Changes in the osmotic pressure of E. coli W7 during the cell cycle

1979 ◽  
Vol 4 (1) ◽  
pp. 121
Author(s):  
C.G. van Eden ◽  
R.W.H. Verwer ◽  
N. Nanninga
Keyword(s):  
Cell Cycle ◽  
Osmotic Pressure ◽  
E Coli

Regulation of the synthesis of surface protein in the cell cycle of e. coli b/r

Cell ◽  
1979 ◽  
Vol 18 (2) ◽  
pp. 287-296 ◽  
Author(s):  
A. Boyd ◽  
I.B. Holland
Keyword(s):  
Cell Cycle ◽  
Surface Protein ◽  
E Coli

YakA, a protein kinase required for the transition from growth to development in Dictyostelium

Development ◽  
1998 ◽  
Vol 125 (12) ◽  
pp. 2291-2302 ◽  
Author(s):  
G.M. Souza ◽  
S. Lu ◽  
A. Kuspa
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Basic Protein ◽  
Mrna Levels ◽  
Wild Type ◽  
E Coli ◽  
Cycle Arrest ◽  
Expression Of Genes ◽  
Extracellular Signal ◽  
Nutrient Rich Medium

When Dictyostelium cells starve they arrest their growth and induce the expression of genes necessary for development. We have identified and characterized a protein kinase, YakA, that is essential for the proper regulation of both events. Amino acid sequence and functional similarities indicate that YakA is a homolog of Yak1p, a growth-regulating protein kinase in S. cerevisiae. Purified YakA expressed in E. coli is able to phosphorylate myelin basic protein. YakA-null cells are smaller and their cell cycle is accelerated relative to wild-type cells. When starved, YakA-null cells fail to decrease the expression of the growth-stage gene cprD, and do not induce the expression of genes required for the earliest stages of development. YakA mRNA levels increase during exponential growth and reach a maximum at the point of starvation, consistent with a role in mediating starvation responses. YakA mRNA also accumulates when cells are grown in medium conditioned by cells grown to high density, suggesting that yakA expression is under the control of an extracellular signal that accumulates during growth. Expression of yakA from a conditional promoter causes cell-cycle arrest in nutrient-rich medium and promotes developmental events, such as the expression of genes required for cAMP signaling. YakA appears to regulate the transition from growth to development in Dictyostelium.

scholarly journals Cultivation at high osmotic pressure confers ubiquinone 8–independent protection of respiration on Escherichia coli

2019 ◽  
Vol 295 (4) ◽  
pp. 981-993 ◽  
Author(s):  
Laura Tempelhagen ◽  
Anita Ayer ◽  
Doreen E. Culham ◽  
Roland Stocker ◽  
Janet M. Wood
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Escherichia Coli ◽  
Electron Transfer ◽  
Oxygen Uptake ◽  
Osmotic Pressure ◽  
Respiratory Chain ◽  
Membrane Lipid ◽  
E Coli ◽  
Uptake Rates

Ubiquinone 8 (coenzyme Q8 or Q8) mediates electron transfer within the aerobic respiratory chain, mitigates oxidative stress, and contributes to gene expression in Escherichia coli. In addition, Q8 was proposed to confer bacterial osmotolerance by accumulating during growth at high osmotic pressure and altering membrane stability. The osmolyte trehalose and membrane lipid cardiolipin accumulate in E. coli cells cultivated at high osmotic pressure. Here, Q8 deficiency impaired E. coli growth at low osmotic pressure and rendered growth osmotically sensitive. The Q8 deficiency impeded cellular O2 uptake and also inhibited the activities of two proton symporters, the osmosensing transporter ProP and the lactose transporter LacY. Q8 supplementation decreased membrane fluidity in liposomes, but did not affect ProP activity in proteoliposomes, which is respiration-independent. Liposomes and proteoliposomes prepared with E. coli lipids were used for these experiments. Similar oxygen uptake rates were observed for bacteria cultivated at low and high osmotic pressures. In contrast, respiration was dramatically inhibited when bacteria grown at the same low osmotic pressure were shifted to high osmotic pressure. Thus, respiration was restored during prolonged growth of E. coli at high osmotic pressure. Of note, bacteria cultivated at low and high osmotic pressures had similar Q8 concentrations. The protection of respiration was neither diminished by cardiolipin deficiency nor conferred by trehalose overproduction during growth at low osmotic pressure, but rather might be achieved by Q8-independent respiratory chain remodeling. We conclude that osmotolerance is conferred through Q8-independent protection of respiration, not by altering physical properties of the membrane.

Effect of osmotic pressure on root growth, cell cycle and cell elongation

PROTOPLASMA ◽  
1968 ◽  
Vol 65 (3) ◽  
pp. 255-262 ◽  
Author(s):  
F. González-Bernáldez ◽  
J. F. López-Sáez ◽  
G. García-Ferrero
Keyword(s):  
Cell Cycle ◽  
Root Growth ◽  
Osmotic Pressure ◽  
Cell Elongation

scholarly journals A study of SeqA subcellular localization in Escherichia coli using photo-activated localization microscopy

2015 ◽  
Vol 184 ◽  
pp. 425-450 ◽  
Author(s):  
Jacek T. Mika ◽  
Aster Vanhecke ◽  
Peter Dedecker ◽  
Toon Swings ◽  
Jeroen Vangindertael ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
Bacterial Genome ◽  
Genetically Engineered ◽  
Replication Initiation ◽  
Cell Protein ◽  
Experimental Conditions ◽  
Localization Microscopy ◽  
E Coli ◽  
Copy Numbers

Escherichia coli (E. coli) cells replicate their genome once per cell cycle to pass on genetic information to the daughter cells. The SeqA protein binds the origin of replication, oriC, after DNA replication initiation and sequesters it from new initiations in order to prevent overinitiation. Conventional fluorescence microscopy studies of SeqA localization in bacterial cells have shown that the protein is localized to discrete foci. In this study we have used photo-activated localization microscopy (PALM) to determine the localization of SeqA molecules, tagged with fluorescent proteins, with a localization precision of 20–30 nm with the aim to visualize the SeqA subcellular structures in more detail than previously possible. SeqA–PAmCherry was imaged in wild type E. coli, expressed from plasmid or genetically engineered into the bacterial genome, replacing the native seqA gene. Unsynchronized cells as well as cells with a synchronized cell cycle were imaged at various time points, in order to investigate the evolution of SeqA localization during the cell cycle. We found that SeqA indeed localized into discrete foci but these were not the only subcellular localizations of the protein. A significant amount of SeqA–PAmCherry molecules was localized outside the foci and in a fraction of cells we saw patterns indicating localization at the membrane. Using quantitative PALM, we counted protein copy numbers per cell, protein copy numbers per focus, the numbers of foci per cell and the sizes of the SeqA clusters. The data showed broad cell-to-cell variation and we did not observe a correlation between SeqA–PAmCherry protein numbers and the cell cycle under the experimental conditions of this study. The numbers of SeqA–PAmCherry molecules per focus as well as the foci sizes also showed broad distributions indicating that the foci are likely not characterized by a fixed number of molecules. We also imaged an E. coli strain devoid of the dam methylase (Δdam) and observed that SeqA–PAmCherry no longer formed foci, and was dispersed throughout the cell and localized to the plasma membrane more readily. We discuss our results in the context of the limitations of the technique.

scholarly journals Escherichia coli Nissle 1917 Distinctively Modulates T-Cell Cycling and Expansion via Toll-Like Receptor 2 Signaling

2005 ◽  
Vol 73 (3) ◽  
pp. 1452-1465 ◽  
Author(s):  
Andreas Sturm ◽  
Klaus Rilling ◽  
Daniel C. Baumgart ◽  
Konstantinos Gargas ◽  
Tay Abou-Ghazalé ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
T Cells ◽  
T Cell ◽  
Peripheral Blood ◽  
Intestinal Inflammation ◽  
Toll Like Receptor ◽  
E Coli ◽  
Toll Like Receptor 2 ◽  
Cell Cycling

ABSTRACT Although the probiotic Escherichia coli strain Nissle 1917 has been proven to be efficacious for the treatment of inflammatory bowel diseases, the underlying mechanisms of action still remain elusive. The aim of the present study was to analyze the effects of E. coli Nissle 1917 on cell cycling and apoptosis of peripheral blood and lamina propria T cells (PBT and LPT, respectively). Anti-CD3-stimulated PBT and LPT were treated with E. coli Nissle 1917-conditioned medium (E. coli Nissle 1917-CM) or heat-inactivated E. coli Nissle 1917. Cyclin B1, DNA content, and caspase 3 expression were measured by flow cytometry to assess cell cycle kinetics and apoptosis. Protein levels of several cell cycle and apoptosis modulators were determined by immunoblotting, and cytokine profiles were determined by cytometric bead array. E. coli Nissle 1917-CM inhibits cell cycling and expansion of peripheral blood but not mucosal T cells. Bacterial lipoproteins mimicked the effect of E. coli Nissle 1917-CM; in contrast, heat-inactivated E. coli Nissle 1917, lipopolysaccharide, or CpG DNA did not alter PBT cell cycling. E. coli Nissle 1917-CM decreased cyclin D2, B1, and retinoblastoma protein expression, contributing to the reduction of T-cell proliferation. E. coli Nissle 1917 significantly inhibited the expression of interleukin-2 (IL-2), tumor necrosis factor α, and gamma interferon but increased IL-10 production in PBT. Using Toll-like receptor 2 (TLR-2) knockout mice, we further demonstrate that the inhibition of PBT proliferation by E. coli Nissle 1917-CM is TLR-2 dependent. The differential reaction of circulating and tissue-bound T cells towards E. coli Nissle 1917 may explain the beneficial effect of E. coli Nissle 1917 in intestinal inflammation. E. coli Nissle 1917 may downregulate the expansion of newly recruited T cells into the mucosa and limit intestinal inflammation, while already activated tissue-bound T cells may eliminate deleterious antigens in order to maintain immunological homeostasis.

scholarly journals Publisher Correction: Osmotic pressure modulates single cell cycle dynamics inducing reversible growth arrest and reactivation of human metastatic cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hubert M. Taïeb ◽  
Daniela S. Garske ◽  
Jörg Contzen ◽  
Manfred Gossen ◽  
Luca Bertinetti ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Single Cell ◽  
Osmotic Pressure ◽  
Growth Arrest ◽  
Metastatic Cells ◽  
Cell Cycle Dynamics

scholarly journals Coordination between E. coli Cell Size and Cell Cycle Mediated by DnaA

2020 ◽  
Author(s):  
Qing Zhang ◽  
Zhichao Zhang ◽  
Hualin Shi
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Dna Replication ◽  
Cell Size ◽  
Doubling Time ◽  
Cell Mass ◽  
Replication Initiation ◽  
General Relationship ◽  
E Coli ◽  
Regulatory Processes

Sixty years ago, bacterial cell size was found as an exponential function of growth rate. Fifty years ago, a more general relationship was proposed, in which the cell mass was equal to the initiation mass multiplied by the ratio of the total time of the C and D periods to the doubling time. This relationship has recently been experimentally confirmed by perturbing doubling time, C period, D period or the initiation mass. However, the underlying molecular mechanism remains unclear. Here, we developed a mechanistic and kinetic model to describe how the initiator protein DnaA mediates the initiation of DNA replication in E. coli. In the model, we introduced an initiation probability function involving competitive binding of DnaA-ATP (active) and DnaA-ADP (inactive) at replication origin to determine the initiation of replication. In addition, we considered RNAP availability, ppGpp inhibition, DnaA autorepression, DnaA titration by chromosomal sites, hydrolysis of DnaA-ATP along with DNA replication, reactivation of DnaA-ADP and established a kinetic description of these DnaA regulatory processes. We simulated DnaA kinetics and obtained a self-consistent cell size and a regular DnaA oscillation coordinated with the cell cycle at steady state. The relationship between the cell size obtained by the simulation and the growth rate, C period, D period or initiation mass reproduces the results of the experiment. This model also predicts how the number of DnaA and the initiation mass vary with the perturbation parameters (including those reflecting the mutation or interference of DnaA regulatory processes), which is comparable to experimental data. The results suggest that the regulatory mechanisms of DnaA level and activity are associated with the invariance of initiation mass and the cell size general relationship for matching frequencies of replication initiation and cell division. This study may provide clues for concerted control of cell size and cell cycle in synthetic biology.

scholarly journals Imaging the Cell Cycle of Pathogen E. coli During Growth in Macrophage

2017 ◽  
pp. 227-236 ◽  
Author(s):  
Gaëlle Demarre ◽  
Victoria Prudent ◽  
Olivier Espéli
Keyword(s):  
Cell Cycle ◽  
E Coli
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