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PubMed1979

[Autoradiographic investigations on the effect of city smog extract on DNA synthesis and cell cycle of mammalian cells in vitro. II. Alterations of the cell cycle of hamsters kidney cells and hamster embryonic cells in presence of city smog extract (author's transl)].

We used the autoradiographic method according to Quastler and Sherman to analyse alterations in the cell cycle under the influence of city smog extracts. Investigations were performed on logarithmically growing cultures of kidney and embryonic cells of the Syrian golden hamster. Low concentrations of city smog extracts (0.125 micrograms/ml Benzo(a)pyren-equivalent) induced a remarkable delay of cell entrance into DNA-synthesis. Furthermore a considerable prolongation of generation time and phase of DNA-synthesis was detected. The number of mitosis was strongly reduced. Already a doubling of concentration of city smog extract caused an almost complete breakdown of the cell cycle and a disappearing of mitosis for a time period of 10 hours. Our results strongly indicate that city smog extracts lead to a severe alteration of the molecular biology of the cell. Taking this in consideration, it can be assumed that a long term exposure of human beings to the city smog could induce an injury of health.

Air Pollutants↗

PubMed1986

DNA adducts and cell cycle.

Cell cycle-dependent differences of transformation sensitivity may be due to alterations in the formation of ultimate electrophilic carcinogens during the cell cycle, preferential primary adduct formation during specific phases of the cell cycle, e.g. binding to single stranded DNA at the replication fork, base-mispairing and mutation of transformation-related genes replicating at critical phases of DNA synthesis, or cell cycle-related differences in the repair of DNA adducts. Some recent data on these subjects are summarized, mainly in context of cell cycle-dependent transformation sensitivity of regenerating rat liver.

Animals↗

PubMed1992

Human immunodeficiency virus infection of cells arrested in the cell cycle.

Cell proliferation is necessary for proviral integration and productive infection of most retroviruses. Nevertheless, the human immunodeficiency virus (HIV) can infect non-dividing macrophages. This ability to grow in non-dividing cells is not specific to macrophages because, as we show here, CD4+ HeLa cells arrested at stage G2 of the cell cycle can be infected by HIV-1. Proliferation is necessary for these same cells to be infected by a murine retrovirus, MuLV. HIV-1 integrates into the arrested cell DNA and produces viral RNA and protein in a pattern similar to that in normal cells. In addition, our data suggest that the ability to infect non-dividing cells is due to one of the HIV-1 core virion proteins. HIV infection of non-dividing cells distinguishes lentiviruses from other retroviruses and is likely to be important in the natural history of HIV infection.

Base Sequence↗

PubMed2001

The temporal control of cell cycle and cell fate in Caenorhabditis elegans.

The nematode Caenorhabditis elegans develops through two major phases: the first phase, embryogenesis, consists of a rapid series of cleavage cell divisions leading to morphogenesis of a first stage larva. The second phase is postembryonic development, which consists of developmentally regulated cell cycles that occur during the four larval stages leading to the adult. Precursor cells set aside during embryogenesis divide through stereotypical cell lineage patterns during the four larval stages to generate larval and adult structures. The precise timing of the postembryonic cell divisions is under strict control, in most cases with a developmentally regulated G1. In certain postembryonic cell lineages, various aspects of the cell division cycle, including cell cycle exit, or G1/S progression, are controlled by temporal regulatory genes of the heterochronic gene pathway. Heterochronic genes also control the timing of numerous other developmental events, indicating that this pathway functions to coordinate the schedule of cell division and cellular differentiation throughout the animal. Some choices of cell fate that occur in response to inductive or lateral signals are linked to cell cycle progression, suggesting that cell cycle phase can confer a critical period for developmental potential in certain cells.

Animals↗

PubMed2003

Cell cycle and cell fate interactions in neural development.

Mechanisms coupling cell cycle and cell fate operate at different steps during neural development. Intrinsic factors control the cell proliferation of distinct brain regions and changes of cell fate competence, whereas components of the cell cycle machinery could play a major role in setting the appropriate timing of the generation of different cell types.

Animals↗

PubMed2003

Bcl-xL/Bcl-2 coordinately regulates apoptosis, cell cycle arrest and cell cycle entry.

Bcl-x(L) and Bcl-2 inhibit both apoptosis and proliferation. In investigating the relationship between these two functions of Bcl-x(L) and Bcl-2, an analysis of 24 Bcl-x(L) and Bcl-2 mutant alleles, including substitutions at residue Y28 previously reported to selectively abolish the cell cycle activity, showed that cell cycle delay and anti-apoptosis co-segregated in all cases. In determining whether Bcl-2 and Bcl-x(L) act in G(0) or G(1), forward scatter and pyronin Y fluorescence measurements indicated that Bcl-2 and Bcl-x(L) cells arrested more effectively in G(0) than controls, and were delayed in G(0)-G(1) transition. The cell cycle effects of Bcl-2 and Bcl-x(L) were reversed by Bad, a molecule that counters the survival function of Bcl-2 and Bcl-x(L). When control and Bcl-x(L) cells of equivalent size and pyronin Y fluorescence were compared, the kinetics of cell cycle entry were similar, demonstrating that the ability of Bcl-x(L) and Bcl-2 cells to enhance G(0) arrest contributes significantly to cell cycle delay. Our data suggest that cell cycle effects and increased survival both result from intrinsic functions of Bcl-2 and Bcl-x(L).

Alleles↗

PubMed1984

Expression of myoblast and myocyte antigens in relation to differentiation and the cell cycle.

Cell cycle parameters and expression of myoblast and myocyte antigens were investigated during exponential growth and during the differentiation phase of rat L8( E63 ) myoblasts by an integrated approach involving microspectrophotometry with DNA fluorochromes, [3H]thymidine autoradiography, and immunofluorescent staining with monoclonal antibodies. In addition to the majority of cells which are recruited into myotubes, two distinct populations of mononucleate cells were resolved in cultures of rat myoblasts undergoing differentiation. These mononucleate cells consist of (1) a population of proliferating cells with a prolonged G1 transit time; (2) a population of non-proliferating cells which remain arrested in G1 for more than 72 h. The latter group was examined with respect to the expression of two marker antigens recognized by two monoclonal antibodies: antibody B58 reacts with a macromolecular component present in undifferentiated myoblasts but not in mature myotubes, and antibody XMlb reacts with a muscle-specific isoform of myosin. All four possible combinations of expression of these antigens by single cells were found: B58 +XM1b -, B58 +XM1b +, B58 - XM1b -, and B58 - XMlb +. The implication of these findings with respect to the transition from the proliferative to the differentiative phase of myogenesis is discussed.

Animals↗

PubMed2003

Cell cycle and cell size regulation in Down syndrome cells.

Although the neuropathological features typical for Down Syndrome obviously result from deregulation of both, cell cycle control and differentiation processes, so far research focused on the latter. Considering the known similarities between the neuropathology of Down Syndrome and Alzheimer's disease and the knowledge, that in Alzheimer's disease neuronal degeneration is associated with the activation of mitogenic signals and cell cycle activation, it is tempting to investigate the consequences of an additional chromosome 21 on mammalian cell cycle regulation. We analysed the distribution of cells in different cell cycle phases on the flowcytometer and the cell size of human amniotic fluid cells with normal karyotypes and with trisomy 21. We could not detect any significant differences suggesting that the presence of an additional copy of the about 225 genes on human chromosome 21 does not trigger cell cycle effects in amniotic fluid cells. These data provide new insights into the cell biology of trisomy 21 cells.

Amniotic Fluid↗

PubMed2006

Control of the AtMAP65-1 interaction with microtubules through the cell cycle.

Cell division depends on the fine control of both microtubule dynamics and microtubule organisation. The microtubule bundling protein MAP65 is a ;midzone MAP' essential for the integrity of the anaphase spindle and cell division. Arabidopsis thaliana MAP65-1 (AtMAP65-1) binds and bundles microtubules by forming 25 nm cross-bridges. Moreover, as AtMAP65-1 bundles microtubules in interphase, anaphase and telophase but does not bind microtubules in prophase or metaphase, its activity through the cell cycle must be under tight control. Here we show that AtMAP65-1 is hyperphosphorylated during prometaphase and metaphase and that CDK and MAPK are involved in this phosphorylation. This phosphorylation inhibits AtMAP65-1 activity. Expression of non-phosphorylatable AtMAP65-1 has a negative effect on mitotic progression resulting in excessive accumulation of microtubules in the metaphase spindle midzone causing a delay in mitosis. We conclude that normal metaphase spindle organisation and the transition to anaphase is dependent on inactivation of AtMAP65-1.

Arabidopsis↗

PubMed2002

P21Waf1 control of epithelial cell cycle and cell fate.

As a broad-acting cyclin-dependent kinase inhibitor, p21(WAF1) occupies a central position in the cell cycle regulation of self-renewing tissues such as oral mucosa and skin. In addition to regulating normal cell cycle progression decisions, p21(WAF1) integrates genotoxic insults into growth arrest and apoptotic signaling pathways that ultimately determine cell fate. As a result of its complex interactions with cell cycle machinery and response to mutagenic agents, p21(WAF1) also has stage-specific roles in epithelial carcinogenesis. Finally, a view is emerging of p21(WAF1) as not merely a cyclin-dependent kinase inhibitor, but also as a direct participant in regulating genes involved in growth arrest, senescence, and aging, thus providing an additional layer of control over matters of the cell cycle. This review discusses these various roles played by p21(WAF1) in cell cycle control, and attempts to relate these to epithelial cell biology, with special emphasis on keratinocytes.

Apoptosis↗

PubMed2004

[Low-intensity microwave blockes cell cycle and regulate cell cycle related gene expression in rabbit lens epithelial cells].

OBJECTIVE: To study the cell cycle arrest induced by different doses of microwave in cultured rabbit lens epithelial cells (RLECs) and its effects on the related gene expression of P21(WAF1), P27(Kip1) and c-myc. METHODS: Cultured rabbit lens epithelial cells were exposed to microwave radiation with frequency of 2450 MHz and power density of 0.10 mW/cm(2) (A group), 0.25 mW/cm(2) (B group), 0.50 mW/cm(2) (C group), 1.00 mW/cm(2) (D group) and 2.00 mW/cm(2) (E group) for 8 hours. The morphological change of RLECs was observed under microscope, effects of microwave radiation on RLECs cell cycle were measured by flow cytometry. Expression of P21(WAF1), P27(Kip1) and c-myc were evaluated by western blot after 2.00 mW/cm(2) microwave radiation for 4 hours, 6 hours and 8 hours respectively. All the results were compared with F group, which was as controls without microwave radiation. RESULTS: 8 hours after radiation, RLECs of C, D and E groups showed RLECs cell swelling, congregation and detachment, the percentage of cells in G(0)/G(1) phase obviously was increased (P < 0.01). No obvious change could be detected in 0.10 mW/cm(2) and 0.25 mW/cm(2) microwave groups. The gene expression of P27(Kip1) was increased and c-myc was decreased after 2.00 mW/cm(2) radiation, it did not affect the gene expression of P21(WAF1). CONCLUSION: Microwave exceeding 0.50 mW/cm(2) can block RLECs cell cycle at G(0)/G(1) phase, which may be related to regulation of P27(Kip1) and c-myc expression, but not P21(WAF1).

Animals↗

PubMed2002

Cell cycle checkpoint signaling: cell cycle arrest versus apoptosis.

Although toxicants may initiate cell damage or stress, the cellular proteins that are involved in control of cell cycle and apoptosis are the final arbiters of cell fate. The biochemical pathways that restrain cell cycle transition and/or induce cell death after stress are known as cell cycle checkpoints. These checkpoints maintain the fidelity of DNA replication, repair, and division. Herein, select cell cycle checkpoint signaling pathways will be discussed and how different components of these pathways are regulated by exogenous and endogenous agents, with focus on the p53 tumor suppressor signaling. The p53 protein is known to play a key role in growth arrest and apoptosis after cell stress, primarily through its ability to regulate the transcription of select downstream target genes in the cell. Further elucidation of the signaling pathways that control growth arrest and apoptosis will continue to provide insights to the complex cellular responses to environmental toxicants.

Animals↗

PubMed1998

A link between cell cycle and cell death: Bax and Bcl-2 modulate Cdk2 activation during thymocyte apoptosis.

Resting thymocytes undergoing apoptosis in response to specific stimuli degrade the cdk inhibitor p27(Kip1) and upregulate Cdk2 kinase activity. Inhibition of Cdk2 kinase activity efficiently blocks cell death via certain apoptosis pathways whereas overexpression of Cdk2 accelerates such cell death, suggesting its involvement in the signal transduction pathways activated by certain apoptotic stimuli. We found that Cdk2 activation during thymocyte apoptosis can be regulated by p53, Bax and Bcl-2. The highly elevated Cdk2 kinase activity in the apoptosing thymocytes is not associated with its canonical cyclins, cyclin E and cyclin A, and requires de novo synthesis of proteins for activation to take place. We therefore propose Cdk2 activation to be a crucial event in distinct pathways of apoptosis and the point at which the cell cycle and cell death pathways interact.

Apoptosis↗

PubMed1994

The steady state levels and structure of the U7 snRNP are constant during the human cell cycle: lack of cell cycle regulation of histone mRNA 3' end formation.

The U7 small nuclear ribonucleoprotein (snRNP) is an essential component of the endonucleolytic cleavage reaction which leads to the production of mature 3'-ends of histone premRNAs. We have examined the relative amount and the structure of the U7 snRNP, as assayed by sensitivity to micrococcal nuclease, during the cell cycle in human HeLa and WI-38 cells. Using an RNase A protection assay, we find no change in the steady state levels of U7 throughout the cell cycle. Similarly, the sensitivity of U7 to micrococcal nuclease remained unchanged in both cell types. Contact inhibited WI-38 cells, that are deemed to have left the cell cycle and entered a quiescent state, displayed similar levels of U7 to cells in S and G1 phases of the cell cycle, however, the U7 snRNA was slightly more resistant to micrococcal nuclease. Histone 3' end mRNA processing was also assayed in HeLa cell cycle phase-specific extracts. In marked contrast to previous observations in extracts prepared from the rodent cell line, C3H10T1/2, (Hoffmann and Birnstiel, 1990), we find that the 3' end processing reaction remained constant throughout the cell cycle.

Base Sequence↗

PubMed2006

Gab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor.

We have shown previously that either Grb2- or Shc-mediated signaling from the oncogenic Met receptor Tpr-Met is sufficient to trigger cell cycle progression in Xenopus oocytes. However, direct binding of these adaptors to Tpr-Met is dispensable, implying that another Met binding partner mediates these responses. In this study, we show that overexpression of Grb2-associated binder 1 (Gab1) promotes cell cycle progression when Tpr-Met is expressed at suboptimal levels. This response requires that Gab1 possess an intact Met-binding motif, the pleckstrin homology domain, and the binding sites for phosphatidylinositol 3-kinase and tyrosine phosphatase SHP-2, but not the Grb2 and CrkII/phospholipase Cgamma binding sites. Importantly, we establish that Gab1-mediated signals are critical for cell cycle transition promoted by the oncogenic Met and fibroblast growth factor receptors, but not by progesterone, the natural inducer of cell cycle transition in Xenopus oocytes. Moreover, Gab1 is essential for Tpr-Met-mediated morphological transformation and proliferation of fibroblasts. This study provides the first evidence that Gab1 is a key binding partner of the Met receptor for induction of cell cycle progression, proliferation, and oncogenic morphological transformation. This study identifies Gab1 and its associated signaling partners as potential therapeutic targets to impair proliferation or transformation of cancer cells in human malignancies harboring a deregulated Met receptor.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Expression of extensin genes is dependent on the stage of the cell cycle and cell proliferation in suspension-cultured Catharanthus roseus cells.

To isolate cDNAs expressed at a specific phase of the cell cycle in a higher plant, we performed differential screening of a cDNA library prepared from the S-phase cells of synchronized cultures of Catharanthus roseus. Sequence analysis shows that two of the identified cDNAs, cyc15 and cyc17, encode extensins that represent a family of cell wall hydroxyproline-rich glycoproteins. Protein sequences deduced from the two cDNAs contain the characteristic pentapeptide repeat sequence, Ser-Pro-Pro-Pro-Pro, which is commonly observed in extensins. The protein sequences also share several other extensin characteristics such as the presence of a N-terminal signal peptide and a high content of Tyr and Lys residues. When C. roseus cell suspension cultures were synchronized by phosphate starvation, the mRNAs of both cyc15 and cyc17 were transiently expressed during the S and G2 phases of the cell cycle. However, significant amounts of the mRNAs also accumulated in phosphate-starved cells arrested in the G1 phase. In asynchronous cultures, both genes were expressed during the stationary phase, when cell proliferation ceased. The observed patterns of expression suggest that the extensin genes, cyc15 and cyc17, are under two types of regulation: one that depends on the stage of the cell cycle and another that is induced during the growth arrest. Thus, the products of these genes may function both during the progression through the cell cycle and in the strengthening of the cell wall after cell division.

Amino Acid Sequence↗

PubMed1999

Aberrations of cell cycle and cell death in normal development of the chick embryo growth plate.

The epiphyses of femurs from 7.5-15 day chicken embryos were studied by electron microscopy. Several forms of aberrant cell cycles were present: (1) in the perichondrium, polyploid metaphases, segmentating large (giant) cells, and mitotic catastrophe (midway between mitosis and apoptosis) were observed; (2) in the resting zone, premature chromosome condensation was found; (3) in the proliferative zone, approximately 5% of divisions were aberrant, representing most often mitosis restitution from metaphase and more seldom from the anaphase; (4) in all layers, 'dark chondrocytes' representing a premortal form of hypersecretory cells undergoing often a-mitotic nuclear segmentation were present. Many of the aberrations of cell cycle were combined with cell death. These deviations omitting or adapting the cell cycle check-points represent evidently the normal epigenetic mechanisms of development and repair. At the same time, by origin and appearances they seem very close to the loss of the growth control displayed by malignant tumours. This connection is briefly analysed in view of some current concepts of carcinogenesis.

Animals↗

PubMed1994

A library of yeast genomic MCM1 binding sites contains genes involved in cell cycle control, cell wall and membrane structure, and metabolism.

The Saccharomyces cerevisiae MCM1 protein, which is essential for viability, participates in both transcription activation and repression as well as DNA replication. However, neither the full network of genes at which MCM1 acts nor whether MCM1 itself mediates a regulatory response is known. Thus far, sites of MCM1 action have been identified by chance during analysis of particular genes. To identify a more complete set of genes on which MCM1 acts, we isolated a library of yeast genomic sequences to which MCM1 binds and then identified known genes within this library. Fragments of genomic DNA, bound to bacterially expressed MCM1 protein, were collected on a nitrocellulose filter, cloned, and analyzed. This selected library contains a large number of genes. As expected, it is enriched for strong MCM1 binding sites and contains cell-type-specific genes known to require MCM1. In addition, it also includes sequences upstream (or near the 5' end) of a number of identified yeast genes that have not yet been shown to be controlled by MCM1. These include genes whose products are involved in (i) the control of cell cycle progression (CLN3, CLB2, and FAR1), (ii) synthesis and maintenance of cell wall or cell membrane structures (PMA1, PIS1, DIT1,2, and GFA1), (iii) cellular metabolism (PCK1, MET2, and CCP1), and (iv) production of a secreted glycoprotein which is heat shock inducible (HSP150). The previously unidentified MCM1 binding site in the essential PMA1 gene is required for expression of a PMA1:lacZ fusion gene, providing evidence that one site is functionally important. We speculate that MCM1 coordinates decisions about cell cycle progression with changes in cell wall integrity and metabolic activity. The presence in the library of three genes involved in cell cycle progression reinforces the idea that one of the functions of MCM1 is indeed analogous to that of the mammalian serum response factor.

Base Sequence↗