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At least 307 records · Page 17Linked to original sources
PubMed1978

Chromosome replication rate and cell shape in Escherichia coli: lack of coupling.

The dimensions of Rep- cells of Escherichia coli K-12 were measured and compared with those of their Rep+ isogenic cells (both Thy-), Rep- cells cultivated identically were longer (but not wider), even though both strains were wider when the rate of chromosome replication was slowed down by lowering the thymine concentration supplied. This eliminates the possibility that cell shape is determined by this rate. Simulating Thy+ phenotype by adding deoxyguanosine resulted in shorter Rep- cells when growth was faster. This excludes a simple relationship between cell elongation and growth rate, but is consistent with a linear proportionality between the rate of surface synthesis and growth. Thymine limitation of fast-growing Thy- E. coli K-12 cells is shown to result in loss of their uniform shape and production of bizarre morphologies, apparently due to imbalanced synthesis of wall components.

Chromosomes, Bacterial↗
PubMed2005

Interplay between septin organization, cell cycle and cell shape in yeast.

Septins are conserved filament-forming proteins that assemble into cortical cytoskeletal structures in animal and fungal cells. Although rapid progress has been made into the functions of septins, the mechanisms governing their localization and organization remain mysterious. In Saccharomyces cerevisiae, Cdc42p organizes the septin cytoskeleton into a ring in preparation for bud formation, following which septins remain as a collar at the mother-bud neck. We have dissected the phenotype of cdc42(V36T,K94E) cells that display an aberrant cell shape correlated with the development of ectopic septin caps and rings within the bud. The results suggest that a well-assembled septin cortex plays a novel role in directing growth to shape the nascent bud, and that a disorganized septin cortex directs improper growth generating an aberrant neck. Conversely, we found that the elongated bud shape arising as a result of the morphogenesis checkpoint cell cycle delay that accompanies septin perturbation can feed back to exacerbate minor defects in septin organization, by maintaining a bud-tip-localized septin assembly activity that competes with the neck-localized septin cortex. Using this exacerbation as a tool, we uncovered septin organization defects in many mutants not previously known to display such defects, expanding the cast of characters involved in proper assembly of the septin cortex to include CLN1, CLN2, BNI1, BNI4, BUD3, BUD4 and BUD5.

Cell Cycle↗
PubMed1998

Hyperactivation of the folded gastrulation pathway induces specific cell shape changes.

During Drosophila gastrulation, mesodermal precursors are brought into the interior of the embryo by formation of the ventral furrow. The first steps of ventral furrow formation involve a flattening of the apical surface of the presumptive mesodermal cells and a constriction of their apical diameters. In embryos mutant for folded gastrulation (fog), these cell shape changes occur but the timing and synchrony of the constrictions are abnormal. A similar phenotype is seen in a maternal effect mutant, concertina (cta). fog encodes a putative secreted protein whereas cta encodes an (alpha)-subunit of a heterotrimeric G protein. We have proposed that localized expression of the fog signaling protein induces apical constriction by interacting with a receptor whose downstream cellular effects are mediated by the cta G(alpha)protein. In order to test this model, we have ectopically expressed fog at the blastoderm stage using an inducible promoter. In addition, we have examined the constitutive activation of cta protein by blocking GTP hydrolysis using both in vitro synthesized mutant alleles and cholera toxin treatment. Activation of the fog/cta pathway by any of these procedures results in ectopic cell shape changes in the gastrula. Uniform fog expression rescues the gastrulation defects of fog null embryos but not cta mutant embryos, arguing that cta functions downstream of fog expression. The normal location of the ventral furrow in embryos with uniformly expressed fog suggests the existence of a fog-independent pathway determining mesoderm-specific cell behaviors and invagination. Epistasis experiments indicate that this pathway requires snail but not twist expression.

Animals↗
PubMed1979

Actin microfilaments, cell shape, and secretory processes in isolated rat hepatocytes. Effect of phalloidin and cytochalasin D.

The effects of phalloidin and cytochalasin D, drugs which, respectively, stabilize and destabilize actin microfilaments, have been tested on isolated rat hepatocytes. Both drugs produced a modification of cell shape, characterized by protrusions bulging from the cytoplasm. In phalloidin-treated hepatocytes, an accumulation of actin microfilamentous network was detectable at the base of each protrusion by electron microscopy, immunofluorescence, and HMM decoration. This accumulation of microfilaments was absent in cytochalasin D-treated cells. The release of triglycerides, an index of very low density lipoprotein secretion, was inhibited by phalloidin or cytochalasin D, and accompanied by an increase in cellular triglycerides. At the electron microscope examination, triglyceride accumulation was represented by fat droplets and vesicle-enclosed, very low density lipoprotein-like particles. Total protein and albumin secretion was only very slightly modified by either one of these drugs. With the use of various phalloidin analogs, a correlation was observed between their respective ability to stabilize F-actin in vitro, and their effects on cell shape and triglyceride secretion. In conclusion, phalloidin, and cytochalasin D: (a) modify the shape of isolated hepatocytes; (b) inhibit lipoprotein secretion. These effects possibly result from a modification of actin microfilament function.

Actins↗
PubMed1996

Effects of Epidermal Cell Shape and Pigmentation on Optical Properties of Antirrhinum Petals at Visible and Ultraviolet Wavelengths.

We used the Mixta+ and mixta- lines of Antirrhinum majus as a model system to investigate the effects of epidermal cell shape and pigmentation on tissue optical properties in the visible and ultraviolet (UV) spectral regions. Adaxial epidermal cells of Mixta+ flowers have a conical-papillate shape; in the mixta- line the cells are slightly domed. Mixta+ cells contained significantly more anthocyanin and other flavonoids than mixta- cells when plants were grown under either high- or low-UV conditions. Mixta+ cells focused light (3.5-4.7 times incident) within their pigmented interiors, whereas mixta- cells focused light (2.1-2.7 times incident) in the unpigmented mesophyll. UV light penetrated the epidermis (commonly 20-50% transmittance at 312 nm) mainly through the unpigmented peripheral regions of the cells that were similar for the two lines, so that overall penetration through Mixta+ and mixta- epidermises was equal. However, maximum UV absorption in the central region of epidermal cells was slightly greater in Mixta+ than mixta-, and intact Mixta+ flowers reflected less light in the spectral regions with intermediate flavonoid absorbance. In both cases, about 50 to 75% of the difference could be attributed to cell shape and resulting changes in the optical pathlength or focusing.

Journal Article↗
PubMed1988

Role of cell-cycle in regulating neuroepithelial cell shape during bending of the chick neural plate.

Neuroepithelial cells transform from spindle-shaped to wedge-shaped within the median and paired dorsolateral hinge points of the bending neural plate, but the mechanisms underlying these localized changes are unclear. This study was designed to evaluate further the hypothesis that localized "wedging" of neuroepithelial cells during bending involves basal cellular expansion resulting from alteration of the cell-cycle. Neurulating chick embryos were treated with tritiated thymidine, and transverse sections through the midbrain were examined autoradiographically. Parameters of the cell-cycle as well as nuclear position and size were assessed in the median hinge point, which contains predominantly wedge-shaped cells, and in adjacent lateral areas of the neural plate, which contain predominantly spindle-shaped cells. Both the DNA-synthetic phase and non-DNA synthetic portion of the cell-cycle were significantly longer in the median hinge point than in lateral neuroepithelial areas, some nuclei in both regions were located basally during these phases, and virtually all basal nuclei in the median hinge point were large. Additionally, the mitotic phase was significantly shorter in the median hinge point than in lateral areas. We present a model to explain how alteration of the cell-cycle in the median hinge point could generate wedging of cells in this region.

Animals↗
PubMed1996

The role of the cortical cytoskeleton: F-actin crosslinking proteins protect against osmotic stress, ensure cell size, cell shape and motility, and contribute to phagocytosis and development.

We generated Dictyostelium double mutants lacking the two F-actin crosslinking proteins alpha-actinin and gelation factor by inactivating the corresponding genes via homologous recombination. Here we investigated the consequences of these deficiencies both at the single cell level and at the multicellular stage. We found that loss of both proteins severely affected growth of the mutant cells in shaking suspension, and led to a reduction of cell size from 12 microns in wild-type cells to 9 microns in mutant cells. Moreover the cells did not exhibit the typical polarized morphology of aggregating Dictyostelium cells but had a more rounded cell shape, and also exhibited an increased sensitivity towards osmotic shock and a reduced rate of phagocytosis. Development was heavily impaired and never resulted in the formation of fruiting bodies. Expression of developmentally regulated genes and the final developmental stages that were reached varied, however, with the substrata on which the cells were deposited. On phosphate buffered agar plates the cells were able to form tight aggregates and mounds and to express prespore and prestalk cell specific genes. Under these conditions the cells could perform chemotactic signalling and cell behavior was normal at the onset of multicellular development as revealed by time-lapse video microscopy. Double mutant cells were motile but speed was reduced by approximately 30% as compared to wild type. These changes were reversed by expressing the gelation factor in the mutant cells. We conclude that the actin assemblies that are formed and/or stabilized by both F-actin crosslinking proteins have a protective function during osmotic stress and are essential for proper cell shape and motility.

Actinin↗
PubMed1990

Phorbol ester mimics ACTH action in corticoadrenal cells stimulating steroidogenesis, blocking cell cycle, changing cell shape, and inducing c-fos proto-oncogene expression.

Cells of the Y-1 corticoadrenal line are: (a) functional, (b) cell cycle-arrested by adrenocorticotropic hormone (ACTH), (c) tumorigenic, and (d) c-Ki-ras overexpressing. We here report that the phorbol ester phorbol 12-myristate 13-acetate (PMA) mimics all ACTH-specific effects in Y-1 cells, namely: (a) steroid-ogenesis stimulation, (b) cell cycle block, and (c) cell shape change. In addition, both ACTH and PMA caused a rapid and transient induction of the c-fos proto-oncogene while having no effect on c-Ki-ras mRNA steady state levels. Dibutyryl cAMP, known to elicit ACTH effects in Y-1 cells, was a poor inducer of the c-fos gene. PMA pretreatment rendered Y-1 cells unresponsive to ACTH. These results suggest that protein kinase C is likely to be involved in the mechanisms of action of ACTH.

Adrenal Cortex Neoplasms↗
PubMed2005

14-3-3 and calmodulin control subcellular distribution of Kir/Gem and its regulation of cell shape and calcium channel activity.

Individual members of the RGK family of Ras-related GTPases, which comprise Rad, Gem/Kir, Rem and Rem2, have been implicated in important functions such as the regulation of voltage-gated calcium channel activity and remodeling of cell shape. The GTPase Kir/Gem inhibits the activity of calcium channels by interacting with the beta-subunit and also regulates cytoskeleton dynamics by inhibiting the Rho-Rho kinase pathway. In addition, Kir/Gem interacts with 14-3-3 and calmodulin, but the significance of this interaction on Kir/Gem function is poorly understood. Here, we present a comprehensive analysis of the binding of 14-3-3 and calmodulin to Kir/Gem. We show that 14-3-3, in conjunction with calmodulin, regulates the subcellular distribution of Kir/Gem between the cytoplasm and the nucleus. In addition, 14-3-3 and calmodulin binding modulate Kir/Gem-mediated cell shape remodeling and downregulation of calcium channel activity. Competition experiments show that binding of 14-3-3, calmodulin and calcium channel beta-subunits to Kir/Gem is mutually exclusive, providing a rationale for the observed regulatory effects of 14-3-3 and calmodulin on Kir/Gem localization and function.

14-3-3 Proteins↗
PubMed1997

Caenorhabditis elegans LET-502 is related to Rho-binding kinases and human myotonic dystrophy kinase and interacts genetically with a homolog of the regulatory subunit of smooth muscle myosin phosphatase to affect cell shape.

We have identified two genes associated with the hypodermal cell shape changes that occur during elongation of the Caenorhabditis elegans embryo. The first gene, called let-502, encodes a protein with high similarity to Rho-binding Ser/Thr kinases and to human myotonic dystrophy kinase (DM-kinase). Strong mutations in let-502 block embryonic elongation, and let-502 reporter constructs are expressed in hypodermal cells at the elongation stage of development. The second gene, mel-11, was identified by mutations that act as extragenic suppressors of let-502. mel-11 encodes a protein similar to the 110- to 133-kD regulatory subunits of vertebrate smooth muscle myosin-associated phosphatase (PP-1M). We suggest that the LET-502 kinase and the MEL-11 phosphatase subunit act in a pathway linking a signal generated by the small GTP-binding protein Rho to a myosin-based hypodermal contractile system that drives embryonic elongation. LET-502 may directly regulate the activity of the MEL-11 containing phosphatase complex and the similarity between LET-502 and DM-kinase suggests a similar function for DM-kinase.

Alleles↗
PubMed1987

Extracellular matrix changes PC12 cell shape and processing of newly synthesized dopamine.

PC12 cells on extracellular matrix (ECM) or plastic were incubated with 3H-tyrosine (3H-TY) in the presence and absence of serum or cold tyrosine. 3H-Dopamine (3H-DA) was determined in medium and cells from 1 to 48 h later with Dowex cation exchange chromatography. In serum-free and tyrosine-free medium, PC12 cells on ECM released significantly more 3H-DA, whereas cells on plastic had a significantly higher cellular content of 3H-DA, but total 3H-DA (medium plus cells) was equal in ECM and plastic cultures. When 3H-TY was added to tyrosine-containing medium, there was a significant decrease in the levels of 3H-DA detected and the differences between ECM and plastic cultures were attenuated, but the patterns of secretion and storage were similar to those observed with tyrosine-free medium and total synthesis did not decline at 48 h. Serum decreased the efficiency of the resin to retain 3H-DA from culture medium, attenuated the difference in dopamine release between ECM and plastic cultures, and contributed to variations in 3H-TY uptake. The morphometric relationship between the cell membrane and the internal compartment in PC12 cells of different shapes was also characterized. The perimeter length and area of the midsection of cells were determined with a modular system for quantitative digital analysis. The perimeter length of cells on ECM was significantly greater than cells on plastic, whereas the internal areas were similar. The ratio of perimeter length to area (P/A) for all cells on ECM was 30% higher than the P/A ratio for cells on plastic. The ratio of P/A for a subpopulation of very flat cells on ECM was 70% higher than the ratio for round cells on plastic. Immunocytochemistry for tyrosine hydroxylase revealed a more diffuse distribution of this enzyme in cells on ECM. These data suggest that there is an increase in the ratio of cell surface area to cell volume as PC12 cells spread on ECM which could facilitate secretory vesicle fusion with the cell membrane, and hence, exocytosis. Although there is a concomitant increase in the secretion of dopamine and a decrease in the storage of dopamine, the change in cell shape does not appear to immediately alter the synthesis of dopamine.

Animals↗
PubMed1994

Origin of spindle-shaped cells in Kaposi sarcoma.

Adult skin microvascular endothelial cells derived from new born foreskin were grown and maintained in tissue culture with and without dibutyryl cyclic AMP (DC-AMP) and isobutyl methyl xanthine (IMX). Whereas in the presence of DC-AMP and IMX, the cells showed the typical cobblestone appearance of endothelium, in the absence of these agents the cultured cells permanently converted to a spindle-shaped configuration. Because this phenomenon of transdifferentiation also occurs in the presence of specific cytokines, the profile of which is notoriously altered in acquired immunodeficiency syndrome (AIDS), the findings support the concept that in Kaposi sarcoma the spindle-shaped cells derive from dysfunction in the microvascular environment.

1-Methyl-3-isobutylxanthine↗
PubMed2002

Mechanical aspects of cell shape regulation and signaling.

Physical forces play a critical role in cell integrity and development, but little is known how cells convert mechanical signals into biochemical responses. This mini-review examines potential molecular mediators like integrins, focal adhesion proteins, and the cytoskeleton in the context of a complex cell structure. These molecules-when activated by cell binding to the extracellular matrix-associate with the skeletal scaffold via the focal adhesion complex. Vinculin is presented as a mechanical coupling protein that contributes to the integrity of the cytoskeleton and cell shape control, and examples are given of how mechanical signals converge into biochemical responses through force-dependent changes in cell geometry and molecular mechanics.

Animals↗
PubMed1988

Blood group antigen deficiencies associated with abnormal red cell shape.

Rare individuals are known with erythrocytes which show an inherited deficiency of certain blood group antigens and also have abnormal red cell shape. Studies of these cells can give an insight into the functional role of blood group active components in maintaining the shape and membrane properties of the normal erythrocyte. The biochemical characterisation of the red cell membrane alterations occurring in two such rare erythrocyte phenotypes--the Leach phenotype and the Rhnull phenotype are reviewed here.

Blood Group Antigens↗
PubMed2000

Regulated interactions between dynamin and the actin-binding protein cortactin modulate cell shape.

The dynamin family of large GTPases has been implicated in the formation of nascent vesicles in both the endocytic and secretory pathways. It is believed that dynamin interacts with a variety of cellular proteins to constrict membranes. The actin cytoskeleton has also been implicated in altering membrane shape and form during cell migration, endocytosis, and secretion and has been postulated to work synergistically with dynamin and coat proteins in several of these important processes. We have observed that the cytoplasmic distribution of dynamin changes dramatically in fibroblasts that have been stimulated to undergo migration with a motagen/hormone. In quiescent cells, dynamin 2 (Dyn 2) associates predominantly with clathrin-coated vesicles at the plasma membrane and the Golgi apparatus. Upon treatment with PDGF to induce cell migration, dynamin becomes markedly associated with membrane ruffles and lamellipodia. Biochemical and morphological studies using antibodies and GFP-tagged dynamin demonstrate an interaction with cortactin. Cortactin is an actin-binding protein that contains a well defined SH3 domain. Using a variety of biochemical methods we demonstrate that the cortactin-SH3 domain associates with the proline-rich domain (PRD) of dynamin. Functional studies that express wild-type and mutant forms of dynamin and/or cortactin in living cells support these in vitro observations and demonstrate that an increased expression of cortactin leads to a significant recruitment of endogenous or expressed dynamin into the cell ruffle. Further, expression of a cortactin protein lacking the interactive SH3 domain (CortDeltaSH3) significantly reduces dynamin localization to the ruffle. Accordingly, transfected cells expressing Dyn 2 lacking the PRD (Dyn 2(aa)DeltaPRD) sequester little of this protein to the cortactin-rich ruffle. Interestingly, these mutant cells are viable, but display dramatic alterations in morphology. This change in shape appears to be due, in part, to a striking increase in the number of actin stress fibers. These findings provide the first demonstration that dynamin can interact with the actin cytoskeleton to regulate actin reorganization and subsequently cell shape.

Amino Acid Sequence↗
PubMed1985

Modulation of epidermal cell shaping and extracellular matrix during caudal fin morphogenesis in the zebra fish Brachydanio rerio.

Distinct changes in epidermal cell shaping largely define the overall pattern of growth and form during generation of the ectodermal ridge and early stages of fin fold morphogenesis. The epidermal portion of the ridge and early fin fold are formed from a strip of epidermal cells that is only six to nine cells wide. There is apparently no increase in the number of these cells during initial formation of the ridge and its subsequent conversion into a fin fold which contains extracellular matrix fibres. Epidermal cells adopt a wedge-shaped morphology during ridge production. Distinct changes in the shaping and contact relationships between basal portions of these cells generate intercellular spaces at several discrete loci within the ridge. These spaces become continuous with each other to form a subepidermal space. Hence, the subepidermal space is not produced by straight-forward folding of an epidermal sheet. Cells flanking the sides of the ridge start to flatten as it is converted into a fin fold. A continuous row of distinctive cells is positioned along the apex of the developing fold. The term 'cleft cells' is suggested for these apical cells. Each cleft cell retains a wedge-shaped form during fold formation and develops a basal cleft-shaped invagination. Invaginations are aligned in neighbouring cleft cells so that these cells cap the distal boundary of the subepidermal space where collagenous extracellular fibres called actinotrichia run anteroposteriorly along the length of the fin fold. This orientation is in direct contrast to the proximodistal orientation of actinotrichia within the remainder of the subepidermal space. During early stages of fold production a temporary set of previously unreported extracellular cross fibres spans the subepidermal space at right angles to actinotrichia. These configurations of extracellular fibres could be advantageous for maintaining the structural integrity of the early fin fold.

Animals↗
PubMed2003

The Sac1 lipid phosphatase regulates cell shape change and the JNK cascade during dorsal closure in Drosophila.

The Sac1 lipid phosphatase dephosphorylates several phosphatidylinositol (PtdIns) phosphates and, in yeast, regulates a diverse range of cellular processes including organization of the actin cytoskeleton and secretion. We have identified mutations in the gene encoding Drosophila Sac1. sac1 mutants die as embryos with defects in dorsal closure (DC). DC involves the migration of the epidermis to close a hole in the dorsal surface of the embryo occupied by the amnioserosa. It requires cell shape change in both the epidermis and amnioserosa and activation of a Jun N-terminal kinase (JNK) MAPK cascade in the leading edge cells of the epidermis [2]. Loss of Sac1 leads to the improper activation of two key events in DC: cell shape change in the amnioserosa and JNK signaling. sac1 interacts genetically with other participants in these two events, and our data suggest that loss of Sac1 leads to upregulation of one or more signals controlling DC. This study is the first report of a role for Sac1 in the development of a multicellular organism.

Animals↗
PubMed1996

Bacillus stearothermophilus cell shape determinant gene, mreC and mreD, and their stimulation of protease production in Bacillus subtilis.

Protease production stimulating genes were isolated from a soybean protein degrading bacterium, Bacillus stearothermophilus HA19. The cloned fragment stimulated production of a 37-kDa protease in B. subtilis. The nucleotide sequence of the genes and their flanking regions were identical to the B. subtilis cell shape determinant genes mreC and mreD [J. Bacteriol., 176, 6729-6742 (1992); J. Bacteriol., 176, 6717-6728 (1992)]. The mreC and mreD genes in B. subtilis stimulate secretion of a neutral protease (37-kDa), and the protease activity in the culture medium reached 2500 U per ml (approximately 10 times higher than the host strain) after 24 h of cultivation in L broth, suggesting the mreCD genes regulate protease expression and the protease is related to the cell shape determination in Bacilli. The protease productions in B. subtilis carrying mreC or mreD deletion plasmids were not elevated, so the 37-kDa protease stimulation requires both mreC and mreD genes. The extracellular protease was purified, and the molecular mass of the enzyme was 37,000 Da by SDS-polyacrylamide gel electrophoresis and gel filtration. The optimum pH and temperature for the enzyme activity were 7.0 and 50 degrees C, respectively, and the enzyme was stable at pH 7-10. The enzyme was inactivated by EDTA, but not by phenylmethyl sulfonyl fluoride and diisopropyl fluorophosphate.

Amino Acid Sequence↗