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.

Tissue economics of hydra: regulation of cell cycle, animal size and development by controlled feeding rates

1977 ◽  
Vol 28 (1) ◽  
pp. 117-132
Author(s):  
J.J. Otto ◽  
R.D. Campbell
Keyword(s):  
Cell Cycle ◽  
Steady State ◽  
Epithelial Cell ◽  
Cycle Time ◽  
Cell Loss ◽  
Tissue Growth ◽  
Tissue Loss ◽  
Feeding Rates ◽  
Cell Cycle Time ◽  
Steady State Condition

Epithelial cell production and epithelial cell loss in 6 different size classes of Hydra attenuata were examined to understand the relationships between growth and morphogenesis. The sizes of adult hydra, the sizes of their buds, and their budding rates are all nearly proportional to the amount of food the hydra eat. Hydra fed at high rates (4-25 Artemia nauplii per day) all have the same epithelial cell cycle time (about 4 days). Budding accounts for most of their cell loss. Hydra fed 4–12 Artemia per day maintain a steady state condition in which tissue loss balances tissue growth. Animals fed 25 Artemia per day are not in a steady state growth condition and change in size. At the lowest feeding rates (0-1 Artemia per day), the epithelial cell cycle time is lengthened to about 16 days. Cell loss from the tentacles accounts for most of the cell loss, and this loss is not completely balanced by growth. As a consequence these animals cease budding and shrink in size.

The relationship between histone H3 phosphorylation and acetylation throughout the mammalian cell cycleThis paper is one of a selection of papers published in this Special Issue, entitled 27th International West Coast Chromatin and Chromosome Conference, and has undergone the Journal's usual peer review process.

2006 ◽  
Vol 84 (4) ◽  
pp. 640-657 ◽  
Author(s):  
Kirk J. McManus ◽  
Michael J. Hendzel
Keyword(s):  
Cell Cycle ◽  
Temporal Dynamics ◽  
Peer Review Process ◽  
Histone H3 ◽  
Specific Cell ◽  
Cell Cycle Time ◽  
Post Translational Modifications ◽  
Amino Terminal ◽  
Spatio Temporal

During interphase, histone amino-terminal tails play important roles in regulating the extent of DNA compaction. Post-translational modifications of the histone tails are intimately associated with regulating chromatin structure: phosphorylation of histone H3 is associated with proper chromosome condensation and dynamics during mitosis, while multiple H2B, H3, and H4 tail acetylations destabilize the chromatin fiber and are sufficient to decondense chromatin fibers in vitro. In this study, we investigate the spatio-temporal dynamics of specific histone H3 phosphorylations and acetylations to better understand the interplay of these post-translational modifications throughout the cell cycle. Using a panel of antibodies that individually, or in combination, recognize phosphorylated serines 10 and 28 and acetylated lysines 9 and 14, we define a series of changes associated with histone H3 that occur as cells progress through the cell cycle. Our results establish that mitosis appears to be a period of the cell cycle when many modifications are highly dynamic. Furthermore, they suggest that the upstream histone acetyltransferases/deacetylases and kinase/phosphatases are temporally regulated to alter their function globally during specific cell cycle time points.

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.

scholarly journals Adenovirus E4orf4 protein induces PP2A-dependent growth arrest in Saccharomyces cerevisiae and interacts with the anaphase-promoting complex/cyclosome

2001 ◽  
Vol 154 (2) ◽  
pp. 331-344 ◽  
Author(s):  
Daniel Kornitzer ◽  
Rakefet Sharf ◽  
Tamar Kleinberger
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Mammalian Cells ◽  
Growth Arrest ◽  
Anaphase Promoting Complex ◽  
Reading Frame ◽  
Cycle Growth ◽  
M Phase ◽  
Dependent Growth ◽  
Synthetically Lethal

Adenovirus early region 4 open reading frame 4 (E4orf4) protein has been reported to induce p53-independent, protein phosphatase 2A (PP2A)–dependent apoptosis in transformed mammalian cells. In this report, we show that E4orf4 induces an irreversible growth arrest in Saccharomyces cerevisiae at the G2/M phase of the cell cycle. Growth inhibition requires the presence of yeast PP2A-Cdc55, and is accompanied by accumulation of reactive oxygen species. E4orf4 expression is synthetically lethal with mutants defective in mitosis, including Cdc28/Cdk1 and anaphase-promoting complex/cyclosome (APC/C) mutants. Although APC/C activity is inhibited in the presence of E4orf4, Cdc28/Cdk1 is activated and partially counteracts the E4orf4-induced cell cycle arrest. The E4orf4–PP2A complex physically interacts with the APC/C, suggesting that E4orf4 functions by directly targeting PP2A to the APC/C, thereby leading to its inactivation. Finally, we show that E4orf4 can induce G2/M arrest in mammalian cells before apoptosis, indicating that E4orf4-induced events in yeast and mammalian cells are highly conserved.

scholarly journals Cooperative effects of genes controlling the G2/M checkpoint

2000 ◽  
Vol 14 (13) ◽  
pp. 1584-1588
Author(s):  
Timothy A. Chan ◽  
Paul M. Hwang ◽  
Heiko Hermeking ◽  
Kenneth W. Kinzler ◽  
Bert Vogelstein
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Mammalian Cells ◽  
Growth Arrest ◽  
Double Knockout ◽  
Specific Test ◽  
Cooperative Effects ◽  
Exogenous Expression ◽  
Induced Genes ◽  
Single Knockout

It is believed that multiple effectors independently control the checkpoints permitting transitions between cell cycle phases. However, this has not been rigorously demonstrated in mammalian cells. The p53-induced genes p21 and 14-3-3ς are each required for the G2 arrest and allow a specific test of this fundamental tenet. We generated human cells deficient in bothp21 and 14-3-3ς and determined whether the double knockout was more sensitive to DNA damage than either single knockout.p21−/−14-3-3ς−/− cells were significantly more sensitive to DNA damage or to the exogenous expression of p53 than cells lacking only p21 or only 14-3-3ς. Thus, p21 and 14-3-3ς play distinct but complementary roles in the G2/M checkpoint, and help explain why genes at the nodal points of growth arrest pathways, like p53, are the targets of mutation in cancer cells.

scholarly journals The proliferative effect of cortisol on bovine endometrial epithelial cells

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Junsheng Dong ◽  
Jun Li ◽  
Jianji Li ◽  
Luying Cui ◽  
Xia Meng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factors ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Tissue Growth ◽  
Mrna Levels ◽  
Physiological Level ◽  
Endometrial Epithelial Cells

Abstract Background Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. Methods BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. Results Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. Conclusions These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways.

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