ViableSaccharomyces cerevisiae cells at high concentrations cause early growth arrest of non-Saccharomyces yeasts in mixed cultures by a cell-cell contact-mediated mechanism

Yeast ◽  
2003 ◽  
Vol 20 (4) ◽  
pp. 331-341 ◽  
Author(s):  
Peter Nissen ◽  
Dennis Nielsen ◽  
Nils Arneborg
Keyword(s):  
Growth Arrest ◽  
Early Growth ◽  
Mixed Cultures ◽  
Cell Contact ◽  
A Cell ◽  
High Concentrations ◽  
Saccharomyces Yeasts ◽  
Cell Cell

Role of cell–cell contact in the preservation of differentiation and response to thyrotrophin in cultured porcine thyroid cells

1987 ◽  
Vol 113 (2) ◽  
pp. 223-NP ◽  
Author(s):  
A. S. Yap ◽  
J. R. Bourke ◽  
S. W. Manley
Keyword(s):  
Follicular Development ◽  
Seeding Density ◽  
Cell Contact ◽  
Culture Dish ◽  
Thyroid Cells ◽  
A Cell ◽  
Free Membrane ◽  
Zero Time ◽  
Cell Cell

ABSTRACT Cultured porcine thyroid cells did not reassociate into functional follicles in the presence of TSH unless the initial seeding density was adequate. At 0·2 × 106 cells/35 mm diameter culture dish the cells rapidly formed a monolayer even in the presence of TSH (128 μu./ml), and radioiodide uptake was not significantly increased compared with that in control cells. Seeding densities of 1–3 × 106 cells/dish resulted in cultures which responded to TSH with follicular development and increased radioiodide uptake. A cell-free membrane fraction of thyroid homogenate restored the ability of cultures seeded at low densities to respond to TSH with development of follicular morphology and increased radioiodide uptake. Delaying the addition of TSH by 48 h markedly reduced the stimulation of follicular development and radioiodide uptake of cultures. Addition of membrane fractions, or an alkali-soluble fraction of membranes, at zero time improved the responses to TSH added after a 48-h delay. It was concluded that maintenance of differentiation and of TSH-responsiveness in cultured thyroid cells was influenced by cell–cell contact. J. Endocr. (1987) 113, 223–229

scholarly journals Loss of Culturability of Salmonella enterica subsp. enterica Serovar Typhimurium upon Cell-Cell Contact with Human Fecal Bacteria

2013 ◽  
Vol 79 (10) ◽  
pp. 3257-3263 ◽  
Author(s):  
Gaspar Avendaño-Pérez ◽  
Carmen Pin
Keyword(s):  
Salmonella Enterica ◽  
Mixed Cultures ◽  
Cell Contact ◽  
Data Sets ◽  
Fecal Bacteria ◽  
Bacterial Cells ◽  
Content Type ◽  
Serovar Typhimurium ◽  
A Cell ◽  
Mechanism Of Growth

ABSTRACTLoss of culturability ofSalmonella entericasubsp.entericaserovar Typhimurium has been observed in mixed cultures with anaerobic fecal bacteria under conditions that allow local interaction between cells, such as cell contact. A reduction of a population of culturableS.Typhimurium on the order of ∼104to 105CFU/ml was observed in batch anaerobic mixed cultures with fecal samples from different human donors. Culturability was not affected either in supernatants collected at several times from fecal cultures, when separated from fecal bacteria by a membrane of 0.45-μm pore size, or when in contact with inactivated fecal bacterial cells. Loss of culturability kinetics was characterized by a sharp reduction of several logarithmic units followed by a pronounced tail. A mathematical model was developed to describe the rate of loss of culturability as a function of the frequency of encounters between populations and the probability of inactivation after encounter. The model termF(S·F)1/2quantifies the effect of the concentration of both populations, fecal bacteria (F) andS.Typhimurium (S), on the loss of culturability ofS.Typhimurium by cell contact with fecal bacteria. When the value ofF(S·F)1/2decreased below ca. 1015(CFU/ml)2, the frequency of encounters sharply decreased, leading to the deceleration of the inactivation rate and to the tailing off of theS.Typhimurium population. The probability of inactivation after encounter,P, was constant, with an estimated value of ∼10−5for all data sets.Pmight be characteristic of the mechanism of growth inhibition after a cell encounter.

scholarly journals Hydrodynamics of transient cell-cell contact: The role of membrane permeability and active protrusion length

2018 ◽  
Author(s):  
Kai Liu ◽  
Brian Chu ◽  
Jay Newby ◽  
Elizabeth L. Read ◽  
John Lowengrub ◽  
...  
Keyword(s):  
Fluid Dynamics ◽  
Aspect Ratio ◽  
Thin Layer ◽  
Membrane Permeability ◽  
Rare Event ◽  
Thermal Fluctuations ◽  
Cell Contact ◽  
Layer Effect ◽  
A Cell ◽  
Cell Cell

AbstractIn many biological settings, two or more cells come into physical contact to form a cell-cell interface. In some cases, the cell-cell contact must be transient, forming on timescales of seconds. One example is offered by the T cell, an immune cell which must attach to the surface of other cells in order to decipher information about disease. The aspect ratio of these interfaces (tens of nanometers thick and tens of micrometers in diameter) puts them into the thin-layer limit, or “lubrication limit”, of fluid dynamics. A key question is how the receptors and ligands on opposing cells come into contact. What are the relative roles of thermal undulations of the plasma membrane and deterministic forces from active filopodia? We use a computational fluid dynamics algorithm capable of simulating 10-nanometer-scale fluid-structure interactions with thermal fluctuations up to seconds-and microns-scales. We use this to simulate two opposing membranes, variously including thermal fluctuations, active forces, and membrane permeability. In some regimes dominated by thermal fluctuations, proximity is a rare event, which we capture by computing mean first-passage times using a Weighted Ensemble rare-event computational method. Our results demonstrate that the time-to-contact increases for smaller cell-cell distances (where the thin-layer effect is strongest), leading to an optimal initial cell-cell separation for fastest receptor-ligand binding. We reproduce a previous experimental observation that fluctuation spatial scales are largely unaffected, but timescales are dramatically slowed, by the thin-layer effect. We also find that membrane permeability would need to be above physiological levels to abrogate the thin-layer effect.Author summaryThe elastohydrodynamics of water in and around cells is playing an increasingly recognized role in biology. In this work, we investigate the flow of extracellular fluid in between cells during the formation of a cell-cell contact, to determine whether its necessary evacuation as the cells approach is a rate-limiting step before molecules on either cell can interact. To overcome the computational challenges associated with simulating fluid in this mechanically soft, stochastic and high-aspect-ratio environment, we extend a computational framework where the cell plasma membranes are treated as immersed boundaries in the fluid, and combine this with computational methods for simulating stochastic rare events in which an ensemble of simulations are given weights according to their probability. We find that the internal dynamics of the membranes has speeds in approximately microseconds, but that as the cells approach, a new slow timescale of approximately milliseconds is introduced. Thermal undulations nor typical amounts of membrane permeability can overcome the timescale, but active forces, e.g., from the cytoskeleton, can. Our results suggest an explanation for differences in molecular interactions in live cells compared to in vitro reconstitution experiments.

scholarly journals Coupling of proadipocyte growth arrest and differentiation. I. Induction by heparinized medium containing human plasma.

1982 ◽  
Vol 94 (2) ◽  
pp. 394-399 ◽  
Author(s):  
B R Krawisz ◽  
R E Scott
Keyword(s):  
Human Plasma ◽  
Adipocyte Differentiation ◽  
Growth Arrest ◽  
Culture Conditions ◽  
Cell Contact ◽  
Low Density ◽  
Prolonged Culture ◽  
Extensive Cell ◽  
High Concentrations

The differentiation of proadipocytes in vitro typically required prolonged culture of cells as a high density in high concentrations of serum and added hormones. With such culture conditions it is difficult to design experiments to determine the mechanisms that control the differentiation process. We now describe the rapid and parasynchronous growth arrest and differentiation of low density murine proadipocytes in heparinized medium containing only human plasma. When low density cells are cultured under these conditions, growth arrest at a distinct state in the G1 phase of the cell cycle occurs within 2 d and the differentiation of 80-100% of the cell population occurs within 4 d thereafter. The factors in human plasma which promote growth arrest and differentiation are heat labile and can be separated by barium adsorption. In the following paper we have used these methods to show that there are five separate phases which regulate the coupling of proadipocyte growth arrest and differentiation. The data reported in this paper establish that: (a) high cell density and extensive cell-to-cell contact are not required for adipocyte differentiation, (b) prolonged culture is not required for adipocyte differentiation, and (c) high concentrations of serum and/or added hormones are not required for adipocyte differentiation.

scholarly journals The CEACAM1-L Glycoprotein Associates with the Actin Cytoskeleton and Localizes to Cell–Cell Contact through Activation of Rho-like GTPases

2000 ◽  
Vol 11 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Svetlana Sadekova ◽  
Nathalie Lamarche-Vane ◽  
Xiaodong Li ◽  
Nicole Beauchemin
Keyword(s):  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Adhesion Molecule ◽  
Control Cell ◽  
Growth Inhibitor ◽  
Cytoplasmic Domain ◽  
Cell Contact ◽  
A Cell ◽  
Rho Family ◽  
Cell Cell

Associations between plasma membrane-linked proteins and the actin cytoskeleton play a crucial role in defining cell shape and determination, ensuring cell motility and facilitating cell–cell or cell–substratum adhesion. Here, we present evidence that CEACAM1-L, a cell adhesion molecule of the carcinoembryonic antigen family, is associated with the actin cytoskeleton. We have delineated the regions involved in actin cytoskeleton association to the distal end of the CEACAM1-L long cytoplasmic domain. We have demonstrated that CEACAM1-S, an isoform of CEACAM1 with a truncated cytoplasmic domain, does not interact with the actin cytoskeleton. In addition, a major difference in subcellular localization of the two CEACAM1 isoforms was observed. Furthermore, we have established that the localization of CEACAM1-L at cell–cell boundaries is regulated by the Rho family of GTPases. The retention of the protein at the sites of intercellular contacts critically depends on homophilic CEACAM1–CEACAM1 interactions and association with the actin cytoskeleton. Our results provide new evidence on how the Rho family of GTPases can control cell adhesion: by directing an adhesion molecule to its proper cellular destination. In addition, these results provide an insight into the mechanisms of why CEACAM1-L, but not CEACAM1-S, functions as a tumor cell growth inhibitor.

scholarly journals Inhibition of cell movement and proliferation by cell–cell contact-induced interaction of Necl-5 with nectin-3

2005 ◽  
Vol 171 (1) ◽  
pp. 165-173 ◽  
Author(s):  
Tsutomu Fujito ◽  
Wataru Ikeda ◽  
Shigeki Kakunaga ◽  
Yukiko Minami ◽  
Mihoko Kajita ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Adhesion Molecule ◽  
Cell Movement ◽  
Cell Contact ◽  
Down Regulation ◽  
Nih3t3 Cells ◽  
Cell Contacts ◽  
Poliovirus Receptor ◽  
A Cell ◽  
Cell Cell

Immunoglobulin-like Necl-5/Tage4/poliovirus receptor (PVR)/CD155, originally identified as the PVR, has been shown to be up-regulated in cancer cells and to enhance growth factor–induced cell movement and proliferation. In addition, Necl-5 heterophilically trans-interacts with nectin-3, a cell–cell adhesion molecule known to form adherens junctions in cooperation with cadherin. We show here that Necl-5 was down-regulated from cell surface upon cell–cell contacts in NIH3T3 cells. This down-regulation of Necl-5 was initiated by its interaction with nectin-3 and was mainly mediated by clathrin-dependent endocytosis. Then, the down-regulation of Necl-5 induced in this way reduced movement and proliferation of NIH3T3 cells. These results indicate that the down-regulation of Necl-5 induced by its interaction with nectin-3 upon cell–cell contacts may be at least one mechanism underlying contact inhibition of cell movement and proliferation.

scholarly journals Identification of a Drosophila homologue of alpha-catenin and its association with the armadillo protein.

1993 ◽  
Vol 121 (5) ◽  
pp. 1133-1140 ◽  
Author(s):  
H Oda ◽  
T Uemura ◽  
K Shiomi ◽  
A Nagafuchi ◽  
S Tsukita ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Lines ◽  
Chromosome Band ◽  
Cell Contact ◽  
Beta Catenin ◽  
Contact Sites ◽  
Adhesion System ◽  
A Cell ◽  
Drosophila Embryos ◽  
Cell Cell

The cadherin cell adhesion system plays a central role in cell-cell adhesion in vertebrates, but its homologues are not identified in the invertebrate. alpha-Catenins are a group of proteins associated with cadherins, and this association is crucial for the cadherins' function. Here, we report the cloning of a Drosophila alpha-catenin gene by low stringent hybridization with a mouse alpha E-catenin probe. Isolated cDNAs encoded a 110-kD protein with 60% identity to mouse alpha E-catenin, and this protein was termed D alpha-catenin. The gene of this protein was located at the chromosome band 80B. Immunostaining analysis using a mAb to D alpha-catenin revealed that it was localized to cell-cell contact sites, expressed throughout development and present in a wide variety of tissues. When this protein was immunoprecipitated from detergent extracts of Drosophila embryos or cell lines, several proteins co-precipitated. These included the armadillo product which was known to be a Drosophila homologue of beta-catenin, another cadherin-associated protein in vertebrates, and a 150-kD glycoprotein. These results strongly suggest that Drosophila has a cell adhesion machinery homologous to the vertebrate cadherin-catenin system.

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