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PubMed2005

Balance between cell division and differentiation during plant development.

The processes which make possible that a cell gives rise to two daughter cells define the cell division cycle. In individual cells, this is strictly controlled both in time and space. In multicellular organisms extra layers of regulation impinge on the balance between cell proliferation and cell differentiation within particular ontogenic programs. In contrast to animals, organogenesis in plants is a post-embryonic process that requires developmentally programmed reversion of sets of cells from different differentiated states to a pluripotent state followed by regulated proliferation and progression through distinct differentiation patterns. This implies a fine coupling of cell division control, cell cycle arrest and reactivation, endoreplication and differentiation. The emerging view is that cell cycle regulators, in addition to controlling cell division, also function as targets for maintaining cell homeostasis during development. The mechanisms and cross talk among different cell cycle regulatory pathways are discussed here in the context of a developing plant.

Arabidopsis↗

PubMed1988

Patterns of cell division in imaginal discs of Drosophila.

A transmission electron microscopic study of cell division in serially sectioned imaginal discs of early third instar fruitfly larvae revealed that mitotic cells maintain a relationship with the basal surface of the disc through thin cytoplasmic extensions abutting on vesicular material. Two patterns of cell division were discerned. In one, cell divisions were isolated and usually found near the peripodial membrane-disc epithelium junction; in the other, cell divisions were clustered. Observations on cell death and cell division in the peripodial membrane are also reported.

Animals↗

PubMed2004

Bacterial cell division and the septal ring.

Cell division in bacteria is mediated by the septal ring, a collection of about a dozen (known) proteins that localize to the division site, where they direct assembly of the division septum. The foundation of the septal ring is a polymer of the tubulin-like protein FtsZ. Recently, experiments using fluorescence recovery after photobleaching have revealed that the Z ring is extremely dynamic. FtsZ subunits exchange in and out of the ring on a time scale of seconds even while the overall morphology of the ring appears static. These findings, together with in vitro studies of purified FtsZ, suggest that the rate-limiting step in turnover of FtsZ polymers is GTP hydrolysis. Another component of the septal ring, FtsK, is involved in coordinating chromosome segregation with cell division. Recent studies have revealed that FtsK is a DNA translocase that facilitates decatenation of sister chromosomes by TopIV and resolution of chromosome dimers by the XerCD recombinase. Finally, two murein hydrolases, AmiC and EnvC, have been shown to localize to the septal ring of Escherichia coli, where they play an important role in separation of daughter cells.

Bacteria↗

PubMed1983

Protein p53 and inducer-mediated erythroleukemia cell commitment to terminal cell division.

Inducer-mediated murine erythroleukemia cell (MELC) differentiation provides a model for examining factors determining terminal cell differentiation. The nuclear protein, p53, has been implicated as a potential determinant of cell cycle progression and cell differentiation. In this study p53 content and synthesis, during inducer-mediated MELC differentiation, has been examined with monoclonal antibodies to p53. A decrease in p53 synthesis and content was demonstrated during induced differentiation. As determined by cell cycle fractionation, the decrease in p53 is manifest at all stages of the cell cycle. Hemin, which induces globin mRNA accumulation but not terminal cell division, fails to decrease p53 content. A MELC variant resistant to inducer-mediated commitment to terminal cell division also fails to decrease p53 levels in response to inducers. These experiments suggest that p53 is implicated in MELC cell proliferation and that an induced decrease in p53 may be responsible for G1 phase prolongation and terminal G1 arrest.

Acetamides↗

PubMed1976

Requirement of a cell division step for stalk formation in Caulobacter crescentus.

Penicillin G at low concentrations blocked cell division in Caulobacter crescentus without inhibiting cell growth. The long filamentous cells formed after two to three generations under these conditions had a stalk at one pole and usually one or more flagella at the opposite pole. The failure of the filaments to form a second stalk at the flagellated pole indicates that stalk formation was dependent upon completion of a step that was also required for cell division. Two observations support this conclusion. (i) Penicillin did not stop the normal development of synchronous swarmer cells into stalked initiation and stalk elongation. (ii) When the action of penicillin was reversed by the addition of penicillinase to cultures of filaments, stalks were not formed at the nonstalked pole until after cell division had occurred; thus the normal order of development events was maintained: cell division leads to stalk formation. These results are consistent with a model in which the organization of the developmental program for stalk formation occurs before cell division as a consequence of steps that branch from the cell division pathway.

Bacteria↗

PubMed1999

Induction of mitotic cell division distrubances and mitotic arrest by pyrethroids in V79 cell cultures.

Five pyrethroids (fenvalerate, deltamethrin, cypermethrin, permethrin, cyfluthrin) differing in their chemical purity were investigated on their cytotoxic effects, especially on their ability to induce mitotic cell division disturbances using Chinese hamster lung cells of line V79. The colony forming ability (CFA) resulted in distinct differences of the cytotoxic effect of the tested pyrethroids, whereby permethrin was found to be most toxic. With the exception of fenvalerate all tested pyrethroids gave rise to inhibition of cell cycle progression as shown by G2/M-arrest of synchronized V79 cells by flow cytometry as well as by the increase of the mitotic index as evaluated by light microscopy. The mitotic arresting activity could be attributed to the occurrence of abnormal mitotic figures such as initial and full C-metaphases. The results however indicate, that pyrethroids per se do not contribute to the cytotoxic effects but that other factors such as chemical impurities, source as well as manufacturing process and isomer composition may be responsible for the observed cytotoxic effects.

Animals↗

PubMed1983

Amino acid transport: its role in cell division and growth of Saccharomyces cerevisiae cells.

The transport of six amino acids was studied in exponentially growing and G1 arrested temperature sensitive mutants of the yeast Saccharomyces cerevisiae. The uptake of three amino acids viz. Gly, Ala and Val was selectively reduced in G1 arrested cells. The reduction in transport was only noticeable when cdc 28 mutant cells were arrested at their non-permissive temperature. Cdc 28 is known to arrest at the point of commitment to the cell cycle 'start'. The uptake, however, was unaffected in G1 arrested cdc 4 and cdc 7 cells. The wild type cells (A364A) when arrested at stationary phase, also demonstrated the reduction in the uptake of Ala and Val. It appears that amino acid transport may be involved in growth and cell division of Saccharomyces cerevisiae.

Amino Acids↗

PubMed1998

FGF is an essential regulator of the fifth cell division in preimplantation mouse embryos.

Fibroblast growth factor (FGF) signaling is required prior to gastrulation in the mouse embryo. To test for the spatial and temporal requirements of FGF signaling, a dominant negative FGF receptor (dnFGFR) was used to make transgenic mouse embryos. In mosaic embryos, cell division ceased at the fifth cell division in all cells that expressed the mutant receptor, but cell death did not increase. After the fifth cell division, the progeny of unaltered cells and cells expressing lacZ continued to accumulate at the same rate, suggesting that the FGF requirement is cell autonomous. In mosaic embryos, lacZ, but not dnFGFR expression was detected in mitotic trophoblasts adjacent to the ICM. Conversely, dnFGFR-expressing extraembryonic ectoderm cells were detected at the abembryonic pole in postmitotic cells. In blastocysts expressing the dnFGFR in all cells, the morphology appeared normal and inner cell masses (ICMs) formed, but resultant embryos had only one-third the number of cells as control embryos. In these blastocysts, cell division had also ceased at the fifth cell division, but cavitation, a concurrent morphogenetic event, initiated and progressed normally. To test for the continuing requirement of FGF, FGFR-3 was overexpressed in all cells and resulted in an increase in cell numbers after the fifth cell cycle. In a model for postimplantation development, addition of FGF-4 to blastocyst outgrowths increased the number of extraembryonic ectoderm cells, suggesting a continuing role for FGF. Thus, FGF signaling induces the cell division of embryonic and extraembryonic cells in the preimplantation mouse embryo starting at the fifth cell division. The signal requirement for FGF is cell autonomous, but is not required to prevent cell death. This provides the first evidence for the necessity of a growth factor before implantation.

Animals↗

PubMed2003

Distinct thresholds for CD8 T cell activation lead to functional heterogeneity: CD8 T cell priming can occur independently of cell division.

To examine the bases for CD8 T cell functional heterogeneity, we analyzed responses to partial vs full agonist Ag. An extended period of interaction with APCs was required to set the threshold required for cell division in response to partial as compared with full agonist Ag. Acquisition of cytolytic function was restricted to the divided T cell population. In contrast, the threshold for commitment to produce IFN-gamma and express some activation markers appeared lower and independent of cell division. Indeed, we characterized a T cell population stimulated in response to the partial agonist that was committed to produce IFN-gamma, but failed to divide or secrete IL-2. Importantly, this activated nondivided population behaved as "primed" rather than "anergized," indicating 1) that priming of CD8 T cells may be induced by suboptimal stimulation independent of cell division and 2) that encounter with Ag does not always induce a complete differentiation program in naive CD8 T cells, as previously reported.

Animals↗

PubMed1997

The Bacillus subtilis DivIVA protein targets to the division septum and controls the site specificity of cell division.

The Bacillus subtilis divIVA gene, first defined by a mutation giving rise to anucleate minicells, has been cloned and characterized. Depletion of DivIVA leads to inhibition of the initiation of cell division. The residual divisions that do occur are abnormally placed and sometimes misorientated relative to the long axis of the cell. The DivIVA phenotype can be suppressed by disruption of the MinCD division inhibitor, suggesting that DivIVA controls the topological specificity of MinCD action and thus septum positioning. A DivIVA-GFP fusion targets to new and used sites of cell division, consistent with it having a direct role in topological specification.

Adenosine Triphosphatases↗

PubMed1987

Human T lymphocytes stimulated by phytohaemagglutinin undergo a single round of cell division without a requirement for interleukin-2 or accessory cells.

Monocyte-depleted human T lymphocytes completed a single round of DNA synthesis and cell division when treated with phytohaemagglutinin (PHA). Direct assay of culture supernatants showed that very low amounts of interleukin-2 (IL-2) were synthesized in these cultures. Furthermore, the first round of cell division was totally unaffected by the addition of saturating amounts of anti-Tac, a monoclonal antibody against the IL-2 receptor. These data strongly suggest that stimulation of IL-2 receptors by IL-2 was not required for the completion of the first round of mitosis. By contrast, proliferation of the daughter cells produced by the first cell doubling required the addition of exogenous IL-2 and was totally abolished by anti-Tac. These results were confirmed by experiments using single lymphocytes, which also showed that accessory cells were not required during the first cell doubling of PHA-stimulated lymphocytes. We therefore propose a modified model for in vitro T-lymphocyte activation, wherein PHA stimulate a single round of cell proliferation without a requirement for stimulation by IL-2. The resulting daughter cells now require IL-2 for further proliferation. By analogy, we suggest that triggering by antigen in vivo (in the context of products of the major histocompatibility locus) may also stimulate a single round of IL-2-independent division in appropriate clones of T lymphocytes, with the resulting population of daughter cells requiring IL-2 for further expansion of the population.

Antibodies, Monoclonal↗

PubMed2001

4-1BB ligand induces cell division, sustains survival, and enhances effector function of CD4 and CD8 T cells with similar efficacy.

A costimulatory member of the TNFR family, 4-1BB, is expressed on activated T cells. Although some reports have suggested that 4-1BB is primarily involved in CD8 T cell activation, in this report we demonstrate that both CD4 and CD8 T cells respond to 4-1BB ligand (4-1BBL) with similar efficacy. CD4 and CD8 TCR transgenic T cells up-regulate 4-1BB, OX40, and CD27 and respond to 4-1BBL-mediated costimulation during a primary response to peptide Ag. 4-1BBL enhanced proliferation, cytokine production, and CTL effector function of TCR transgenic T cells. To compare CD4 vs CD8 responses to 4-1BBL under similar conditions of antigenic stimulation, we performed MLRs with purified CD4 or CD8 responders from CD28(+/+) and CD28(-/-) mice. We found that CD8 T cells produced IL-2 and IFN-gamma in a 4-1BBL-dependent manner, whereas under the same conditions the CD4 T cells produced IL-2 and IL-4. 4-1BBL promoted survival of CD4 and CD8 T cells, particularly at late stages of the MLR. CD4 and CD8 T cells both responded to anti-CD3 plus s4-1BBL with a similar cytokine profile as observed in the MLR. CD4 and CD8 T cells exhibited enhanced proliferation and earlier cell division when stimulated with anti-CD3 plus anti-CD28 compared with anti-CD3 plus 4-1BBL, and both subsets responded comparably to anti-CD3 plus 4-1BBL. These data support the idea that CD28 plays a primary role in initial T cell expansion, whereas 4-1BB/4-1BBL sustains both CD4 and CD8 T cell responses, as well as enhances cell division and T cell effector function.

4-1BB Ligand↗

PubMed2001

Structural and functional studies of MinD ATPase: implications for the molecular recognition of the bacterial cell division apparatus.

Proper placement of the bacterial cell division site requires the site-specific inactivation of other potential division sites. In Escherichia coli, selection of the correct mid-cell site is mediated by the MinC, MinD and MinE proteins. To clarify the functional role of the bacterial cell division inhibitor MinD, which is a membrane-associated ATPase that works as an activator of MinC, we determined the crystal structure of a Pyrococcus furiosus MinD homologue complexed with a substrate analogue, AMPPCP, and with the product ADP at resolutions of 2.7 and 2.0 A, respectively. The structure reveals general similarities to the nitrogenase iron protein, the H-Ras p21 and the RecA-like ATPase domain. Alanine scanning mutational analyses of E.coli MinD were also performed in vivo. The results suggest that the residues around the ATP-binding site are required for the direct interaction with MinC, and that ATP binding and hydrolysis play a role as a molecular switch to control the mechanisms of MinCDE-dependent bacterial cell division.

Adenosine Triphosphatases↗

PubMed1995

Cell division does not increase transepithelial permeability of LLC-PK1 cell sheets.

The transepithelial electrical resistance (TER) across LLC-PK1 cell sheets is unstable for several days postseeding, even when the cells are trypsinized from a previously confluent culture and replated at confluent density. We therefore followed the TER of LLC-PK1 cells plated at confluent density to elucidate characteristics of the TER fluctuations after plating of the cells. Control cultures reached a maximum TER of 1800 omega.cm2 approximately 24 h after plating. TER then declined sharply, reaching generally stable values (approximately 175 omega.cm2) only after 4 days. Cell cycle activity ([3H]-thymidine incorporation) peaked approximately 22 h after plating, prior to the peak in TER values, and then followed a decline similar to that of the TER. Treatment of cells with EGF at 24 h after plating caused the TER values reached at 3-4 days postseeding to exceed time matched controls by approximately 100%. This EGF-treated group showed a concomitant increase in [3H]thymidine incorporation and cell density compared to control. Transepithelial fluxes of [14C]D-mannitol across control vs EGF-treated cell sheets were not, however, significantly different at the 4-day time point, indicating that a change in tight junction sieving on the basis of size had not occurred. Diffusion and bi-ionic potential studies indicated that the change in TER in EGF-treated cells was instead due to altered charge selectivity at the tight junction and/or intercellular space. We conclude: (1) TER across LLC-PK1 cell sheets does not stabilize until 4 days after seeding at confluent density and (2) cell division and resultant increased cell density in LLC-PK1 cell sheets can correlate with elevated TER values, due to altered ion permeability of the paracellular pathway. Permeability to both Na+ and Cl- decreased as a result of EGF treatment but the decline in chloride permeability was significantly greater. Not only was there a decrease in the permeabilities of all halide anions after exposure of cell sheets to EGF, but the permeability sequence changed after EGF exposure.

Animals↗

PubMed2005

Targeting the cell division cycle in cancer: CDK and cell cycle checkpoint kinase inhibitors.

The cyclin-dependent kinase (CDK) family of serine/threonine kinases regulate progression through each stage of the cell division cycle and as such are major targets for deregulation in cancer. This has led to the development of several small-molecule inhibitors of CDKs as potential therapeutic agents for the treatment of this disease. Progression through the cell cycle is also monitored at several positions known as cell cycle checkpoints, two of which occur during G1 and G2 in response to DNA damage. These are often defective in cancer, leading to the suggestion that inhibition of one or both of the cell cycle checkpoint kinases CHK1 and CHK2 may drive a cancer cell that already has defects in its cell cycle checkpoints towards death.

Cell Cycle↗

PubMed2000

[Expression of the Cholinesterase-Related Cell Division Controller Gene in Peripheral Blood Cell from Patients with Myelodysplastic Syndrome]

To investigate the expression of the cholinesterase-related cell division controller (CHED) gene in the patients with myelodysplastic syndrome (MDS), CHED gene expression was assayed by RT-PCR and its relative expression rate (RER) was determined by the semi-quantitative RT-PCR analysis in peripheral blood mononuclear cells from 21 patients with MDS, 12 normal individuals served as controls. Results showed that RER of CHED in the patients (2.69 +/- 0.76) was significantly higher than that in controls (1.12 +/- 0.51, P < 0.01), the RER out of 85.7% of the patients was higher than the mean value of the controls, in which three patients developed into acute leukemia; the RER out of 61.9% of the patients was higher than the upper limit of the mean value of the controls; three patients whose RER was lower than the mean value of the controls did not developed into leukemia. These findings suggested that the expression of CHED gene in patients with MDS was significantly higher than in controls.

Journal Article↗

PubMed1987

A conceptual model of cell division in neoplasia.

A model of cell division as it occurs in the neoplastic cell is presented. The two basic features of the model are that firstly cell division is autonomous and secondly it is incomplete because not all of the processes which take place during normal division occur in the disordered division of neoplasia. As a result cellular structures may not be replicated along with the rest of the cell and they are therefore deficient. The deficiency of particular structures is then used to explain certain observations made of neoplastic cells eg. disturbances of metabolism and morphology, heterogeneity of the cell population, malignancy and immortalisation. Oncogenes are then introduced into the model in an attempt to understand their role in the development of cancer.

Cell Division↗

PubMed1976

Action of delta 9-tetrahydrocannabinol on cell division and macromolecular synthesis in division-synchronized protozoa.

Delta 9-Tetrahydrocannabinol (THC) elicited a dose-dependent (3.2-24 muM) response for form/movement, cellular growth and division in log growth phase and division-synchronized Tetrahymena pyriformis GL. Progressive dose-dependent action of THC on division delays in division-synchronized cell cultures was correlated with a concomitant reduction of division maxima and the percent of cells that completed division I. THC depressed the incorporation of 5-3H-uridine, 2-14C-thymidine and L-3-14C-phenylalanine into RNA, DNA and protein macromolecules respectively of division-synchronized Tetrahymena during division I. The depression of incorporation of 5-3H-uridine into nucleic acid macromolecules was correlated with a reduction of exogenous precursor in the cellular pool. The specific activity of radiolabeled mRNA and nascent polypeptides of polyribosomal fractions from synchronized cells was reduced by THC treatment. THC caused an inhibition of the incorporation of 5-3H-uridine into ribosomal RNA (17S and 25S RNA) and ribosomal precursor RNA (35S RNA) of synchronized cells.

Cannabis↗