Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cell Shape”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed1999

High expression of HHV-8-encoded ORF73 protein in spindle-shaped cells of Kaposi's sarcoma.

Human herpesvirus 8 (HHV-8) has been demonstrated previously in Kaposi's sarcoma (KS) tissues by immunohistochemistry, in situ polymerase chain reaction, and in situ hybridization. The HHV-8-encoded protein ORF73 is a 222- or 234-kd protein named latent nuclear antigen (LNA) or latency-associated nuclear antigen (LANA) that is identified in HHV-8-infected cell lines by immunofluorescence assay. In the present study, a rabbit antibody against a recombinant ORF73 protein was developed. Immunofluorescent staining of a HHV-8-infected cell line, TY-1, showed that the staining pattern of the anti-ORF73 antibody overlapped completely the LANA staining pattern obtained using KS patients' sera. Immunoblotting analysis showed that the anti-ORF73 antibody reacted specifically with 222- and 234-kd proteins that were present in TY-1 and BCBL-1 cell lysates. Immunohistochemistry using a catalyzed signal amplification system demonstrated that the anti-ORF73 antibody reacted exclusively with the majority of KS spindle-shaped cells, showing a nuclear dot-like staining pattern. Some of the ORF73 protein-positive cells also expressed CD34 and vimentin but not CD68 or factor-VIII-related antigen. These data indicate that the anti-ORF73 antibody recognizes LANA and that most KS cells are infected with HHV-8 in the latent phase. Our findings also suggest that ORF73 protein plays an important role in the pathogenesis of KS.

Animals↗
PubMed1998

Immunoelectron microscopic studies indicate the existence of a cell shape preserving cytoskeleton in prokaryotes.

Immunoelectron microscopic studies of prokaryotes were performed with anti-actin antibodies directed against the C terminus of actin. Studies on ultrathin sections revealed high proportions of the overall label close to the cell periphery in Escherichia coli, Ralstonia eutropha, Thermoanaerobacterium thermosulfurigenes, T. thermosaccharolyticum, and Methanococcus jannaschii. Substantial label also in the cytoplasm was observed in Bacillus sp., Methanococcus voltae, and Methanobacterium thermoautotrophicum. Only very minor amounts of label were found in the nucleoid region of the cells. Whole-mount immunogold studies, combined with negative staining, revealed the existence of an intracellular network of fibrils which could be labeled by anti-actin antibodies. This network is assumed to be located below the cytoplasmic membrane all around the cytoplasm. It appears to have properties that would allow its function as a cytoskeleton-like structure preserving cell shape.

Actins↗
PubMed1990

Involvement of cell shape in the replication and segregation of chromosomes in Escherichia coli.

Chromosome replication appears to initiate in E. coli when the dnaA boxes in oriC become filled with DnaA protein, which could simultaneously mediate both the unwinding of the origin for the start of polymerization and the attachment of oriC to the cell envelope (Bramhill and Kornberg, 1988; Løbner-Olesen et al., 1989; Pierucci et al., 1989). The attachment takes place somewhere within the cell half in which the oriC resides. The boundaries of this attachment/replication zone, which cannot include the polar cap, could be demarcated by the polar and centrally located periseptal annuli (Rothfield, this Forum). Since attachment and polymerization are two aspects of the same process, the attachment probably takes place via the polymerizing strand. Once polymerization begins, the oriC with the older template strand moves away from the younger one, by mechanisms unknown, to eventually take up residence in the equivalent domain of the complementary sister cell. Thus, the template strand that stays within its domain corresponds to the strand that was attached during the previous round of replication, and the template that moves away is the one that was not attached. The driving force for this translocation is not specified by our model, but a number of plausible alternatives have been proposed by others (reviewed in Leonard and Helmstetter, 1990). Throughout the ensuing replication and cell division, the chromosomes are located (or can move freely) within the attachment/replication zone of the developing daughter cell (lateral cylinder and septum). At some time during the course of this process, but before the next initiation event, the replication origins must be released from the attachment sites so that the entire process can be repeated. Thus, the probabilistic non-random chromosome segregation is due to the asymmetry of the attachment/replication zone in the cell, whereas the partitioning system itself must possess a mechanism to discriminate between template strands of different ages. This apparent mechanistic relationship between chromosome replication, chromosome partitioning and the maintenance of cell shape may provide an interesting framework for future experiments.

Biomechanical Phenomena↗
PubMed1996

Cell autonomous expression of perlecan and plasticity of cell shape in embryonic muscle of Caenorhabditis elegans.

Perlecan, a component of the extracellular matrix (ECM), is essential for myofilament formation and muscle attachment in Caenorhabditis elegans. We show here that perlecan is a product of muscle and that it behaves in a cell autonomous fashion. That is, perlecan expressed in an individual muscle cell does not spread beyond the borders of the ECM underlying that cell. Using a polyclonal antibody that recognizes all isoforms of perlecan, we demonstrate that this protein first appears extracellularly at the comma stage (approx. 350 min) of development. We also show that during morphogenesis muscle cells have a heretofore undescribed plasticity of shape. This ability to regulate cell shape allows cells within a muscle quadrant to compensate for missing cells and to form a functional quadrant. A dramatic example of this morphological flexibility can be observed in animals in which the D blastomere has been removed by laser ablation. Such animals, lacking 20 of the 81 embryonic body wall muscle cells, can survive to become viable adult animals indistinguishable from wildtype animals. This demonstrates that the assembly of an embryo via a stereotypic lineage does not preclude a more general regulation during morphogenesis. It appears that embryos are flexible enough to immediately compensate for drastic alterations in tissue composition, a feature of development that may be of general importance during evolution.

Animals↗
PubMed1981

The influence of cell shape on the induction of functional differentiation in mouse mammary cells in vitro.

To define more clearly the in vitro conditions permissive for hormonal induction of functional differentiation, we cultured dissociated normal mammary cells from prelactating mice in or on a variety of substrates. Cultivation of an enriched epithelial cell population in association with living adult mammary stroma in the presence of lactogenic hormones resulted in both morphological and biochemical differentiation. This differentiation, however, was not enhanced over that seen when the cells were associated with killed stroma, provided that the killed stroma had a flexibility similar to that of the living stroma. Cells cultured in inflexible killed stroma usually did not differentiate. Cells cultured within the flexible environment of a collagen gel, but removed from the gas-medium interface, differentiated in a manner similar to those cultured in flexible stroma. Cells cultured on the surface of an attached collagen gel were squamous, and their basolateral surfaces were sequestered from the medium; they did not differentiate. Cells cultured on floating collagen gels were cuboidal-columnar, with basolateral surfaces exposed to the medium, and showed good functional differentiation. Cells cultured on inflexible floating collagen gels were extremely flattened and had exposed basolateral surfaces, and showed no evidence of functional differentiation. We infer that assumption of cuboidal to columnar shapes differentiation in vitro. The additional requirement of basolateral cell surface exposure also is important.

Adipose Tissue↗
PubMed2002

The endoplasmic reticulum cation P-type ATPase Cta4p is required for control of cell shape and microtubule dynamics.

Here we describe the phenotypic characterization of the cta4+ gene, encoding a novel member of the P4 family of P-type ATPases of fission yeast. The cta4Delta mutant is temperature sensitive and cold sensitive lethal and displays several morphological defects in cell polarity and cytokinesis. Microtubules are generally destabilized in cells lacking Cta4p. The microtubule length is decreased, and the number of microtubules per cell is increased. This is concomitant with an increase in the number of microtubule catastrophe events in the midzone of the cell. These defects are likely due to a general imbalance in cation homeostasis. Immunofluorescence microscopy and membrane fractionation experiments revealed that green fluorescent protein-tagged Cta4 localizes to the ER. Fluorescence resonance energy transfer experiments in living cells using the yellow cameleon indicator for Ca2+ indicated that Cta4p regulates the cellular Ca2+ concentration. Thus, our results reveal a link between cation homeostasis and the control of cell shape, microtubule dynamics, and cytokinesis, and appoint Ca2+ as a key ion in controlling these processes.

Adenosine Triphosphatases↗
PubMed2003

PINCH-1 is an obligate partner of integrin-linked kinase (ILK) functioning in cell shape modulation, motility, and survival.

PINCH-1 is a widely expressed focal adhesion protein that forms a ternary complex with integrin-linked kinase (ILK) and CH-ILKBP/actopaxin/alpha-parvin (abbreviated as alpha-parvin herein). We have used RNA interference, a powerful approach of reverse genetics, to investigate the functions of PINCH-1 and ILK in human cells. We report here the following. First, PINCH-1 and ILK, but not alpha-parvin, are essential for prompt cell spreading and motility. Second, PINCH-1 and ILK, like alpha-parvin, are crucial for cell survival. Third, PINCH-1 and ILK are required for optimal activating phosphorylation of PKB/Akt, an important signaling intermediate of the survival pathway. Whereas depletion of ILK reduced Ser473 phosphorylation but not Thr308 phosphorylation of PKB/Akt, depletion of PINCH-1 reduced both the Ser473 and Thr308 phosphorylation of PKB/Akt. Fourth, PINCH-1 and ILK function in the survival pathway not only upstream but also downstream (or in parallel) of protein kinase B (PKB)/Akt. Fifth, PINCH-1, ILK and to a less extent alpha-parvin are mutually dependent in maintenance of their protein, but not mRNA, levels. The coordinated down-regulation of PINCH-1, ILK, and alpha-parvin proteins is mediated at least in part by proteasomes. Finally, increased expression of PINCH-2, an ILK-binding protein that is structurally related to PINCH-1, prevented the down-regulation of ILK and alpha-parvin induced by the loss of PINCH-1 but failed to restore the survival signaling or cell shape modulation. These results provide new insights into the functions of PINCH proteins in regulation of ILK and alpha-parvin and control of cell behavior.

Actinin↗
PubMed1991

Cell shape and organization of the contractile apparatus in cultured adult cardiac myocytes.

The isolation and culture of adult cardiac myocytes has proved to be an ideal model system to explore myocardial biology at the cellular level. A major criticism of this model, however, has been that organ-specific characteristics such as cell shape and subcellular structural organization cannot be retained in vitro for prolonged periods of time. Encasing freshly isolated myocytes in a matrix of calcium alginate enables one to maintain the rod-like, three-dimensional (3D) shape of the cultured myocyte. Such preparations more closely resemble their in vivo counterparts with respect to the organization of the contractile apparatus, the transverse tubular system and the sarcoplasmic reticulum than do heart cells cultured on a two-dimensional (2D) plastic surface. Stereologic measurements reveal that myofibrillar volume density (VvMYF) decreases in both non-beating preparations over a 2-week interval, but VvMYF is conserved in cells cultured in an alginate matrix when compared to those myocytes maintained on a laminin-coated substratum. The present observations suggest that in the absence of contractile function myofibrillar atrophy appears responsible for the decline in VvMYF in alginate (3D) preparations, whereas atrophy and subcellular remodelling probably mediate the myofibrillar loss and reorganization that develops when adult heart cells are cultured on a 2D surface.

Alginates↗
PubMed1993

Transformation efficiency of EMS-induced mutants of Streptococcus mutans of altered cell shape.

Some Streptococcus mutans strains change shape from bacillary to coccal or ellipsoid form in response to the ratio of bicarbonate to potassium or of borate to potassium in growth media. So that insight into determinants of shape of these streptococci could be gained, and future genetic studies facilitated, the shapes of a series of transformable and nontransformable strains of S. mutans were studied and attempts made to isolate a mutant of augmented transformability. Several strains were mutagenized by ethylmethane sulfonate and mutants with altered colonial and cellular morphologies isolated. Cell shapes were studied by Gram stain and Nomarski interference microscopy, and by scanning and transmission electron microscopy. Diverse shape-altered mutants were isolated from seven transformable and two nontransformable strains of S. mutans. Among these, length-to-width ratios ranged from > 10 to about 0.25. Regulation of timing of cell division, septum formation, or septum completion events may have been altered in these mutants. While most mutants substantially or completely lost transformability, mutant LT11 had transformation efficiency of 1.3 x 10(-4) to 2.3 x 10(-3), more than two to three orders of magnitude greater than its parental UA159 and the well-known transformable strain GS5(HK), respectively. There was no evidence of production of competence factor by LT11. Competence of LT11 was maintained for at least six months upon storage at -70 degrees C, facilitating its use for genetic studies. While the morphologies of several shape-altered mutants were no longer responsive to changes of the bicarbonate/potassium, unlike those of their parentals, the morphology of LT11 persisted in its response to this condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Ethyl Methanesulfonate↗
PubMed1993

Two novel protein kinase C-related genes of fission yeast are essential for cell viability and implicated in cell shape control.

Two novel protein kinase C (PKC)-like genes, pck1+ and pck2+ were isolated from fission yeast by PCR. Both contain common domains of PKC-related molecules, but lack a putative Ca(2+)-binding domain so that they may belong to the nPKC group. Gene disruption of pck1+ and pck2+ establishes that they share an overlapping essential function for cell viability. Cells of a single pck2 deletion display severe defects in cell shape; they are irregular and sometimes pear-like instead of cylindrical. In contrast, the induced overexpression of pck2+ is lethal, producing multiseptated and branched cells. These results suggest that fission yeast PKC-like genes are involved in the polarity of cell growth control. We show that pck2 is allelic to sts6, a locus we have previously identified by its supersensitivity to staurosporine, a potent protein kinase inhibitor [Toda et al. (1991) Genes Dev., 5, 60-73]. In addition, the lethal overexpression of pck2+ can be suppressed by staurosporine, indicating that fission yeast pck1 and pck2 are molecular targets of this inhibitor.

Alkaloids↗
PubMed1976

Time-lapse filming of cellular interactions within living tissues. III. The role of cell shape.

By a further development of the technique for time-lapse filming of organ cultures, it has become possible to observe the internal structure of the living tissues and to study the dynamics of intercellular contacts within the tissue. This method has been applied to a study of the interaction between the tissues of the chick chorioallantoic membrane and non-malignant fibroblasts, polyoma virus-transformed fibroblasts, and Harding-Passey melanoma cells. The behaviour of these cells in the absence and in the presence of colcemid has been investigated. From these studies it is concluded that disturbances in cell shape brought about by colcemid do not affect the invasive properties whereas the surface polypodial activity shown by the malignant cells is a major factor in tumour invasion.

Cell Membrane↗
PubMed1992

The divIVB region of the Bacillus subtilis chromosome encodes homologs of Escherichia coli septum placement (minCD) and cell shape (mreBCD) determinants.

Mutation of the divIVB locus in Bacillus subtilis causes frequent misplacement of the division septum, resulting in circular minicells, short rods, and filaments of various sizes. The divIVB1 mutant allele maps to a region of the chromosome also known to encode sporulation (spo0B, spoIVF, spoIIB) and cell shape (rodB) determinants. This study reports the cloning and sequence analysis of 4.4 kb of the B. subtilis chromosome encompassing the divIVB locus. This region contains five open reading frames (ORFs) arranged in two functionally distinct gene clusters (mre and min) and transcribed colinearly with the direction of replication. Although sequence analysis reveals potential promoters preceding each gene cluster, studies with integrational plasmids suggest that all five ORFs are part of a single transcription unit. The first gene cluster contains three ORFs (mreBCD) homologous to the mre genes of Escherichia coli. We show that rodB1 is allelic to mreD and identify the rodB1 mutation. The second gene cluster contains two ORFs (minCD) homologous to minC and minD of E. coli but lacks a minE homolog. We show that divIVB1 is allelic to minD and identify two mutations in the divIVB1 allele. Insertional inactivation of either minC or minD or the presence of the divIVB region on plasmids produces a severe minicell phenotype in wild-type cells. Moreover, E. coli cells carrying the divIVB region on a low-copy-number plasmid produce minicells, suggesting that a product of this locus may retain some function across species boundaries.

Alleles↗
PubMed2000

act up controls actin polymerization to alter cell shape and restrict Hedgehog signaling in the Drosophila eye disc.

Cells in the morphogenetic furrow of the Drosophila eye disc undergo a striking shape change immediately prior to their neuronal differentiation. We have isolated mutations in a novel gene, act up (acu), that is required for this shape change. acu encodes a homolog of yeast cyclase-associated protein, which sequesters monomeric actin; we show that acu is required to prevent actin filament polymerization in the eye disc. In contrast, profilin promotes actin filament polymerization, acting epistatically to acu. However, both acu and profilin are required to prevent premature Hedgehog-induced photoreceptor differentiation ahead of the morphogenetic furrow. These findings suggest that dynamic changes in actin filaments alter cell shape to control the movement of signals that coordinate a wave of differentiation.

Actins↗
PubMed1979

Determinants of cell shape and orientation: a comparative Golgi analysis of cell-axon interrelationships in the developing neocortex of normal and reeler mice.

Patterns of dendritic development in the neocortex of normal and reeler E15-17 mouse embryos are studied in Golgi impregnations. Interactions between dendrites and axon-rich strata appear to be critical determinants of dendritic morphology in both genotypes. Firstly, axon-dendrite proximity appears to stimulate dendritic sprouting, elongation and branching. Secondly, the position of the axon-rich strata with respect to the differentiating cell appears to determine the direction of dendritic growth and thereby the ultimate configuration of the dendritic arbor. With regard to specific cell configurations, a multipolar form is generated when the cell is embedded in an axon-rich zone. A monopolar or bipolar configuration is achieved when the cell lies in the axon-poor cortical plate and addresses and axon-rich stratum with one or both radially extended migratory processes. Such variations in the configuration of neurons with polar dendritic systems may be observed uniquely in the mutant cortex because axon-rich zones are stratified anomalously at multiple levels in the cortical plate. As a consequence, polar dendritic systems develop from either the superior, the inferior or both somatic poles of postmigratory cells. Pyramidal cells may, therefore, develop a normal upright or an abnormal "upside-down" disposition. Regardless of the orientation of the polar dendritic system, the axon emerges from the inferior aspect of the cell suggesting that there has been no rotation of the original migratory axis of the cell.

Afferent Pathways↗
PubMed1987

Cell shape modulation alters glycosylation of a metastatic melanoma cell-surface antigen.

B16-F1 melanoma cells cultivated in vitro as spheroids on a non-adhesive substrate acquire in a reversible fashion an increase in lung colonization in vivo as compared to cells cultured as a monolayer. After neuraminidase treatment of protein blots, the spheroidal cells expressed an increased binding of 125I-labelled peanut lectin (PNA) to a unique glycoprotein of Mr 78,000 (gp78) which after desialylation migrated in SDS-polyacrylamide gels as an Mr 86,000 protein. Antibodies were generated against this glycoprotein purified on PNA-Sepharose and its expression on the surface of viable B16-F1 cells was demonstrated. Growth of B16-F1 melanoma cells in suspension is associated with the altered glycosylation of gp78 which may be related to the increased metastatic ability of these cells. In vitro treatment of B16-F1 cells with anti-gp78 Fab fragments prior to their injection into the tail veins of syngeneic mice resulted in a 2-fold increase in the appearance of tumor lung colonies.

Animals↗
PubMed2002

p60(v-src) and serum control cell shape and apoptosis via distinct pathways in quail neuroretina cells.

We made use of QNR cells transformed by a thermosensitive (tsNY68) strain of the Rous sarcoma virus (RSV) to compare the effect of p60(v-src) and serum in cultured nerve cells. In this system, both p60(v-src) heat inactivation and serum removal resulted in growth arrest in G1. In both cases, growth arrest was reversible since cell proliferation was rapidly re-induced following respectively p60v-src renaturation or serum re-addition. However, cells did not fully recover their ability to grow in soft agar, suggesting that, in contrast to the cell cycle machinery, the transforming capacities of these cells have been irreversibly altered. We found that p60(v-src) kinase activity prevented detachment from the substratum and cell death following serum removal. Thermal inactivation of p60(v-src) at restrictive temperature (41.5 degrees C), but not serum removal, resulted in dramatic morphological changes, which occurred 4 h after temperature shift up to 41.5 degrees C. Later on, typical features of apoptotic cells could be observed. Cell death was greatly reduced by the caspase-3 inhibitor ZVAD.FMK, but not by the caspase-1 inhibitor Ac-YVAD.CHO. Together, these results suggested that p60(v-src) and serum factors act on distinct pathways, at least in part. In an attempt to identify the signalling pathways involved in the cell response to p60(v-src) down regulation, we found that Erk and Rac were rapidly inactivated following temperature shift up to 41.5 degrees C. Thus, the combined effects of p60(v-src) and serum factors on the cytoskeleton dynamics and the apoptosis machinery are essential for full neoplastic transformation of neuroretina cells.

Animals↗
PubMed1997

v-src-induced cell shape changes in rat fibroblasts require new gene transcription and precede loss of focal adhesions.

The mechanism of v-src-induced morphological transformation is still obscure. We compared LA29 rat fibroblasts, which express a temperature-sensitive (ts) v-src mutant, with D1025 rat fibroblasts, transfected with a ts mutant of v-fps. Upon transformation, LA29 cells adopted an elongated shape with reduced focal adhesions and loss of actin stress fibers. In contrast, activation of v-fps in D1025 cells had little effect on morphology. In both cells, paxillin was strongly tyrosine phosphorylated upon activation of the kinases. This indicates that paxillin phosphorylation is not required, or not sufficient, for the v-src-induced disruption of focal adhesions. As previously described by others, v-src activated the ras-MAP kinase (MAPK) pathway, as indicated by tyrosine phosphorylation of the rasGAP-associated proteins p62 and p190 and MAPK phosphorylation. Since MAPK affects transcription, this suggested that novel gene transcription was required. This notion was confirmed using actinomycin D and cycloheximide, which did not impair activation of v-src kinase activity, but completely blocked v-src-induced morphological changes, as demonstrated using image analysis. Furthermore, we observed that v-src-induced changes in cell shape occurred before the reduction in number and size of focal adhesions. We conclude that v-src-induced transformation of rat fibroblasts depends on synthesis of a protein, which induces rapid changes in cell shape that precede the loss of focal adhesions.

Actin Cytoskeleton↗
PubMed1993

Red cell shape changes following trigger finger fatigue in subjects with chronic tiredness and healthy controls.

AIMS: To investigate the possibility of a correlation between the percentage of nondiscocytic erythrocytes and muscle fatiguability in subjects with the symptom of chronic tiredness. METHODS: Sixty nine volunteers suffering from persisting or intermittent tiredness and 72 healthy controls provided 3-drop samples of venous blood for red cell shape analysis before and after inducing fatigue in the trigger finger muscles by repeatedly pulling the trigger of an antique revolver. Elapsed time and the number of pulls were recorded. A work index was calculated from the number of trigger pulls divided by the time in seconds then multiplied by the number of trigger pulls. RESULTS: Subjects with tiredness had fewer discoid cells (males 62.5% vs 69.2%, p = 0.029; females 65.8% vs 71.8%, p = 0.002) than controls. They also had fewer trigger pulls (males 62.3 vs 84.0, p = 0.003; females 29.5 vs 36.8, p = 0.042) and lower "work indices" (males 75.6 vs 104.7, p = 0.001; females 26.1 vs 39.6, p = 0.001) than controls at the first trigger pulling. After 5 minutes rest the number of trigger pulls for males was fewer than the controls (56.0 vs 64.2) but the difference was not significant, but the female values (24.3 vs 33.2) were significantly different (p = 0.008). Work indices for both sexes were significantly different from controls (males p = 0.020, females p = 0.001). CONCLUSIONS: The association of increased nondiscocytes and impaired muscle function could indicate a cause and effect relationship. This would be in agreement with the physiological concept of fatigue as a consequence of inadequate oxygen delivery.

Adult↗