Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CELL DIVISION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1997

A promoter for the first nine genes of the Escherichia coli mra cluster of cell division and cell envelope biosynthesis genes, including ftsI and ftsW.

We constructed a null allele of the ftsI gene encoding penicillin-binding protein 3 of Escherichia coli. It caused blockage of septation and loss of viability when expression of an extrachromosomal copy of ftsI was repressed, providing a final proof that ftsI is an essential cell division gene. In order to complement this null allele, the ftsI gene cloned on a single-copy mini-F plasmid required a region 1.9 kb upstream, which was found to contain a promoter sequence that could direct expression of a promoterless lacZ gene on a mini-F plasmid. This promoter sequence lies at the beginning of the mra cluster in the 2 min region of the E. coli chromosome, a cluster of 16 genes which, except for the first 2, are known to be involved in cell division and cell envelope biosynthesis. Disruption of this promoter, named the mra promoter, on the chromosome by inserting the lac promoter led to cell lysis in the absence of a lac inducer. The defect was complemented by a plasmid carrying a chromosomal fragment ranging from the mra promoter to ftsW, the fifth gene downstream of ftsI, but not by a plasmid lacking ftsW. Although several potential promoter sequences in this region of the mra cluster have been reported, we conclude that the promoter identified in this study is required for the first nine genes of the cluster to be fully expressed.

Bacterial Proteins↗
PubMed1980

A spatial analysis of the localization of cell division and cell death in relationship with the morphogenesis of the chick optic cup.

In an attempt to analyze the possible mechanisms underlying the morphogenesis of the optic cup and the optic fissure, two features of generally accepted morphogenetic importance, mitosis and cell death, were studied in their spatial distribution in the chick. The mitotic figures and necrotic remnants visible in serial sections as stained with Feulgen/naphthol yellow-S, were marked on photomicrographs and traced on glass-plates. By piling up the plates, glass reconstructions of five successive developmental phases in the course of the third day of incubation were obtained. Mitotic figures in the walls of the optic vesicle and cup appeared to be distributed at random in all phases. Four areas of cell death, in the lateral wall of the optic vesicle, in the ventral part of the proximal optic stalk, in the uppermost part of the optic cup rim and in the outer layer of the optic cup, were found lying in a frontal plane somewhat rostral from the center of invagination. Evidence for the role of local differences in cell division and localized cell death during the morphogenesis of the optic cup, was not found. Current theories in literature and our observations were discussed. We concluded that for the present, current or conceivable theories can only be teleological explanations of circumstantial evidence. A topographical relationship between cell death and the outgrowth of the optic nerve fibers probably does exist, however. This relationship is born out by studies of congenital anomalies. Possible avenues for further investigation are suggested.

Animals↗
PubMed2004

Arabidopsis E2Fa plays a bimodal role in regulating cell division and cell growth.

The onset of cell cycle in mammalian systems is primarily controlled by E2F-like transcription factors. Recent evidence shows that plant E2F homologs and their associated proteins likely play similar roles in higher plant development. We studied the function of plant E2F in gene regulation and morphogenesis using transgenic Arabidopsis plants over-expressing AtE2Fa. Examination of rosettes showed that AtE2Fa over-expression resulted in increased expression of both cell cycle promoters and cell cycle inhibitors. The positive factors up-regulated by AtE2Fa emcompassed genes for G1/S transition, DNA synthesis and mitosis, and the negative factors up-regulated by AtE2Fa included RB1 , encoding the E2F binding protein, as well as KRP3 and KRP5 , encoding the plant CDK inhibitors. Moreover, AtE2Fa over-expression in rosettes led to elevated expression of ATPK19 , the homolog of the highly conserved S6 kinase that is known to enhance cell growth. The transgenic plants exhibited narrower rosette leaves when compared to wild-type control. Consistent with elevated expression of cell cycle inhibitors and ATPK19 , the mature rosette leaves displayed reduced cell number but increased cell size. These results demonstrate that AtE2Fa controls cell division and plant development by assuming a bimodal function in balancing the expression of both positive and negative regulators involved in cell division and growth.

Animals↗
PubMed1978

Mutants altered in the control co-ordinating cell division with cell growth in the fission yeast Schizosaccharomyces pombe.

The control co-ordinating cell division with cell growth has been investigated in the fission yeast Schizosaccharomyces pombe. Twenty-five mutants altered in this control have been isolated which have the same growth rate as wild type but divide at a smaller cell size. The mutants define two genes wee 1 and wee 2, both of which are involved in a control initiating mitosis when the cell attains a critical size.

Cell Count↗
PubMed2005

Counting human somatic cell replications: methylation mirrors endometrial stem cell divisions.

Cell proliferation may be altered in many diseases, but it is uncertain exactly how to measure total numbers of divisions. Although it is impossible to count every division directly, potentially total numbers of stem cell divisions since birth may be inferred from numbers of somatic errors. The idea is that divisions are surreptitiously recorded by random errors that occur during replication. To test this "molecular clock" hypothesis, epigenetic errors encoded in certain methylation patterns were counted in glands from 30 uteri. Endometrial divisions can differ among women because of differences in estrogen exposures or numbers of menstrual cycles. Consistent with an association between mitotic age and methylation, there was an age-related increase in methylation with stable levels after menopause, and significantly less methylation was observed in lean or older multiparous women. Methylation patterns were diverse and more consistent with niche rather than immortal stem cell lineages. There was no evidence for decreased stem cell survival with aging. An ability to count lifetime numbers of stem cell divisions covertly recorded by random replication errors provides new opportunities to link cell proliferation with aging and cancer.

Adolescent↗
PubMed1995

Rat intestinal crypt-cell replication factor with homology to early S-phase proteins required for cell division.

Cell proliferation requires inhibitory and permissive factors to monitor cell-cycle progression and control DNA replication. The small intestine has a high rate of proliferation and a very low incidence of cancer, suggestive of efficient mechanisms for control of the cell cycle and assuring fidelity of DNA replication. We have isolated a cDNA from a rat crypt-cell library which hybridized to a 3.0-kb mRNA specific for crypt cells, the proliferative cell compartment of the intestine. Its amino-acid sequence indicates that it is a new member of a family of replication proteins found in yeast, Cenorhabditis elegans, mouse and humans. Its transcripts were markedly increased in fetal rat intestine and liver, decreased in long-term confluent and serum-starved tissue culture cells (IEC cells, a cell line derived from rat crypt cells), increased with serum repletion as cells resumed proliferation, and appeared to be species specific. Isolation and functional characterization of small intestinal crypt-cell replication factors should help explain this organ's low incidence of cancer.

Amino Acid Sequence↗
PubMed2002

Tryptophan deprivation sensitizes activated T cells to apoptosis prior to cell division.

Cells expressing indoleamine 2,3-dioxygenase (IDO), an enzyme which catabolizes tryptophan, prevent T-cell proliferation in vitro, suppress maternal antifetal immunity during pregnancy and inhibit T-cell-mediated responses to tumour-associated antigens. To examine the mechanistic basis of these phenomena we activated naïve murine T cells in chemically defined tryptophan-free media. Under these conditions T cells expressed CD25 and CD69 and progressed through the first 12 hr of G0/G1 phase but did not express CD71, cyclin D3, cdk4, begin DNA synthesis, or differentiate into cytotoxic effector cells. In addition, activated T cells with their growth arrested by tryptophan deprivation exhibited enhanced tendencies to die via apoptosis when exposed to anti-Fas antibodies. Apoptosis was inhibited by caspase inhibitor and was not observed when T cells originated from Fas-deficient mice. These findings suggest that T cells activated in the absence of free tryptophan entered the cell cycle but cell cycle progression ceased in mid-G1 phase and T cells became susceptible to death via apoptosis, in part though Fas-mediated signalling. Thus, mature antigen-presenting cells expressing IDO and Fas-ligand may induce antigen-specific T-cell tolerance by blocking T-cell cycle progression and by rapid induction of T-cell activation induced cell death in local tissue microenvironments.

Animals↗
PubMed1993

Relationship between local cell division and cell displacement during regeneration of embryonic Xenopus eye fragments.

We examined the relationship between early healing modes and extra cell division (via tritiated thymidine incorporation) during embryonic retinal regeneration. Nasal (N) and dorsal (D) one-third sized eye fragments were surgically created in stage 32 Xenopus laevis embryos. Embryos were injected with tritiated thymidine two days postsurgery (stage 43), and then fixed and processed for autoradiography one day postinjection (stage 46). Histological analysis revealed that all nasal one-third sized fragments showed cell displacement in healing regions. These displaced cells were located in the ventral retinal region and showed heavy thymidine label incorporation. Alternatively, most dorsal one-third sized fragments showed little cell displacement during healing; in addition, no extra thymidine incorporation was evident. A minority of dorsal one-third sized fragments showed cell displacement during healing, and also showed significant local label ventrally through all regions of the eye. Therefore, in both dorsal and nasal one-third sized retinal fragments, when cell displacements were observed during early healing, associated mitosis was apparent in ventral retinal regions. Furthermore, by 60 hours postsurgery, all eyes which showed cell displacements during healing were greater in volume than those eyes which showed little cell displacement. Increases in volume appear to be derived from a combination of both cells migrating in from underlying optic stalk tissue and from related extra cell division during healing. These data further support a model which predicts that specific healing interactions which involve cell displacement during embryonic retinal regeneration and subsequent intercalary growth underlie visuotectal pattern formation.

Animals↗
PubMed1972

Regulation of cell division and cell enlargement by turgor pressure.

Isolated radish (Raphanus sativus L., var. Red Prince) cotyledons were incubated in growth medium plus graded concentrations of mannitol (-1 to -16 bars) for 28 hours. At the end of the incubation period, turgor pressures were measured using thermocouple psychrometers. Cell division, as measured by DNA increase, was greatly stimulated by increasing turgor from 5 to 6 bars. Cell enlargement was stimulated as turgor increased above 3 bars. The critical turgor pressure for increased cell division thus appeared significantly greater than that for increased cell enlargement.

Journal Article↗
PubMed2003

cki-1 links cell division and cell fate acquisition in the C. elegans somatic gonad.

The formation of a complex multicellular organism requires the precise specification of many diverse cell types at the correct time and position throughout development. This may be achieved by coordinating cell fate specification processes with progression through the cell cycle. Here, we show that the extra distal tip cells (DTCs) associated with the loss of cki-1, a Caenorhabditis elegans homologue of the cyclin-dependent kinase inhibitor p27, do not arise from duplications of pre-existing DTCs, but that they are formed from another cell type within the somatic gonad. Results from our laser microsurgery experiments suggest that the extra DTCs are caused by aberrant somatic gonadal precursor cell divisions in the absence of cki-1, resulting in abnormal daughter cell fates. cki-1(RNAi) animals also possess extra anchor cells and ectopic gonad arms with variable sheath cell numbers and positioning. In addition, cki-1(RNAi) animals display an endomitotic oocyte (Emo) phenotype. Our results uncover a novel role of this CKI in cell fate acquisition, either by directly influencing specification, or through a more conventional role in appropriately linking cell cycle phase with this process.

Animals↗
PubMed2000

Involvement of ethylene and gibberellin signalings in chromosaponin I-induced cell division and cell elongation in the roots of Arabidopsis seedlings.

Chromosaponin I (CSI), a triterpenoid saponin isolated from pea, stimulates the growth of roots in Arabidopsis thaliana seedlings on wetted filter paper in the light for 14 d. The growth rates of roots in Columbia (Col) and Landsberg erecta (Ler) wild-types were 0.92 and 0.26 mm d(-1), respectively, and they were accelerated to 3.46 (Col) and 2.20 (Ler) mm d(-1) by treating with 300 microM CSI. The length of mature epidermal cells was increased by 1.8-fold (Col) and 2.81-fold (Ler) compared with control and the number of epidermal cells was increased by a factor of 1.65 (Col) and 2.12 (Ler). Treatment with 2-aminoethoxyvinylglycine (AVG), an inhibitor of ethylene biosynthesis, also increased cell length but not cell number. The effects of CSI on root growth were not detected in the ethylene-insensitive mutant ein2-1. CSI did not inhibit ethylene production but stimulated the growth of roots in ctr1-1, the constitutive triple response mutant for ethylene, indicating that CSI inhibits ethylene signaling, especially downstream of CTR1. In the GA-insensitive mutant gai and the mutant spy-3, in which the basal level of GA signaling is activated, CSI did not increase cell number, although both CSI and AVG stimulated cell elongation in these mutants. These results suggest that the inhibition of ethylene signaling is the cause of CSI-induced cell elongation. A possible involvement of both GA and ethylene signalings is discussed for the CSI-induced cell division.

Aminobutyrates↗
PubMed2004

Interplay between cell division and cell death during TCR triggering.

Cell death is crucial to avoid excessive T cell expansion. During primary T cell expansion in response to pathogen or after vaccination, the amount of foreign Ag determines the degree of clonal amplification and death. Here, we studied the balance between cell proliferation and death, as well as susceptibility to cell death, during TCR triggering. After priming of CD4 T cells from AND-TCR (Vbeta3, Valpha11)-transgenic mice with a high dose of pigeon cytochrome c peptide 88-104, the cell expansion rate was significantly reduced by marked clonal elimination compared to lower Ag doses, whereas the number of cell divisions reached was similar at all Ag doses. TCR re-engagement on activated T cells induced cell death, irrespective of the dose of Ag encountered during primary stimulation. Surprisingly, commitment to apoptosis occurred as early as the first division on all dividing cells both in vitro and in vivo. This phenomenon was highly selective, as activated but non-dividing cells did not undergo cell death, whereas cells that had divided once became susceptible to cell death. These findings have direct implications for the peripheral homeostatic mechanism following Ag challenge and for designing primary/booster vaccine strategies.

Animals↗
PubMed1978

Cell division and cell allocation in early mouse development.

Cell division was observed in intact and dissociated mouse embryos between the 2-cell stage and the blastocyst in embryos developing in culture. Division to the 4-cell stage was usually asynchronous. The first cell to divide to the 4-cell stage produced descendants which tended to divide ahead of those cells produced by its slow partner at all subsequent stages of development up to the blastocyte stage. The descendants of the first cell to divide to the 4-cell stage did not subsequently have short cell cycles. The first cell or last cell to divide from the 4-cell stage was labelled with tritiated thymidine. The embryo was reassembled, and it was found that the first pair of cells to reach the 8-cell stage contributed disproportionately more descendants to the ICM when compared with the last cell to divide to the 8-cell stage.

Animals↗
PubMed1975

Control of cell division and cell differentiation by deoxynucleotides in the early embryo of Xenopus laevis.

It is proposed that the deoxyriboside triphosphates present in the egg of Xenopus laevis support the synchronous cell divisions occurring during the earliest phase of embryonic development and that, as long as synchrony prevails, the cells are prevented from undergoing differentiation. This hypothesis has been tested by injecting deoxyribonucleotides into fertilized eggs. The following effects were observed: 1) the duration of synchrony is prolonged, 2) the morphological development is suppressed, an effect which is greatest when four nucleotides are injected together and 3) the synthesis of all kinds of RNA is inhibited, including the mRNA required for differentiation to occur.

Adenosine Triphosphate↗
PubMed1981

[Cell division and cell cycle].

The paper gives a short review of biochemical and genetic analyses of the eukaryotic cell cycle and cell division. Emphasis is placed on the interrelationship of macromolecular syntheses during chromosome replication, the possible involvement of protein phosphorylation in chromosome condensation, the function of contractile proteins in mitosis and cytokinesis and on mechanisms which trigger cell proliferation.

Actins↗
PubMedDate not supplied

[Radiosensitive mutants of yeast-Saccharomyces with disruptions in the cell division cycle. Cell inactivation by restrictive temperature, ultra-violet and ionizing radiation in relation to the passage of the generated cycle].

Three thermo- and radiosensitive mutants of yeast-Saccharomyces were used to study cell inactivation under the effect of elevated temperature, UV-light, and ionizing radiation. The forms of cell inactivation were shown to be identical with all the factors under study and to resemble lethal "terminal phenotypes" of Hartwell cds mutants. It is suggested that the cell division cycle is blocked due to the disorders in the system of gene product synthesis and not to defects in the enzymes themselves.

Cell Division↗
PubMed1989

Inhibition of growth of ftsQ, ftsA, and ftsZ mutant cells of Escherichia coli by amplification of a chromosomal region encompassing closely aligned cell division and cell growth genes.

Amplification of a 2.6-kilobase chromosomal fragment of the mra region of Escherichia coli encompassing the ftsI(pbpB) gene and an open reading frame upstream with lethal to E. coli strains with mutations of the flanking cell division genes ftsQ, ftsA, and ftsZ. A shortened fragment in which the major portion of ftsI was deleted also had lethal effects on ftsQ and ftsZ mutants.

Bacterial Proteins↗