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At least 109 records · Page 6Linked to original sources
PubMed2004

The Arabidopsis GNARLED gene encodes the NAP125 homolog and controls several actin-based cell shape changes.

In plants many aspects of cell shape regulation are controlled by actin-dependent processes. The ARP2/3 complex has been recognized as a regulator of actin organization. Mutations in genes encoding components of the ARP2/3 complex lead to cell shape defects in several cell types, including trichomes, epidermal pavement cells and hypocotyl cells. We show here that mutations in the GNARLED (GRL) gene cause a similar range of phenotypes. The GRL gene encodes the Arabidopsis homolog of NAP125, which in animals is known to act as one regulator of the ARP2/3-regulating complex WAVE-HSPC300. As an HSPC300 homolog is present in the Arabidopsis genome but no WAVE homolog has yet been found, the existence of a related regulation pathway was doubtful. Our finding that GRL encodes a putative regulator of the WAVE-HSPC300 complex, NAP125, combined with the phenotypic similarity between arp2/3 and grl mutants, provides evidence that the ARP2/3 complex is indeed regulated by the above mentioned pathway in Arabidopsis.

Actins↗
PubMed1998

D2 dopamine-receptor-mediated inhibition of proliferation of rat lactotropes in culture is accompanied by changes in cell shape.

Dopaminergic agonists are effective in vivo in inhibiting lactotrope proliferation and prolactin (PRL)-secreting pituitary tumors. The purpose of the present study was to demonstrate in vitro actions of dopaminergic agents on proliferation and cell shape of rat lactotropes. Anterior pituitary cells cultured with serum-free, chemically defined medium were treated with dopaminergic agents and were labeled with 5-bromo-2'-deoxyuridine (BrdU) for 3 h before the end of culture. BrdU-labeling indices indicative of the proliferation rate of lactotropes were determined by double immunofluorescence staining for BrdU and PRL. Treatment with dopamine for 21 h decreased BrdU-labeling indices of lactotropes in a dose-dependent manner with a nadir at 3 x 10(-7) M. The inhibitory action of 10(-5) M dopamine appeared 15 h after the initiation of treatment and became pronounced with time up to 33 h. The dopamine action was mimicked by treatment with the D2 receptor agonist bromocriptine at concentrations over 10(-9) M. Phase-contrast microscopy revealed that the flat polygonal cell shape of cultured lactotropes had changed to a round refractive cell shape after treatment with dopamine or bromocriptine, and that these changes in cell shape exactly paralleled those in the BrdU-labeling index. The changes in cell shape of lactotropes were accompanied by changes in subcellular distribution of actin filaments. Pretreatment with 10(-7) M eticlopride, a D2 receptor antagonist, blocked the dopamine- or bromocriptine-induced changes in both BrdU-labeling index and cell shape. These results suggest that (1) the in vitro experimental system established in the present study is a good model for studying the mechanism of the antiproliferative action of dopamine and (2) D2-receptor-mediated inhibition of proliferation of lactotropes in serum-free culture is closely related to changes in actin organization and cell shape.

Actins↗
PubMed2005

Distinct protease pathways control cell shape and apoptosis in v-src-transformed quail neuroretina cells.

Intracellular proteases play key roles in cell differentiation, proliferation and apoptosis. In nerve cells, little is known about their relative contribution to the pathways which control cell physiology, including cell death. Neoplastic transformation of avian neuroretina cells by p60(v-src) tyrosine kinase results in dramatic morphological changes and deregulation of apoptosis. To identify the proteases involved in the cellular response to p60(v-src), we evaluated the effect of specific inhibitors of caspases, calpains and the proteasome on cell shape changes and apoptosis induced by p60(v-src) inactivation in quail neuroretina cells transformed by tsNY68, a thermosensitive strain of Rous sarcoma virus. We found that the ubiquitin-proteasome pathway is recruited early after p60(v-src) inactivation and is critical for morphological changes, whereas caspases are essential for cell death. This study provides evidence that distinct intracellular proteases are involved in the control of the morphology and fate of v-src-transformed cells.

Animals↗
PubMed2006

Mitosis-specific mechanosensing and contractile-protein redistribution control cell shape.

Because cell-division failure is deleterious, promoting tumorigenesis in mammals, cells utilize numerous mechanisms to control their cell-cycle progression. Though cell division is considered a well-ordered sequence of biochemical events, cytokinesis, an inherently mechanical process, must also be mechanically controlled to ensure that two equivalent daughter cells are produced with high fidelity. Given that cells respond to their mechanical environment, we hypothesized that cells utilize mechanosensing and mechanical feedback to sense and correct shape asymmetries during cytokinesis. Because the mitotic spindle and myosin II are vital to cell division, we explored their roles in responding to shape perturbations during cell division. We demonstrate that the contractile proteins myosin II and cortexillin I redistribute in response to intrinsic and externally induced shape asymmetries. In early cytokinesis, mechanical load overrides spindle cues and slows cytokinesis progression while contractile proteins accumulate and correct shape asymmetries. In late cytokinesis, mechanical perturbation also directs contractile proteins but without apparently disrupting cytokinesis. Significantly, this response only occurs during anaphase through cytokinesis, does not require microtubules, and is independent of spindle orientation, but is dependent on myosin II. Our data provide evidence for a mechanosensory system that directs contractile proteins to regulate cell shape during mitosis.

Animals↗
PubMed1988

Culture of granulosa cells in collagen gels: the influence of cell shape on steroidogenesis.

The gonadotropic regulation of granulosa cells steroidogenesis in vitro has been shown to be accompanied by cellular rounding. In this study, the possible relationship between cell shape, microtubules, and granulosa cell steroidogenesis in vitro was further explored by culturing (24 h) granulosa cells obtained from antral follicles of pregnant mare's serum gonadotropin-treated rats in either Eagles's Minimum Essential Medium alone (MEM-cells) or in collagen gels (GEL-cells) in the absence or presence of colchicine, a microtubule-depolymerizing agent previously shown to inhibit cell-spreading in vitro. Cellular morphology was assessed by electron microscopy and compared with that seen in vivo. In addition, the influence of the various culture conditions on progesterone and 20 alpha-hydroxy-pregn-4-en-3-one (20 alpha-OH-progesterone) secretion was determined by specific radioimmunoassays. Whereas the majority of granulosa cells in sections of antral follicles appeared rounded in shape, cells cultured in MEM underwent considerable spreading and assumed a variety of shapes at the end of 24 h of culture. GEL-cells, on the other hand, remained rounded and had cellular diameters only slightly larger than those observed in vivo. They also secreted more progesterone (almost 3-fold) and less 20 alpha-OH-progesterone (0.6-fold) than MEM-cells. Colchicine increased the secretion of progesterone (1.6-fold) and 20 alpha-OH-progesterone (1.8-fold) comparably in MEM-cells but had no influence on the secretion of either progestin by GEL-cells. Hence, although colchicine-stimulated progestin secretion by granulosa cell monolayers appeared to reflect increased metabolism of substrate-possibly due to a closer association between lipid droplets and mitochondria, the elevated secretion of progesterone by GEL-cells may have been largely due to a shift in the equilibrium between progesterone and its inactive 20 alpha-reduced metabolite. The high ratio of 20 alpha-OH-progesterone to progesterone secretion seen in MEM-cultured cells may be an adaptation of granulosa cell metabolism to culture as monolayers on plastic or glass surfaces. The morphology of GEL-rather than MEM-cells resembled closely that seen in vivo. This culture method may represent a more physiologic approach to the maintenance of granulosa and other steroidogenic cells in vitro and provide a more appropriate means of assessing cytoskeletal function in the regulation of steroid hormone production.

20-alpha-Dihydroprogesterone↗
PubMed1981

Changes in cell shape and induction of cell differentiation in the protozoan Herpetomonas samuelpessoai by cholinergic drugs.

Carbamylcholine, Pilocarpine and Atropine, but not Epinephrine, inhibited the motility of Herpetomonas samuelpessoai, when added to the suspension medium for 1 h. In addition, protozoan cells became spherical under the influence of atropine. This drug also induced the formation of the more differentiated opistomastigote form of the protozoan, in 60 per cent of growing cells, whereas these forms represented less than 5 per cent in untreated cultures. This may indicate that cholinergic receptors are present in this protozoan.

Animals↗
PubMed1993

Binding of cyclosporine by erythrocytes: influence on cell shape and deformability.

Cyclosporine is a widely used immunosuppressive drug with a high affinity for erythrocytes. It was hypothesized that the hydrophobic agent would interact with the erythrocyte membrane, which could cause a shape change and alter cell deformability. Administration of 300 mg cyclosporine in vivo and incubation of erythrocytes with concentrations up to 100 mg l-1 in vitro at room temperature showed that cyclosporine is found in the cytoplasm, but not in the membrane of erythrocytes and that cell shape or deformability were not affected. Incubation of erythrocytes with the highest cyclosporine concentration (100 mg l-1) at 37 degrees C lead to a time-dependent, slight stomatocytic shape transformation, indicating that the drug is intercalated preferentially into the inner hemileaflet of the membrane under these conditions. Cyclosporine metabolites had no effect on the cell shape. The shape of erythrocyte ghosts was neither affected by cyclosporine nor by its metabolites. It is concluded that cyclosporine is bound in the erythrocyte cytoplasm and does not affect the cell membrane and cell deformability at therapeutic concentrations. These results may contribute to a better understanding of the interactions of cyclosporine with cells.

Adult↗
PubMed2005

Epithelial cell shape and Rho small GTPases.

In epithelial cells, morphology is intrinsically related to function. Typically, polarization (i.e. acquisition of a cuboidal cell shape) must occur prior to terminal differentiation and functionality of epithelial sheets. Extensive work has been performed to understand the initial steps that drive cell-cell contact assembly, a process that is essential for polarization. However, not much is known about the subsequent steps that lead to remodelling of actin cytoskeleton and concomitant cell shape changes. Here we review what is known about actin organization during epithelial polarization, and discuss current models for junction assembly, actin reorganization and signalling pathways that may contribute to the generation of a polarized epithelial morphology.

Animals↗
PubMed2005

Nuclear receptor NHR-25 is required for cell-shape dynamics during epidermal differentiation in Caenorhabditis elegans.

Epithelial cell shape changes underlie important events in animal development. During the postembryonic life of the nematode Caenorhabditis elegans, stem epidermal seam cells lose and actively renew mutual adherens junction contacts after each asymmetric division that separates them. The seam cell contacts are important for epidermal differentiation, but what regulates the cell-shape changes that restore them is unknown. Here, we show that NHR-25, a transcription factor of the nuclear receptor family, is expressed in the seam cells and is necessary for these cells to elongate and reach their neighbors after the asymmetric divisions. A failure to do so, caused by nhr-25 RNA interference, compromises the subsequent fate of seam-cell anterior daughters. Unexpectedly, the lack of cell-cell contacts does not prevent a unique seam cell to produce a neuroblast, even though a homeotic gene (mab-5) that normally prevents the neuroblast commitment is ectopically expressed in the absence of nhr-25 function. Seam cells lacking mutual contacts display reduced expression of a Fat-like cadherin marker cdh-3::gfp. Although some seam cells retain the ability to fuse at the final larval stage, the resulting syncytium shows gaps and bifurcations, translating into anomalies in cuticular ridges (alae) produced by the syncytium. nhr-25 RNAi markedly enhances branching of the alae caused by a mutant cuticular collagen gene rol-6. Silencing of nhr-25 also disturbs epidermal ultrastructure, which is probably the cause of compromised cuticle secretion and molting. Cell shape dynamics and molting thus represent distinct roles for NHR-25 in epidermal development.

Animals↗
PubMed1998

Activation of inositol 1,4,5-trisphosphate receptors induces transient changes in cell shape of fertilized Xenopus eggs.

Injection of inositol 1,4,5-trisphosphate (InsP3) into fertilized Xenopus eggs induced transient changes in cell shape. The region around the injected site contracted during the first 2 min, followed by swelling. These changes which initiated at the injected site extended toward the opposite side. Injection of adenophostin B, a potent InsP3 receptor agonist, also induced similar morphological changes, which suggested that InsP3 receptor activation, and not the action of InsP3 metabolites, is responsible for these changes. To determine whether these changes correlate to InsP3 receptor-mediated calcium release, we examined the morphological changes and those in intracellular free calcium concentrations ([Ca2+]i). A calcium wave was observed to precede the propagation of changes in cell shape by about 2 min. The extent of propagation of cell shape changes varied with the eggs but consistently depended on the extent of the calcium wave propagation. Changes in cell shape were inhibited in eggs injected with the calcium chelator, BAPTA, indicating that calcium released from the InsP3-sensitive calcium store is required for cell shape changes. During the cell shape changes, the contracted region was strongly stained with rhodamine-phalloidin, which suggests that structural changes of actin filaments are involved in the cortical changes. We propose that spatiotemporally controlled elevation of intracellular calcium induces successive cortical cytoskeletal changes that are responsible for changes in cell shape. These observations provide insight into the potency of InsP3/calcium signaling in the regulation of cortical cytoskeleton.

Actin Cytoskeleton↗
PubMed1990

Cell shape changes during gastrulation in Drosophila.

The first morphogenetic movement during Drosophila development is the invagination of the mesoderm, an event that folds a one-layered epithelium into a multilayered structure. In this paper, we describe the shape changes and behaviour of the cells participating in this process and show how mutations that change cell fate affect this behaviour. We divide the formation of the mesodermal germ layer into two phases. During the first phase, the ventral epithelium folds into a tube by a series of concerted cell shape changes (ventral furrow formation). Based on the behaviour of cells in this phase, we conclude that the prospective mesoderm is not a homogeneous cell population, but consists of two subpopulations. Each subpopulation goes through a distinctive sequence of specific cell shape changes which together mediate the invagination of the ventral furrow. In the second phase, the invaginated tube of mesoderm loses its epithelial character, the mesoderm cells disperse, divide and then spread out along the ectoderm to form a single cell layer. To test how ventral furrow formation depends on cell fates in the mesoderm and in neighbouring cells we alter these fates genetically using maternal and zygotic mutations. These experiments show that some of the aspects of cell behaviour specific for ventral furrow cells are part of an autonomous differentiation programme. The force driving the invagination is generated within the region of the ventral furrow, with the lateral and dorsal cell populations contributing little or none of the force. Two known zygotic genes that are required for the formation of the mesoderm, twist and snail, are expressed in ventral furrow cells, and the correct execution of cell shape changes in the mesoderm depends on both. Finally, we show that the region where the ventral furrow forms is determined by the expression of mesoderm-specific genes, and not by mechanical or other epigenetic properties of the egg.

Animals↗
PubMed1997

Phenotype and proliferation characteristics of cultured spindle-shaped cells obtained from normal human skin and lesions of dermatofibroma, Kaposi's sarcoma, and dermatofibrosarcoma protuberans: a comparison with fibroblast and endothelial cells of the dermis.

Normal human dermis contains mesenchymal cells that are generally referred to as fibroblasts. However the relationships between fibroblasts and endothelial cells with respect to the types of spindle-shaped cells that are present in cultures obtained from tumor bearing-skin is unclear. To explore the potential heterogeneity amongst dermal-derived cells that grow in culture with a spindle-shaped morphology, we compared the immunophenotype and growth characteristics of several types of cells. Besides dermal fibroblasts and microvascular endothelial cells derived from normal adult skin, we also studied large vessel-derived endothelial cells, and spindle-shaped cells derived from three different tumor-bearing dermal-based neoplasms. Kaposi's sarcoma (KS), dermatofibroma (DF), and dermatofibrosarcoma protuberans (DFSP). A broad panel of eight different antibodies were used to immunophenotype the multi-passaged cultured cells. Spindle-shaped cells from all three neoplasms could be distinguished from the normal skin derived fibroblasts by their constitutive expression of factor XIIIa, and the gamma-interferon induced expression of VCAM-1. All seven types of cultured cells stained positive for s-actin and proline-4-hydroxylase, and none of the cells expressed CD34. Both large and small-vessel derived endothelial cells expressed factor VIII, ELAM-1, and VCAM-1. Using two different types of growth media, significant differences were also observed amongst these cultured cell types. Spindle-shaped cells from DFSP did not grow in DMEM containing 10% fetal bovine serum (DMEM-FBS); but they proliferated in KS cell growth medium (KSGM). Spindle-shaped cells from DF grew best in KSGM, but not in DMEM-FBS. KS tumor cells grew well in KSGM, but not in DMEM-FBS. Fibroblasts proliferated in DMEM-FBS, but failed to grow in KSGM; and even when pre-treated with conditioned medium from a transformed KS cell line (i.e. SLK cells), no fibroblast proliferation could be induced in KSGM. These results indicate that KS cell line (i.e. SLK cells), no fibroblast proliferation could be induced in KSGM. These results indicate that even though dermal-derived cells can have an identical spindle-shape by light microscopy, significant heterogeneity can be defined amongst such cells from normal and tumor-bearing human skin. Having established culture conditions to propagate these different cell types and phenotypic criteria to distinguish them from one another, will provide new research opportunities to explore the function and ontogeny of the diverse mesenchymal cells that take on a spindle-shaped morphology in culture.

Adult↗
PubMed1994

The seventh Datta Lecture. Membrane bending energy concept of vesicle- and cell-shapes and shape-transitions.

The main objective of this lecture is to discuss the role of lipid-bilayer elasticity (1) for the self-organization of lipid/protein-bilayers (2) for the stabilization of domain structures and shapes of cell membranes and (3) for the control of shape transitions (e.g. bud- and pit-formation) and shape instabilities (vesicle fission). It is demonstrated that many complex shape transitions of cell membranes can be mimicked by single lipid bilayer vesicles by simply varying the area-to-volume ratio or by chemically induced bending moments suggesting that these processes are governed by the universal minimum bending energy concept of closed shells composed of stratified membranes. The essential role of the coupling between curvature and phase separation in mixed membranes for the formation and stabilization of local pits and buds or the fission of budded vesicles is demonstrated. Finally, we discuss the consequences of the pronounced thermally excited bending undulations of the hyperelastic membranes for the membrane tension, the material exchange at membrane surfaces and the control of the adhesion of vesicles (or cells) on solid substrates.

Biophysical Phenomena↗
PubMed2003

Control of cell morphogenesis in bacteria: two distinct ways to make a rod-shaped cell.

Cell shape in most eubacteria is maintained by a tough external peptidoglycan cell wall. Recently, cell shape determining proteins of the MreB family were shown to form helical, actin-like cables in the cell. We used a fluorescent derivative of the antibiotic vancomycin as a probe for nascent peptidoglycan synthesis in unfixed cells of various Gram-positive bacteria. In the rod-shaped bacterium B. subtilis, synthesis of the cylindrical part of the cell wall occurs in a helical pattern governed by an MreB homolog, Mbl. However, a few rod-shaped bacteria have no MreB system. Here, a rod-like shape can be achieved by a completely different mechanism based on use of polar growth zones derived from the division machinery. These results provide insights into the diverse molecular strategies used by bacteria to control their cellular morphology, as well as suggesting ways in which these strategies may impact on growth rates and cell envelope structure.

Bacillus subtilis↗
PubMed2000

Cell shape and organelle modification in apoptotic U937 cells.

U937 cells induced to apoptosis, progressively and dramatically modified their cell shape by intense blebbing formation, leading to the production of apoptotic bodies. The blebs evolved with time; milder forms of blebbing involving only a region or just the cortical part of the cytoplasm were observed within the first hour of incubation with puromycin; blebbing involving the whole cell body with very deep constrictions is the most frequent event observed during late times of incubation. The ultrastructural analysis of apoptotic cells revealed characteristic features of nuclear fragmentation (budding and cleavage mode) and cytoplasmatic modifications. The cytoplasm of blebs does not contain organelles, such as ribosomes or mitochondria. Scarce presence of endoplasmic reticulum can be observed at the site of bleb detachment. However, blebbing is a dispensable event as evaluated by using inhibitor of actin polymerization. In the present study, the progressive modifications of the nucleus, mitochondria, nuclear fragmentation, cytoplasmic blebs formation and production of apoptotic bodies in U937 monocytic cells induced to apoptosis by puromycin (an inhibitor of protein synthesis) were simultaneously analyzed.

Apoptosis↗
PubMed1998

PDGF and TGF-beta induce cell shape changes in invertebrate immunocytes via specific cell surface receptors.

The presence of PDGF receptor-alpha- and -beta- and TGF-beta-receptor (type II)-like molecules on the plasma membranes of the immunocytes of the mollusc Mytilus galloprovincialis was demonstrated by an immunocytochemical procedure. Furthermore, the present study provides evidence that PDGF-AB and TGF-beta1 provoke cell shape changes in immunocytes via interactions with the respective receptors and that these extracellular signals are transduced along the phosphoinositide signaling pathway.

Animals↗