the calcium channel blocker D-600 resulted in a reduction of the field-induced response. When external calcium was elevated stepwise from 0 to 10 mM, the field-induced response increased correspondingly. Electric stimulation in the presence of the calcium ionophore A23187 resulted in an increase of spindle-shaped cells with no preferential orientation. This response was blocked by calcium depletion and lanthanum, but not by D-600. The anticalmodulin drug W-13 inhibited the field-induced responses observed in normal buffer as well as in the presence of A23187. Some cell death resulted from prolonged electric field exposure, and the mortality was reduced by calcium depletion, lanthanum or D-600, but was not affected by W-13. We postulate that local calcium influx through channels opened by the electric field produces areas of high intracellular calcium which stimulate the cytoskeletal network to induce lamellar retraction. Prolonged field-induced calcium influx may eventually overcome the cell's mitochondrial calcium-buffer system, leading to necrotic calcification.

Animals↗
PubMed2006

Galphaq-TRPC6-mediated Ca2+ entry induces RhoA activation and resultant endothelial cell shape change in response to thrombin.

RhoA activation and increased intracellular Ca(2+) concentration mediated by the activation of transient receptor potential channels (TRPC) both contribute to the thrombin-induced increase in endothelial cell contraction, cell shape change, and consequently to the mechanism of increased endothelial permeability. Herein, we addressed the possibility that TRPC signals RhoA activation and thereby contributes in actinomyosin-mediated endothelial cell contraction and increased endothelial permeability. Transduction of a constitutively active Galphaq mutant in human pulmonary arterial endothelial cells induced RhoA activity. Preventing the increase in intracellular Ca2+ concentration by the inhibitor of Galphaq or phospholipase C and the Ca2+ chelator, BAPTA-AM, abrogated thrombin-induced RhoA activation. Depletion of extracellular Ca2+ also inhibited RhoA activation, indicating the requirement of Ca2+ entry in the response. RhoA activation could not be ascribed to storeoperated Ca2+ (SOC) entry because SOC entry induced with thapsigargin or small interfering RNA-mediated inhibition of TRPC1 expression, the predominant SOC channel in these endothelial cells, failed to alter RhoA activity. However, activation of receptor-operated Ca2+ entry by oleoyl-2-acetyl-sn-glycerol, the membrane permeable analogue of the Galphaq-phospholipase C product diacylglycerol, induced RhoA activity. Receptor-operated Ca2+ activation was mediated by TRPC6 because small interfering RNA-induced TRPC6 knockdown significantly reduced Ca2+ entry. TRPC6 knockdown also prevented RhoA activation, myosin light chain phosphorylation, and actin stress fiber formation as well as inter-endothelial junctional gap formation in response to either oleoyl-2-acetyl-sn-glycerol or thrombin. TRPC6-mediated RhoA activity was shown to be dependent on PKCalpha activation. Our results demonstrate that Galphaq activation of TRPC6 signals the activation of PKCalpha, and thereby induces RhoA activity and endothelial cell contraction.

Biological Transport↗