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PubMed1984

Lysine tRNA and cell division: a G1 cell cycle mutant is temperature sensitive for the modification of tRNA5Lys to tRNA4Lys.

Ts-694 is a temperature sensitive mutant of hamster cells which is blocked in the G1 phase of the cell cycle at the restrictive temperature of 39 degrees. A comparison of the Lys-tRNA isoacceptors by RPC-5 chromatography showed a decrease in tRNA5Lys and an increase in tRNA4Lys at 39 degrees. This was identical to the changes seen in confluent cultures at the permissive temperature of 33 degrees. These Lys-tRNA changes were not seen in ts-694 cells blocked in G1 by isoleucine deficiency, nor in two other G1 ts mutants at the restrictive temperature. Cells trapped in S phase by a thymidine block also contained decreased levels of tRNA4Lys when raised to 39 degrees. Both tRNA4Lys levels and cell division increased when the cells were returned to the permissive temperature. An in vitro assay was established for the modification of tRNA5Lys to tRNA4Lys with tRNA6Lys and tRNA2Lys as intermediates. The first reaction is the synthesis of tRNA6Lys which involves the introduction of a modified uridine at the third position of the anticodon. Extracts of 694 cells grown at 33 degrees were able to modify rat liver [3H] tRNA5Lys to tRNA6Lys and tRNA4Lys in vitro when assayed at 25 degrees but not at 39 degrees. Extracts of Balb/c 3T3 cells, however, were more active at 39 degrees than at 25 degrees showing that the normal enzyme is not temperature sensitive. Ts-694 cell tRNA, isolated from cells grown at 33 degrees was aminoacylated at both 25 degrees and 39 degrees with rat liver synthetases. tRNA4Lys was present at both temperatures indicating that ts-694 cells do not contain a temperature sensitive tRNA4Lys.

Animals↗
PubMed1983

The interferon-induced hyporesponsive state in variant and parental L cells: a requirement for cell division.

L cells grown for 18 to 22 months in the presence of interferon (IFN) retained their sensitivity to the antiviral effect of IFN but were less sensitive to cell growth inhibition by IFN. Moreover, the parental and variant lines became hyporesponsive (i.e. less responsive to virus induction of IFN) with different kinetics after IFN treatment. Experiments using mitomycin C to inhibit cell division suggested that cell division is required to enter the hyporesponsive state.

Animals↗
PubMed1996

The mechanism of bacterial asymmetric cell division.

Asymmetric cell division generates two cells that contain different regulatory proteins and express different fates. In an example of asymmetric cell division from B. subtilis, a site on the membrane of the dividing cell is chosen to establish the initial asymmetry. Recent results show that a key regulatory protein, SpoIIE, is localized to one side of a sporulating B. subtilis cell, and subsequently functions in an asymmetric manner. SpoIIE is a phosphatase at the beginning of a regulatory cascade that leads to activation of a cell fate-determining transcription factor in only one daughter cell.

Bacillus subtilis↗
PubMed1982

Studies on cell division in mammalian cells: VI. A temperature-sensitive mutant blocked in both G1 and G2 phases of the cell cycle.

A temperature-sensitive mammalian cell cycle mutant with blocks in G1 and G2 phases of the cell cycle has been isolated in culture. When shifted from the permissive temperature of 33 degrees C to the nonpermissive temperature of 39 degrees C, the fraction of cells initiating DNA synthesis as well as the fraction of cells entering mitosis decreased rapidly. Combined cytophotometric and autoradiographic analysis on the cells at 39 degrees C showed that G1 cells, with the exception of those in late G1, were arrested in that phase. Cells is S phase at the time of temperature shift, together with the late g1 cells which subsequently entered S, continued through S into G2, but were blocked in that phase of the cell cycle and unable to initiate mitosis. Those cells already in mitosis completed cell division at 39 degrees C. The G1 block point of ts-550C was found to be located after the serum starvation and isoleucine deprivation arrest points, approximately 3 h before initiation of DNA synthesis.

Aged↗
PubMed1997

Dynamics of phragmoplastin in living cells during cell plate formation and uncoupling of cell elongation from the plane of cell division.

The cell plate is formed by the fusion of Golgi apparatus-derived vesicles in the center of the phragmoplast during cytokinesis in plant cells. A dynamin-like protein, phragmoplastin, has been isolated and shown to be associated with cell plate formation in soybean by using immunocytochemistry. In this article, we demonstrate that similar to dynamin, phragmoplastin polymerizes to form oligomers. We fused soybean phragmoplastin with the green fluorescence protein (GFP) and introduced it into tobacco BY-2 cells to monitor the dynamics of early events in cell plate formation. We demonstrate that the chimeric protein is functional and targeted to the cell plate during cytokinesis in transgenic cells. GFP-phragmoplastin was found to appear first in the center of the forming cell plate, and as the cell plate grew outward, it redistributed to the growing margins of the cell plate. The redistribution of phragmoplastin may require microtubule reorganization because the microtubule-stabilizing drug taxol inhibited phragmoplastin redistribution. Our data show that throughout the entire process of cytokinesis, phragmoplastin is concentrated in the area in which membrane fusion is active, suggesting that phragmoplastin participates in an early membrane fusion event during cell plate formation. Based on the dynamics of GFP-phragmoplastin, it appears that the process of cell plate formation is completed in two phases. The first phase is confined to the cylinder of the phragmoplast proper and is followed by a second phase that deposits phragmoplast vesicles in a concentric fashion, resulting in a ring of fluorescence, with the concentration of vesicles being higher at the periphery. In addition, overexpression of GFP-phragmoplastin appears to act as a dominant negative, slowing down the completion of cell plate formation, and often results in an oblique cell plate. The latter appears to uncouple cell elongation from the plane of cell division, forming twisted and elongated cells with longitudinal cell divisions.

Antibodies↗
PubMed2004

Asymmetric cell division.

Asymmetric cell division is a conserved mechanism for partitioning information during mitosis. Over the past several years, significant progress has been made in our understanding of how cells establish polarity during asymmetric cell division and how determinants, in the form of localized proteins and mRNAs, are segregated. In particular, genetic studies in Drosophila and Caenorhabditis elegans have linked cell polarity, G protein signaling and regulation of the cytoskeleton to coordination of mitotic spindle orientation and localization of determinants. Also, several new studies have furthered our understanding of how asymmetrically localized cell fate determinants, such as the Numb, a negative regulator Notch signaling, functions in biasing cell fates in the developing nervous system in Drosophila. In vertebrates, analysis of dividing neural progenitor cells by in vivo imaging has raised questions about the role of asymmetric cell divisions during neurogenesis.

Animals↗
PubMed1989

Control of cell division in hepatoma cells by exogenous heparan sulfate proteoglycan.

The effects of cell surface heparan sulfate proteoglycan (HSPG) prepared from log and confluent monolayers of a rat hepatoma cell line on hepatoma cell growth were studied. When HSPG isolated from confluent cells was added exogenously to log phase cells, it was internalized and free heparan sulfate (HS) chains appeared transiently in the nucleus. Concurrently, the growth of the treated cells was inhibited, but the cells resumed logarithmic growth as the level of nuclear HS fell, and the cells grew to confluence and became contact inhibited. When HSPG prepared from log-phase hepatoma cells was added exogenously to log phase cells, it was internalized but very little of the internalized HS appeared in the nucleus, and there was no change in the rate of cell growth. However, when the rate of cell growth was reduced by culture of the cells in serum- and insulin-deficient medium, HSPG prepared from log-phase cells stimulated the growth rate of these slow-growing cells. The cell cycle dependency of HSPG uptake and growth inhibition was studied in cultures synchronized by a thymidine/aphidicolin double block. When [35SO4]HSPG from confluent cells was added to synchronized cells just as they were released from the second block, a portion of the [35SO4]HSPG was internalized and [35SO4]HS appeared in the nucleus. However, at mitosis the [35SO4]HS disappeared almost completely from all of the cellular pools, and after mitosis, more of the [35SO4]HSPG was taken up and [35SO4]HS reappeared in the nucleus and remained in the nucleus until the cells divided again. When cultures were released from the aphidicolin block, both control and HSPG-treated cells progressed through the S, the G2, and the M phases of the cell cycle. However, the length of the G1 phase of the cycle was increased in the HSPG-treated cells. The treated cultures then progressed through the second S, G2, and M phases. Thus, the inhibition of cell division occurred in the G1 phase of the cell cycle, prior to the G1/S boundary. Addition of the HSPG to the synchronized cultures just after the first mitosis resulted in an immediate arrest of the cell cycle in G1.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1962

Cell division in a species of Erwinia III. Reversal of inhibition of cell division caused by D-amino acids, penicillin, and ultraviolet light.

Grula, E. A. (Oklahoma State University, Stillwater) and Mary M. Grula. Cell division in a species of Erwinia. III. Reversal of inhibition of cell division caused by d-amino acids, penicillin, and ultraviolet light. J. Bacteriol. 83:981-988. 1962.-Inhibition of cell division in an Erwinia sp. occurs in the presence of any of six d-amino acids, penicillin, or ultraviolet light. Cell-division inhibition caused by d-amino acids is pH-dependent; however, elongation caused by penicillin occurs over a wide range of pH. Bulging and spheroplast formation in the presence of penicillin occurs only at pH values below 7.6; however, division continues to be inhibited at higher pH levels. Reversal of cell-division inhibition caused by two d-amino acids (phenylalanine and histidine) can be partially overcome by their respective l-isomers. Divalent cations (Zn, Ca, Mn) cause varying amounts of reversal of division inhibition in all systems studied; each system appears to have an individual requirement. All induced division inhibitions, including that caused by penicillin, can be reversed by pantoyl lactone or omega-methylpantoyl lactone. Evidence is presented and discussed concerning the possible importance of pantoyl lactone and divalent cations in terminal steps of the cell-division process in this organism.

Amino Acids↗
PubMed1998

Polar localization of the MinD protein of Bacillus subtilis and its role in selection of the mid-cell division site.

Cell division in rod-shaped bacteria is initiated by formation of a ring of the tubulin-like protein FtsZ at mid-cell. Division site selection is controlled by a conserved division inhibitor MinCD, which prevents aberrant division at the cell poles. The Bacillus subtilis DivIVA protein controls the topological specificity of MinCD action. Here we show that DivIVA is targeted to division sites late in their assembly, after some MinCD-sensitive step requiring FtsZ and other division proteins has been passed. DivIVA then recruits MinD to the division sites preventing another division from taking place near the newly formed cell poles. Sequestration of MinD to the poles also releases the next mid-cell sites for division. Remarkably, this mechanism of DivIVA action is completely different from that of the equivalent protein MinE of Escherichia coli, even though both systems operate via the same division inhibitor MinCD.

Adenosine Triphosphatases↗
PubMed2006

Mutations in the Diageotropica (Dgt) gene uncouple patterned cell division during lateral root initiation from proliferative cell division in the pericycle.

In angiosperms, root branching requires a continuous re-initiation of new root meristems. Through some unknown mechanism, in most eudicots pericycle cells positioned against the protoxylem change identity and initiate patterned division, leading to formation of lateral root primordia that further develop into lateral roots. This process is auxin-regulated. We have observed that three mutations in the Diageotropica (Dgt) gene in tomato prevent primordium formation. Detailed analysis of one of these mutants, dgt1-1, demonstrated that the mutation does not abolish the proliferative capacity of the xylem-adjacent pericycle in the differentiated root portion. Files of shortened pericycle cells found in dgt1-1 roots were unrelated to primordium formation. Auxin application stimulated this unusual proliferation, leading to formation of a multi-layered xylem-adjacent pericycle, but did not rescue the primordium formation. In contrast to wild type, auxin could not induce any cell divisions in the pericycle of the most distal dgt1-1 root-tip portion. In wild-type roots, the Dgt gene promoter was expressed strongly in lateral root primordia starting from their initiation, and on auxin treatment was induced in the primary root meristem. Auxin level and distribution were altered in dgt1-1 root tissues, as judged by direct auxin measurements, and the tissue-specific expression of an auxin-response reporter was altered in transgenic plants. Together, our data demonstrate that the Dgt gene product, a type-A cyclophilin, is essential for morphogenesis of lateral root primordia, and that the dgt mutations uncouple patterned cell division in lateral root initiation from proliferative cell division in the pericycle.

Arabidopsis↗
PubMed2001

Translational repression determines a neuronal potential in Drosophila asymmetric cell division.

Asymmetric cell division is a fundamental strategy for generating cellular diversity during animal development. Daughter cells manifest asymmetry in their differential gene expression. Transcriptional regulation of this process has been the focus of many studies, whereas cell-type-specific 'translational' regulation has been considered to have a more minor role. During sensory organ development in Drosophila, Notch signalling directs the asymmetry between neuronal and non-neuronal lineages, and a zinc-finger transcriptional repressor Tramtrack69 (TTK69) acts downstream of Notch as a determinant of non-neuronal identity. Here we show that repression of TTK69 protein expression in the neuronal lineage occurs translationally rather than transcriptionally. This translational repression is achieved by a direct interaction between cis-acting sequences in the 3' untranslated region of ttk69 messenger RNA and its trans-acting repressor, the RNA-binding protein Musashi (MSI). Although msi can act downstream of Notch, Notch signalling does not affect MSI expression. Thus, Notch signalling is likely to regulate MSI activity rather than its expression. Our results define cell-type-specific translational control of ttk69 by MSI as a downstream event of Notch signalling in asymmetric cell division.

3' Untranslated Regions↗
PubMed1991

A factor that positively regulates cell division by activating transcription of the major cluster of essential cell division genes of Escherichia coli.

Cell division in Escherichia coli requires the products of the ftsQ, ftsA and ftsZ genes. It is not known how the cell regulates the cellular concentrations of these essential elements of the division system. We describe here a factor that activates cell division by specifically increasing transcription from one of the two promoters that lie immediately upstream of the ftsQAZ gene cluster. The trans-acting factor is the product of the sdiA gene, which was isolated on the basis of its ability to suppress the division inhibitory effect of the MinC/MinD division inhibitor. In addition, the sdiA gene product suppressed the action of other chromosomally encoded division inhibitors, induced minicell formation in wild type cells, and restored division activity to an ftsZ temperature-sensitive mutant grown under nonpermissive conditions. All of these properties were explained by the ability of the sdiA gene product specifically to increase transcription of the ftsQAZ gene cluster, resulting in an increase in cellular concentration of the FtsZ protein. The sdiA gene product is the first factor thus far identified that specifically regulates expression of this key group of cell division genes.

Amino Acid Sequence↗
PubMed1980

Cell division and giant cell formation in Kupffer cell cultures.

A method is described allowing the isolation and culture of relatively pure preparations of murine Kupffer cells for long-term morphological and functional studies. In vivo labelling experiments showed no evidence of significant blood monocyte contamination. The use of a density gradient allowed removal of fibroblasts, cell debris and a relative enrichment of Kupffer cells. After 24 hr in culture the cells were phagocytic, contained non-specific esterase and exhibited an Fc receptor. During the first 3 weeks, cell clumps, epithelioid cells and multinucleate giant cells appeared. Mitoses were seen in the Kupffer cells, cell numbers increased and in vitro labelling with 3H-thymidine at 49 days showed that 33% of the cells underwent DNA synthesis in a 24-hr period. Experiments suggested that giant cell formation was produced both by cell fusion and nuclear division. The experiments show that Kupffer cells are capable of cell division and giant cell formation in culture.

Animals↗
PubMed1993

Oscillator control of cell division in Euglena: cyclic AMP oscillations mediate the phasing of the cell division cycle by the circadian clock.

The achlorophyllous ZC strain of Euglena gracilis exhibits a circadian rhythm of cell division in constant darkness (DD). Mitosis occurs during a restricted part of the circadian cycle, corresponding to the dark intervals in a light-dark cycle comprising 12 h of light and 12 h of darkness. We have demonstrated that division-phased cultures also exhibit bimodal, circadian changes of cyclic AMP level. Maximum cyclic AMP levels occurred at the beginning of the light period (CT (circadian time) 00-02), and at the beginning of darkness (CT 12-14). These variations persisted in cultures that had been transferred into DD and appeared to be under the control of the circadian oscillator rather than to be cell division cycle (CDC)-dependent, since they continued in cultures that had reached the stationary phase of growth. In the experiments reported in this paper, we tested for the possible role of this periodic cyclic AMP signal in the generation of cell division rhythmicity by examining the effects of exogenous cyclic AMP signals and of forskolin, which permanently increased the cyclic AMP level, on the cell division rhythm. Perturbations of the cyclic AMP oscillation by exogenous cyclic AMP resulted in the temporary uncoupling of the CDC from the circadian timer. The addition of cyclic AMP during the subjective day resulted in delays (up to 9 h) of the next synchronous division step. In contrast, mitosis was stimulated when cyclic AMP was administered in the middle of the subjective night. Measurement of the DNA content of cells by flow cytometry indicated that cyclic AMP injected at CT 06-08 delayed progression through S phase, and perhaps also through mitosis. When added at CT 18-20, cyclic AMP accelerated the G2/M transition. The circadian oscillator was not perturbed by the addition of exogenous cyclic AMP: the division rhythm soon returned to its original phase. On the other hand, the permanent elevation of cyclic AMP levels in the presence of forskolin induced a rapid loss of cell division rhythmicity. These findings are consistent with the hypothesis that cyclic AMP acts downstream from the oscillator and that the cyclic AMP oscillation is an essential component of the signaling pathway for the control of the CDC by the circadian oscillator. The receptors for cyclic AMP in Euglena have been shown to be two cyclic AMP-dependent kinases (cPKA and cPKB). Pharmacological studies using cyclic AMP analogs suggested that cPKA mediates cyclic AMP effects during the subjective day, and cPKB during the subjective night.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Cell division promoting activity of naturally occurring dehydrodiconiferyl glucosides: do cell wall components control cell division?

Naturally occurring isomers of the dehydrodiconiferyl glucosides have been isolated from Vinca rosea crown gall tumors and have been tested for cell division promoting activities in the tobacco pith and leaf assay systems. The enantiomeric isomers A and B are active, although they are required at concentrations up to 2 orders of magnitude higher than zeatin riboside to promote comparable growth. We estimate that the active dehydrodiconiferyl glucosides are present in rapidly growing tissues (tumor tissue, habituated tissue, cultured nontransformed tissue) in micromolar concentrations. In quiescent tobacco pith tissue, the levels of these compounds are reduced by a factor of 100. These results suggest that cytokinin may exert control of cell division through the accumulation of molecules (the dehydrodiconiferyl glucosides) that are apparent cell wall components.

Cell Division↗
PubMed2005

Cell division theory and individual-based modeling of microbial lag: part I. The theory of cell division.

This series of two papers deals with the theory of cell division and its implementation in an individual-based modeling framework. In this first part, the theory of cell division is studied on an individual-based level in order to learn more about the mechanistic principles behind microbial lag phenomena. While some important literature on cell division theory dates from 30 to 40 years ago, until now it has hardly been introduced in the field of predictive microbiology. Yet, it provides a large amount of information on how cells likely respond to changing environmental conditions. On the basis of this theory, a general theory on microbial lag behavior caused by a combination of medium and/or temperature changes has been developed in this paper. The proposed theory then forms the basis for a critical evaluation of existing modeling concepts for microbial lag in predictive microbiology. First of all, a more thorough definition can be formulated to define the lag time lambda and the previously only vaguely defined physiological state of the cells in terms of mechanistically defined parameters like cell mass, RNA or protein content, specific growth rate and time to perform DNA replication and cell division. On the other hand, existing predictive models are evaluated with respect to the newly developed theory. For the model of , a certain fitting parameter can also be related to physically meaningful parameters while for the model of [Augustin, J.-C., Rosso, L., Carlier, V.A. 2000. A model describing the effect of temperature history on lag time for Listeria monocytogenes. Int. J. Food Microbiol. 57, 169-181] a new, mechanistically based, model structure is proposed. A restriction of the proposed theory is that it is only valid for situations where biomass growth responds instantly to an environment change. The authors are aware of the fact that this assumption is not generally acceptable. Lag in biomass can be caused, for example, by a delayed synthesis of some essential growth factor (e.g., enzymes). In the second part of this series of papers [Dens, E.J., Bernaerts, K., Standaert, A.R., Kreft, J.-U., Van Impe, J.F., this issue. Cell division theory and individual-based modeling of microbial lag: part II. Modeling lag phenomena induced by temperature shifts. Int. J. Food Microbiol], the theory of cell division is implemented in an individual-based simulation program and extended to account for lags in biomass growth. In conclusion, the cell division theory applied to microbial populations in dynamic medium and/or temperature conditions provides a useful framework to analyze microbial lag behavior.

Algorithms↗