scholarly journals A cell-cycle-phase-specific mutant of amoeba

1984 ◽  
Vol 68 (1) ◽  
pp. 95-111
Author(s):  
A. Gangopadhyay ◽  
S. Chatterjee
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Size Structure ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Membrane Properties ◽  
Cycle Phase ◽  
Mutagenic Action ◽  
A Cell ◽  
Characteristic Features

The treatment of Amoeba indica with ethylmethanesulphonate (EMS) at early S, late S and late G2 phases of the cell cycle leads to the production of mini amoeba cells in the G2 period. Among them, only a few of the mini cells that originated from EMS treatment at early S phase have been found to be viable and to give rise to stable clones. These mini amoebae show stable and altered characteristic features in cell size, structure, membrane properties, cell-cycle timing and the patterns of macromolecular syntheses as compared to the parental cells. It is suggested that the mini amoeba cell is a size mutant that has a cell-cycle-phase-specific origin. The finding is discussed in relation to preferential mutagenic action involving the functional state of DNA leading to the production of viable mutant amoebae.

scholarly journals Heterogeneous Nuclear Ribonucleoprotein C Modulates Translation of c-myc mRNA in a Cell Cycle Phase-Dependent Manner

2003 ◽  
Vol 23 (2) ◽  
pp. 708-720 ◽  
Author(s):  
Jong Heon Kim ◽  
Ki Young Paek ◽  
Kobong Choi ◽  
Tae-Don Kim ◽  
Bumsuk Hahm ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Phase ◽  
In Vitro Translation ◽  
Cycle Phase ◽  
Dependent Manner ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
M Phase ◽  
Hnrnp C ◽  
A Cell ◽  
Nuclear Ribonucleoprotein

ABSTRACT The c-myc proto-oncogene plays a key role in the proliferation, differentiation, apoptosis, and regulation of the cell cycle. Recently, it was demonstrated that the 5′ nontranslated region (5′ NTR) of human c-myc mRNA contains an internal ribosomal entry site (IRES). In this study, we investigated cellular proteins interacting with the IRES element of c-myc mRNA. Heterogeneous nuclear ribonucleoprotein C (hnRNP C) was identified as a cellular protein that interacts specifically with a heptameric U sequence in the c-myc IRES located between two alternative translation initiation codons CUG and AUG. Moreover, the addition of hnRNP C1 in an in vitro translation system enhanced translation of c-myc mRNA. Interestingly, hnRNP C was partially relocalized from the nucleus, where most of the hnRNP C resides at interphase, to the cytoplasm at the G2/M phase of the cell cycle. Coincidently, translation mediated through the c-myc IRES was increased at the G2/M phase when cap-dependent translation was partially inhibited. On the other hand, a mutant c-myc mRNA lacking the hnRNP C-binding site, showed a decreased level of translation at the G2/M phase compared to that of the wild-type message. Taken together, these findings suggest that hnRNP C, via IRES binding, modulates translation of c-myc mRNA in a cell cycle phase-dependent manner.

Dynamically-enhanced retention of gold nanoclusters in HeLa cells following X-rays exposure: A cell cycle phase-dependent targeting approach

2016 ◽  
Vol 119 (3) ◽  
pp. 544-551 ◽  
Author(s):  
Yan Liu ◽  
Weiqiang Chen ◽  
Pengcheng Zhang ◽  
Xiaodong Jin ◽  
Xinguo Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hela Cells ◽  
Gold Nanoclusters ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
X Rays ◽  
A Cell

scholarly journals DNA damage checkpoint dynamics drive cell cycle phase transitions

2017 ◽  
Author(s):  
Hui Xiao Chao ◽  
Cere E. Poovey ◽  
Ashley A. Privette ◽  
Gavin D. Grant ◽  
Hui Yan Chao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Phase Transitions ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Dna Damage Checkpoint ◽  
Cycle Progression ◽  
Dna Damage Checkpoints

ABSTRACTDNA damage checkpoints are cellular mechanisms that protect the integrity of the genome during cell cycle progression. In response to genotoxic stress, these checkpoints halt cell cycle progression until the damage is repaired, allowing cells enough time to recover from damage before resuming normal proliferation. Here, we investigate the temporal dynamics of DNA damage checkpoints in individual proliferating cells by observing cell cycle phase transitions following acute DNA damage. We find that in gap phases (G1 and G2), DNA damage triggers an abrupt halt to cell cycle progression in which the duration of arrest correlates with the severity of damage. However, cells that have already progressed beyond a proposed “commitment point” within a given cell cycle phase readily transition to the next phase, revealing a relaxation of checkpoint stringency during later stages of certain cell cycle phases. In contrast to G1 and G2, cell cycle progression in S phase is significantly less sensitive to DNA damage. Instead of exhibiting a complete halt, we find that increasing DNA damage doses leads to decreased rates of S-phase progression followed by arrest in the subsequent G2. Moreover, these phase-specific differences in DNA damage checkpoint dynamics are associated with corresponding differences in the proportions of irreversibly arrested cells. Thus, the precise timing of DNA damage determines the sensitivity, rate of cell cycle progression, and functional outcomes for damaged cells. These findings should inform our understanding of cell fate decisions after treatment with common cancer therapeutics such as genotoxins or spindle poisons, which often target cells in a specific cell cycle phase.

scholarly journals Expression of mRNA for Adenosine A1, A2a, A2b, and A3 Receptors in HL-60 Cells: Dependence on Cell Cycle Phases

2011 ◽  
pp. 913-920 ◽  
Author(s):  
M. HOFER ◽  
L. DUŠEK ◽  
Z. HOFEROVÁ ◽  
L. STIXOVÁ ◽  
M. POSPÍŠIL
Keyword(s):  
Cell Cycle ◽  
Mrna Expression ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Block Method ◽  
Physiological Mechanisms ◽  
Adenosine A1 ◽  
Adenosine A2a ◽  
Adenosine A2b

The present studies investigated changes in expression of mRNA for adenosine A1, A2a, A2b, and A3 receptors in samples of HL-60 promyelocytic cells differing in the actual presence of cells in various phases of the cell cycle induced by the double thymidine block method. Real-time PCR technique was used for obtaining data on mRNA expression. Statistical analysis of the data revealed that the mRNA expression of adenosine A1, A2a, and A3 receptors is dependent on the cell cycle phase. G0/G1 and G2/M phases were characterized by a higher mRNA expression of adenosine A1 receptors and a lower one of adenosine A2a and A3 receptors whereas the opposite was true for the S phase. Interestingly, expression of mRNA of the adenosine A2b receptors was independent on the cell cycle phase. The results indicate the plasticity of mRNA expression of adenosine receptors in the investigated promyelocytic cells and its interaction with physiological mechanisms of the cell cycle.

DNA Damage Induced by DNA Topoisomerase I- and Topoisomerase II- Inhibitors Detected by Histone H2AX Phosphorylation in Leukemic Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4240-4240
Author(s):  
Dorota H. Halicka ◽  
Xuan Huang ◽  
Fevzi M. Ozkaynak ◽  
Karen Seiter ◽  
Frank Traganos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Topoisomerase I ◽  
Caspase 3 ◽  
S Phase ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Dna Topoisomerase I ◽  
H2ax Phosphorylation ◽  
Dna Topoisomerase ◽  
Histone H2ax

Abstract Histone H2AX is phosphorylated on Ser-139 by ATM kinase in response to damage that induces dsDNA breaks. Immunocytochemical detection of phosphorylated H2AX (γH2AX), thus, reveals the presence of dsDNA breaks in chromatin. Multiparameter cytometry was presently used to correlate the appearance of γH2AX with: (a) cell cycle phase; (b) caspase-3 activation; and (c) apoptosis-associated DNA fragmentation in individual human leukemic HL-60 cells treated with the DNA topoisomerase I (topo1) inhibitors topotecan (TPT) and camptothecin (CPT) or with the topo2 inhibitor mitoxantrone (MTX). In response to TPT or CPT maximal increase of γH2AX immunofluorescence was seen in S-phase cells by 90 min. In contrast, following MTX treatment the maximal rise of γH2AX was detected at 2 h in G1 cells and the cell cycle phase specificity was much less apparent. A linear relationship between the drug concentration and increase of γH2AX immunofluorescence was seen only up to 200 nM TPT; a decline in γH2AX was apparent at a concentration range between 0.4 and 1.6 μM TPT. Thus, the intensity of γH2AX immunofluorescence, as a marker of cell survival following TPT treatment, can be used only within a limited range of drug concentration. Following treatment with TPT, CPT or MTX the peak of H2AX phosphorylation preceded caspase-3 activation and the appearance of apoptosis-associated DNA fragmentation, both selective to S-phase cells. Progression of apoptosis was paralleled by a decrease in γH2AX immunofluorescence. On the basis of our laboratory results, the present clinical study is evaluating ex vivo the feasibility of assessing DNA damage induced by treatment with topoisomerase inhibitors in patients with acute leukemias.

scholarly journals Dependence of cell-type proportioning and sorting on cell cycle phase in Dictyostelium discoideum

1984 ◽  
Vol 70 (1) ◽  
pp. 133-145 ◽  
Author(s):  
C.J. Weijer ◽  
G. Duschl ◽  
C.N. David
Keyword(s):  
Cell Cycle ◽  
Stationary Phase ◽  
Dictyostelium Discoideum ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Cell Type ◽  
Slime Mould ◽  
Synchronous Cell ◽  
A Cell ◽  
The Relationship

The relationship between the cell cycle phase of vegetative amoebae and prestalk and prespore differentiation in the slug stage were investigated in the slime mould Dictyostelium discoideum. Cells were synchronized by release from the stationary phase. Samples were taken at various times during the course of a synchronous cell doubling, fluorescently labelled and mixed with cells of random cell cycle phase from exponentially growing cultures. The fate of the fluorescently labelled cells was recorded at the slug stage. Cells early in the cycle exhibit strong prestalk sorting; cells taken later in the cycle exhibit strong prespore sorting. The period of prestalk sorting occurs immediately following mitosis and lasts about 1 h in a cell cycle of about 7 h duration. Accompanying the altered sorting behaviour is a marked changed in the prestalk-prespore proportions in slugs formed from synchronized populations of cells. Cells synchronized early in the cycle form slugs with 55% prespore cells; cells synchronized late in the cycle form slugs with 90% prespore. The results are discussed in terms of models for the formation of the prestalk-prespore pattern in slugs.

scholarly journals Visualizing Cell Cycle Phase Organization and Control During Neural Lineage Elaboration

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2112
Author(s):  
Fatma Rabia Urun ◽  
Adrian W Moore
Keyword(s):  
Cell Cycle ◽  
Cell Fate ◽  
Cell Types ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Cell Cycle Regulators ◽  
Neural Lineage ◽  
Fate Control ◽  
A Cell ◽  
Cell Fate Control

In neural precursors, cell cycle regulators simultaneously control both progression through the cell cycle and the probability of a cell fate switch. Precursors act in lineages, where they transition through a series of cell types, each of which has a unique molecular identity and cellular behavior. Thus, investigating links between cell cycle and cell fate control requires simultaneous identification of precursor type and cell cycle phase, as well as an ability to read out additional regulatory factor expression or activity. We use a combined FUCCI-EdU labelling protocol to do this, and then apply it to the embryonic olfactory neural lineage, in which the spatial position of a cell correlates with its precursor identity. Using this integrated model, we find the CDKi p27KIP1 has different regulation relative to cell cycle phase in neural stem cells versus intermediate precursors. In addition, Hes1, which is the principle transcriptional driver of neural stem cell self-renewal, surprisingly does not regulate p27KIP1 in this cell type. Rather, Hes1 indirectly represses p27KIP1 levels in the intermediate precursor cells downstream in the lineage. Overall, the experimental model described here enables investigation of cell cycle and cell fate control linkage from a single precursor through to a lineage systems level.

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