La cinétique cellulaire au cours de la segmentation du germe d'Axolotl: proposition d'un modèle statistique

Development ◽  
1977 ◽  
Vol 42 (1) ◽  
pp. 5-14
Author(s):  
Par J. Signoret
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Statistical Distribution ◽  
Cyclic Process ◽  
Blastula Stage ◽  
Cell Cycle Time ◽  
Cycle Times ◽  
Division Process ◽  
Kinetics Of ◽  
Cell Division Control

The present work is based on the study of individual cell cycle times for a given category of cells. The material considered in detail is the Axolotl embryo during the eleventh cleavage cycle. In spite of the exceptional homogeneity of this population, individual cycle times show a remarkable variation from cell to cell, coinciding with a characteristic statistical distribution. To describe the kinetics of cell proliferation, we propose a model for which the theoretical distribution of cycle times fits with the distribution observed in our material. Numerous observations allow us to generalize the model to other types of populations. According to this concept the notion of cell cycle time disappears in favour of the notion of a statistical distribution of individual cycle times. This varïability is integral to the cell division process itself. We suggest that in the cycle there is a particular event the probability of occurrence of which is constant beginning with a critical state. The cells would therefore remain a certain time in this state, overcoming it at a characteristic rate. To this exponential distribution variability would be added the variability of other events whose cumulative effects would result in a normal distribution. The resultant of both factors conforms to the frequency distribution implicated in our kinetic model. Discussing in a more general way the distributions of the cycle times of each cell division during cleavage, we propose the following interpretation of this development. The introduction of new events in the cyclic process would imply the switching on of certain essential genetic activities. The final consequences would be the desynchronization and the lengthening of the cycles observed at the blastula stage. Thus considered, this period of embryonic development would be eminently suitable for the study of the factors of cell division control.

Protein kinase cascades in meiotic and mitotic cell cycle control

1990 ◽  
Vol 68 (12) ◽  
pp. 1297-1330 ◽  
Author(s):  
Steven L. Pelech ◽  
Jasbinder S. Sanghera ◽  
Maleki Daya-Makin
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Protein Kinase ◽  
Tyrosine Kinases ◽  
Somatic Cells ◽  
Protein Tyrosine Kinases ◽  
Sea Star ◽  
Protein Tyrosine ◽  
Threonine Kinases ◽  
Cell Division Control

Eukaryotic cell cycle progression during meiosis and mitosis is extensively regulated by reversible protein phosphorylation. Many cell surface receptors for mitogens are ligand-stimulated protein-tyrosine kinases that control the activation of a network of cytoplasmic and nuclear protein-serine(threonine) kinases. Over 30 plasma membrane associated protein-tyrosine kinases are encoded by proto-oncogenes, i.e., genes that have the potential to facilitate cancer when disregulated. Proteins such as ribosomal protein S6, microtubule-associated protein-2, myelin basic protein, and casein have been used to detect intracellular protein-serine(threonine) kinases that are activated further downstream in growth factor signalling transduction cascades. Genetic analysis of yeast cell division control (cdc) mutants has revealed another 20 or so protein-serine(threonine) kinases. One of these, specified by the cdc-2 gene in Schizosaccharomyces pombe, has homologs that are stimulated during M phase in maturing sea star and frog oocytes and mammalian somatic cells. Furthermore, during meiotic maturation in these echinoderm and amphibian oocytes, this is followed by activation of many of the same protein-serine(threonine) kinases that are stimulated when quiescent mammalian somatic cells are prompted with mitogens to traverse from G0 to G1 phase. These findings imply that a similar protein kinase cascade may oversee progression at multiple points in the cell cycle.Key words: protein kinases, mitosis, meiosis, oncogenes, cell division control.

scholarly journals Thylakoid membrane biogenesis in Chlamydomonas reinhardtii 137+. II. Cell-cycle variations in the synthesis and assembly of pigment.

1982 ◽  
Vol 93 (2) ◽  
pp. 411-416 ◽  
Author(s):  
D R Janero ◽  
R Barrnett
Keyword(s):  
Cell Cycle ◽  
Chlamydomonas Reinhardtii ◽  
Thylakoid Membrane ◽  
Direct Analysis ◽  
Cellular Level ◽  
Periodic Pattern ◽  
Cell Cycle Time ◽  
Pigment Synthesis ◽  
Thylakoid Biogenesis ◽  
Kinetics Of

Synthesis of the chlorophyll and the major carotenoid pigments and their assembly into thylakoid membrane have been studied throughout the 12-h light/12-h dark vegetative cell cycle of synchronous Chlamydomonas reinhardtii 137+ (wild-type). Pulse exposure of cells to radioactive acetate under conditions in which labeling accurately reflects lipogenesis, followed by cellular fractionation to purify thylakoid membrane, allowed direct analysis of the pigment synthesis and assembly attendant to thylakoid biogenesis. All pigments are synthesized and assembled into thylakoids continuously, but differentially, with respect to cell-cycle time. Highest synthesis and assembly rates are confined to the photoperiod (mid-to-late G1) and support chlorophyll and carotenoid accretion before M-phase. The lower levels at which these processes take place during the dark period (S, M, and early-to-mid G1) have been ascribed to pigment turnover. Within this general periodic pattern, pigment synthesis and assembly occur in a "multi-step" manner, i.e., by a temporally-ordered, stepwise integration of the various pigments into the thylakoid membrane matrix. The cell-cycle kinetics of pigment assembly at the subcellular level mirror the kinetics of pigment synthesis at the cellular level, indicating that pigment synthesis not only provides chlorophyll and carotenoid for thylakoid biogenesis but may also serve as a critical rate-determinant to pigment assembly.

Modulation of in vitro proliferation kinetics and primitive hematopoietic potential of individual human CD34+CD38–/lo cells in G0

Blood ◽  
2005 ◽  
Vol 105 (8) ◽  
pp. 3109-3116 ◽  
Author(s):  
Edward F. Srour ◽  
Xia Tong ◽  
Ki Woong Sung ◽  
P. Artur Plett ◽  
Susan Rice ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Severe Combined Immunodeficiency ◽  
Extrinsic Factors ◽  
In Vitro Proliferation ◽  
Cell Divisions ◽  
Human Cd34 ◽  
Cytokine Stimulation ◽  
Kinetics Of

AbstractWhether cytokines can modulate the fate of primitive hematopoietic progenitor cells (HPCs) through successive in vitro cell divisions has not been established. Single human marrow CD34+CD38–/lo cells in the G0 phase of cell cycle were cultured under 7 different cytokine combinations, monitored for proliferation on days 3, 5, and 7, then assayed for long-term culture-initiating cell (LTC-IC) function on day 7. LTC-IC function was then retrospectively correlated with prior number of in vitro cell divisions to determine whether maintenance of LTC-IC function after in vitro cell division is dependent on cytokine exposure. In the presence of proliferation progression signals, initial cell division was independent of cytokine stimulation, suggesting that entry of primitive HPCs into the cell cycle is a stochastic property. However, kinetics of proliferation beyond day 3 and maintenance of LTC-IC function were sensitive to cytokine stimulation, such that LTC-IC underwent an initial long cell cycle, followed by more synchronized shorter cycles varying in length depending on the cytokine combination. Nonobese diabetic/severe combined immunodeficiency (NOD/SCID) transplantation studies revealed analogous results to those obtained with LTC-ICs. These data suggest that although exit from quiescence and commitment to proliferation might be stochastic, kinetics of proliferation, and possibly fate of primitive HPCs, might be modulated by extrinsic factors.

scholarly journals Simulated Cell Division Processes of the Xenopus Cell Cycle Pathway by Genomic Object Net

2004 ◽  
Vol 1 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Mika Matsui ◽  
Sachie Fujita ◽  
Shunichi Suzuki ◽  
Hiroshi Matsuno ◽  
Satoru Miyano
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Petri Net ◽  
Notch Signaling Pathway ◽  
Hybrid Functional ◽  
Dynamic Cell ◽  
Cell Cycle Pathway ◽  
Cell Division Control

Summary Matsuno et al.[1] modeled and simulated that multicellular patterning by the Drosophila Delta-Notch signaling pathway by using the software “Genomic Object Net” which was developed based on hybrid functional Petri net (HFPN) architecture. In this model, cellular formation is fixed throughout the simulation. This paper constructs an HFPN model of the Xenopus cell cycle pathway, which includes the mechanism for cell division control as well as checkpoint processes. This model simulates dynamic cell division processes of the early Xenopus embryo, including the changes in cell division cycles from synchronous to asynchronous.

MORPHOMETRIC ANALYSIS OF YEAST CELLS: III. SIZE DISTRIBUTION OF 2-DEOXYGLUCOSE-INDUCED LYSING SCHIZOSACCAROMYCES POMBE CELLS AND THEIR SITES OF LYSIS

1974 ◽  
Vol 16 (3) ◽  
pp. 593-598 ◽  
Author(s):  
Byron F. Johnson ◽  
Calvin Lu ◽  
Sidney Brandwein
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Stationary Phase ◽  
Morphometric Analysis ◽  
Initial Dose ◽  
Low Dose ◽  
Yeast Cells ◽  
High Dose ◽  
Division Process ◽  
Low Dosage

To cultures of Schizosaccharomyces pombe, 2-deoxyglucose (2DG) was added, either as 7 μg/ml during inoculation of the cultures (low dosage), or as 250 μg/ml during the log phase (high dosage). Samples were removed from the cultures, and lysing and non-lysing cells were measured and tabulated. Addition of the high dosage was followed immediately by lysis, with over 85% of the lysing cells found in cytolysis at their primary growing ends Lysis ensued only at the beginning of the stationary phase in the low dosage experiments; 64% of the affected cells lysed at their cell plates. Cells lysing at their primary ends (high dose experiments) were shorter than the controls; cells lysing at their cell plates (low dose experiments) were longer than the controls. The cell division process of the last cell cycle completed in the culture is unusual in its susceptibility to the low initial dose of 2DG, suggesting that cell division metabolism is fundamentally different from wall extension metabolism in the fission yeast.

scholarly journals Transcriptional Networks Controlling the Cell Cycle

2013 ◽  
Vol 3 (1) ◽  
pp. 75-90 ◽  
Author(s):  
Martin Bonke ◽  
Mikko Turunen ◽  
Maria Sokolova ◽  
Anna Vähärautio ◽  
Teemu Kivioja ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Size ◽  
Transcriptional Networks ◽  
Protein Homeostasis ◽  
Transcriptional Program ◽  
Regulatory Systems ◽  
Genome Wide ◽  
A Genome ◽  
Division Process

Abstract In this work, we map the transcriptional targets of 107 previously identified Drosophila genes whose loss caused the strongest cell-cycle phenotypes in a genome-wide RNA interference screen and mine the resulting data computationally. Besides confirming existing knowledge, the analysis revealed several regulatory systems, among which were two highly-specific and interconnected feedback circuits, one between the ribosome and the proteasome that controls overall protein homeostasis, and the other between the ribosome and Myc/Max that regulates the protein synthesis capacity of cells. We also identified a set of genes that alter the timing of mitosis without affecting gene expression, indicating that the cyclic transcriptional program that produces the components required for cell division can be partially uncoupled from the cell division process itself. These genes all have a function in a pathway that regulates the phosphorylation state of Cdk1. We provide evidence showing that this pathway is involved in regulation of cell size, indicating that a Cdk1-regulated cell size checkpoint exists in metazoans.

scholarly journals Isolation and Characterization of New Fission Yeast Cytokinesis Mutants

Genetics ◽  
1998 ◽  
Vol 149 (3) ◽  
pp. 1265-1275 ◽  
Author(s):  
Mohan K Balasubramanian ◽  
Dannel McCollum ◽  
Louise Chang ◽  
Kelvin C Y Wong ◽  
Naweed I Naqvi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Genetic Screen ◽  
Contractile Ring ◽  
Medial Region ◽  
Septum Formation ◽  
Isolation And Characterization ◽  
Gtp Binding ◽  
Division Process

Abstract Schizosaccharomyces pombe is an excellent organism in which to study cytokinesis as it divides by medial fission using an F-actin contractile ring. To enhance our understanding of the cell division process, a large genetic screen was carried out in which 17 genetic loci essential for cytokinesis were identified, 5 of which are novel. Mutants identifying three genes, rng3+, rng4+, and rng5+, were defective in organizing an actin contractile ring. Four mutants defective in septum deposition, septum initiation defective (sid)1, sid2, sid3, and sid4, were also identified and characterized. Genetic analyses revealed that the sid mutants display strong negative interactions with the previously described septation mutants cdc7-24, cdc11-123, and cdc14-118. The rng5+, sid2+, and sid3+ genes were cloned and shown to encode Myo2p (a myosin heavy chain), a protein kinase related to budding yeast Dbf2p, and Spg1p, a GTP binding protein that is a member of the ras superfamily of GTPases, respectively. The ability of Spg1p to promote septum formation from any point in the cell cycle depends on the activity of Sid4p. In addition, we have characterized a phenotype that has not been described previously in cytokinesis mutants, namely the failure to reorganize actin patches to the medial region of the cell in preparation for septum formation.

scholarly journals ECM remodeling and spatial cell cycle coordination determine tissue growth kinetics

2020 ◽  
Author(s):  
Anna P. Ainslie ◽  
John Robert Davis ◽  
John J. Williamson ◽  
Ana Ferreira ◽  
Alejandro Torres-Sánchez ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Temporal Dynamics ◽  
Growth Arrest ◽  
Tissue Expansion ◽  
Tissue Growth ◽  
Cell Cycle Time ◽  
Ecm Remodeling ◽  
Cycle Times ◽  
Spatially Correlated ◽  
Developmental Growth

SummaryDuring development, multicellular organisms undergo stereotypical patterns of tissue growth to yield organs of highly reproducible sizes and shapes. How this process is orchestrated remains unclear. Analysis of the temporal dynamics of tissue growth in the Drosophila abdomen reveals that cell cycle times are spatially correlated and that growth termination occurs through the rapid emergence of a population of arrested cells rather than a gradual slowing down of cell cycle time. Reduction in apical tension associated with tissue crowding has been proposed as a developmental growth termination mechanism. Surprisingly, we find that growth arrest in the abdomen occurs while apical tension increases, showing that in this tissue a reduction in tension does not underlie the mechanism of growth arrest. However, remodeling of the extracellular matrix is necessary for tissue expansion. Thus, changes in the tissue microenvironment, and a rapid exit from proliferation, control the formation of the adult Drosophila abdomen.

scholarly journals Two different cell-cycle processes determine the timing of cell division in Escherichia coli

2021 ◽  
Author(s):  
Alexandra Colin ◽  
Gabriele Micali ◽  
Louis Faure ◽  
Marco Cosentino Lagomarsino ◽  
Sven van Teeffelen
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
Cell Division ◽  
Single Cells ◽  
Chromosome Replication ◽  
Replication Initiation ◽  
Cell Width ◽  
Division Process ◽  
Balanced Contributions ◽  
Independent Process

AbstractCells must control the cell cycle to ensure that key processes are brought to completion. In Escherichia coli, it is controversial whether cell division is tied to chromosome replication or to a replication-independent inter-division process. A recent model suggests instead that both processes may limit cell division with comparable odds in single cells. Here, we tested this possibility experimentally by monitoring single-cell division and replication over multiple generations at slow growth. We then perturbed cell width, causing an increase of the time between replication termination and division. As a consequence, replication became decreasingly limiting 21 for cell division, while correlations between birth and division and between subsequent replication-initiation events were maintained. Our experiments support the hypothesis that both chromosome replication and a replication-independent inter-division process can limit cell division: the two processes have balanced contributions in non-perturbed cells, while our width perturbations increase the odds of the replication-independent process being limiting.

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