scholarly journals Galactoglucomannans Increase Cell Population Density and Alter the Protoxylem/Metaxylem Tracheary Element Ratio in Xylogenic Cultures of Zinnia

2006 ◽  
Vol 142 (2) ◽  
pp. 696-709 ◽  
Author(s):  
Anna Beňová-Kákošová ◽  
Catherine Digonnet ◽  
Florence Goubet ◽  
Philippe Ranocha ◽  
Alain Jauneau ◽  
...  
Keyword(s):  
Population Density ◽  
Cell Population ◽  
Tracheary Element ◽  
Element Ratio

scholarly journals Effect of cell population density on G2 arrest in Tetrahymena.

1975 ◽  
Vol 67 (3) ◽  
pp. 518-522 ◽  
Author(s):  
I L Cameron ◽  
N C Bols
Keyword(s):  
Cell Cycle ◽  
Population Density ◽  
Cell Population ◽  
Tritiated Thymidine ◽  
Tetrahymena Pyriformis ◽  
High Cell ◽  
Ciliated Protozoan ◽  
G2 Phase ◽  
Cell Densities ◽  
Two Peaks

The ciliated protozoan, Tetrahymena pyriformis strain GL-C, has been used to study the effect of cell population density during starvation on the synchrony obtained after refeeding and on the number of cells arrested in G2 phase of the cell cycle. At high cell densities two peaks of division indices were observed after refeeding while only one was observed at low cell densities. Cell division began earlier in cultures starved at high cell densities. Most importantly, the proportion of cells in G2 was considerably higher in populations starved at high cell densities. When tritiated thymidine was present during the refeeding period, radioautographs of cell samples at different times showed that the first cells to exhibit division furrows contained unlabeled nuclei. The first peak in the division index after refeeding was observed only at higher cell densities and is attributed to the cells arrested in G2. These results suggest that Tetrahymena is an excellent organism to study the concept of resting stages in the cell cycle and their control.

scholarly journals CytoplasmicEscherichia coliADP sugar pyrophosphatase binds to cell membranes in response to extracellular signals as the cell population density increases

2008 ◽  
Vol 288 (1) ◽  
pp. 25-32 ◽  
Author(s):  
María Teresa Morán-Zorzano ◽  
Manuel Montero ◽  
Francisco José Muñoz ◽  
Nora Alonso-Casajús ◽  
Alejandro Miguel Viale ◽  
...  
Keyword(s):  
Population Density ◽  
Cell Population ◽  
Cell Membranes ◽  
Extracellular Signals

scholarly journals Loss of cell-population-density-dependent incorporation of fucose into the lipid fraction of cultured human tumour cells

1978 ◽  
Vol 172 (1) ◽  
pp. 181-184 ◽  
Author(s):  
M Gacto
Keyword(s):  
Population Density ◽  
Cell Population ◽  
Lipid Fraction ◽  
Tumour Cells ◽  
Human Tumour ◽  
Density Dependent ◽  
Human Tumour Cells ◽  
Normal Human ◽  
Tumour Cell Lines ◽  
Human Tumour Cell Lines

The incorporation of radioactively labelled fucose into the lipid fraction of cultured normal human cells and several human tumour-cell lines was examined as a function of the cell population density. Normal cells exhibited a density-dependent pattern of incorporation, whereas in tumour cells the radioactivity incorporated was independent of the cell population density. An exception was found among the tumour cells, which suggests a possible correlation between the loss of this marker and the ability to produce tumours.

scholarly journals Quorum sensing and the population-dependent control of virulence

2000 ◽  
Vol 355 (1397) ◽  
pp. 667-680 ◽  
Author(s):  
Paul Williams ◽  
Miguel Camara ◽  
Andrea Hardman ◽  
Simon Swift ◽  
Deborah Milton ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Population Density ◽  
Cell Population ◽  
Cell Communication ◽  
Immunomodulatory Activity ◽  
Signal Molecules ◽  
Dependent Manner ◽  
Virulence Determinants ◽  
Signal Molecule ◽  
Cell Cell

One crucial feature of almost all bacterial infections is the need for the invading pathogen to reach a critical cell population density sufficient to overcome host defences and establish the infection. Controlling the expression of virulence determinants in concert with cell population density may therefore confer a significant survival advantage on the pathogen such that the host is overwhelmed before a defence response can be fully initiated. Many different bacterial pathogens are now known to regulate diverse physiological processes including virulence in a cell–density–dependent manner through cell–cell communication. This phenomenon, which relies on the interaction of a diffusible signal molecule (e.g. an N –acylhomoserine lactone) with a sensor or transcriptional activator to couple gene expression with cell population density, has become known as ‘quorum sensing’ . Although the size of the ‘quorum’ is likely to be highly variable and influenced by the diffusibility of the signal molecule within infected tissues, nevertheless quorum–sensing signal molecules can be detected in vivo in both experimental animal model and human infections. Furthermore, certain quorum–sensing molecules have been shown to possess pharmacological and immunomodulatory activity such that they may function as virulence determinants per se . As a consequence, quorum sensing constitutes a novel therapeutic target for the design of small molecular antagonists capable of attenuating virulence through the blockade of bacterial cell–cell communication.

scholarly journals Invasion fronts and adaptive dynamics in a model for the growth of cell populations with heterogeneous mobility

2021 ◽  
pp. 1-18
Author(s):  
T. LORENZI ◽  
B. PERTHAME ◽  
X. RUAN
Keyword(s):  
Population Density ◽  
Density Function ◽  
Cell Population ◽  
Adaptive Dynamics ◽  
Reaction Diffusion Equation ◽  
Cell Populations ◽  
Maximum Point ◽  
Front Edge ◽  
Cell Mobility ◽  
Local Cell

We consider a model for the dynamics of growing cell populations with heterogeneous mobility and proliferation rate. The cell phenotypic state is described by a continuous structuring variable and the evolution of the local cell population density function (i.e. the cell phenotypic distribution at each spatial position) is governed by a non-local advection–reaction–diffusion equation. We report on the results of numerical simulations showing that, in the case where the cell mobility is bounded, compactly supported travelling fronts emerge. More mobile phenotypic variants occupy the front edge, whereas more proliferative phenotypic variants are selected at the back of the front. In order to explain such numerical results, we carry out formal asymptotic analysis of the model equation using a Hamilton–Jacobi approach. In summary, we show that the locally dominant phenotypic trait (i.e. the maximum point of the local cell population density function along the phenotypic dimension) satisfies a generalised Burgers’ equation with source term, we construct travelling-front solutions of such transport equation and characterise the corresponding minimal speed. Moreover, we show that, when the cell mobility is unbounded, front edge acceleration and formation of stretching fronts may occur. We briefly discuss the implications of our results in the context of glioma growth.

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