Gap Phase Introduction in Every Cell Cycle of C. elegans Embryogenesis

2018 ◽  
Author(s):  
Ming-Kin Wong ◽  
Vincy Wing Sze Ho ◽  
Xiaotai Huang ◽  
Lu-yan Chan ◽  
Runsheng Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Gap Phase

scholarly journals Evidence that the cell cycle is a series of uncoupled, memoryless phases

2018 ◽  
Author(s):  
Hui Xiao Chao ◽  
Randy I. Fakhreddin ◽  
Hristo K. Shimerov ◽  
Rashmi J. Kumar ◽  
Gaorav P. Gupta ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Cell Cycle Progression ◽  
Phase 1 ◽  
Cell Cycle Phase ◽  
Cell Cycle Checkpoints ◽  
Cycle Phase ◽  
Erlang Distribution ◽  
Cycle Progression ◽  
Gap Phase

The cell cycle is canonically described as a series of 4 phases: G1 (gap phase 1), S (DNA synthesis), G2 (gap phase 2), and M (mitosis). Various models have been proposed to describe the durations of each phase, including a two-state model with fixed S-G2-M duration and random G1 duration1,2; a “stretched” model in which phase durations are proportional3; and an inheritance model in which sister cells show correlated phase durations2,4. A fundamental challenge is to understand the quantitative laws that govern cell-cycle progression and to reconcile the evidence supporting these different models. Here, we used time-lapse fluorescence microscopy to quantify the durations of G1, S, G2, and M phases for thousands of individual cells from three human cell lines. We found no evidence of correlation between any pair of phase durations. Instead, each phase followed an Erlang distribution with a characteristic rate and number of steps. These observations suggest that each cell cycle phase is memoryless with respect to previous phase durations. We challenged this model by perturbing the durations of specific phases through oncogene activation, inhibition of DNA synthesis, reduced temperature, and DNA damage. Phase durations remained uncoupled in individual cells despite large changes in durations in cell populations. To explain this behavior, we propose a mathematical model in which the independence of cell-cycle phase durations arises from a large number of molecular factors that each exerts a minor influence on the rate of cell-cycle progression. The model predicts that it is possible to force correlations between phases by making large perturbations to a single factor that contributes to more than one phase duration, which we confirmed experimentally by inhibiting cyclin-dependent kinase 2 (CDK2). We further report that phases can show coupling under certain dysfunctional states such as in a transformed cell line with defective cell cycle checkpoints. This quantitative model of cell cycle progression explains the paradoxical observation that phase durations are both inherited and independent and suggests how cell cycle progression may be altered in disease states.

scholarly journals Leptolstatin from Streptomyces sp. SAM1595, a new gap phase-specific inhibitor of the mammalian cell cycle. II. Physico-chemical properties and structure.

1993 ◽  
Vol 46 (5) ◽  
pp. 735-740 ◽  
Author(s):  
KEIICHI ABE ◽  
MINORU YOSHIDA ◽  
HIDEO NAOK ◽  
SUEHARU HORINOUCHI ◽  
TERUHIKO BEPPU
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Chemical Properties ◽  
Specific Inhibitor ◽  
Streptomyces Sp ◽  
Physico Chemical ◽  
Mammalian Cell Cycle ◽  
Gap Phase

The regulation of the cell cycle during Drosophila embryogenesis: the transition to polyteny

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 997-1008 ◽  
Author(s):  
A.V. Smith ◽  
T.L. Orr-Weaver
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Developmental Regulation ◽  
Mitotic Cell ◽  
Mitotic Cell Cycle ◽  
Drosophila Embryogenesis ◽  
First Instar ◽  
Late Embryogenesis ◽  
Gap Phase ◽  
Different Tissues

The process of polytenization plays a crucial role in Drosophila development, and most of the larval tissues are polytene. By analyzing the pattern of DNA replication in embryos pulse-labeled with BrdU, we show that many larval tissues undergo a transition to begin becoming polytene late in embryogenesis. Our results demonstrate that in these larval tissues polyteny results from a modified cell cycle, the endo cell cycle, in which there is only an S (synthesis) phase and a G (gap) phase. A key regulator of the mitotic cell cycle, the product of the string gene (the Drosophila homologue of cdc25), is not required for the endo cell cycle. The developmental regulation of the endo cell cycle is striking in that tissue-specific domains undergo polytene DNA replication in a dynamic pattern at defined times in embryogenesis. During subsequent rounds of the endo cell cycle in late embryogenesis and first instar larval development, the domains are subdivided and the temporal control is not as rigid. The length of the G phase varies among different tissues. By quantifying DNA content, we show that during the early polytene S phases the genome is not fully duplicated.

scholarly journals Cell Cycle Analysis and Stimulation of Rat Kangaroo Cells (PtK2) after Pulse Labeling

1971 ◽  
Vol 26 (7) ◽  
pp. 722-724 ◽  
Author(s):  
Peter R. Lorenz ◽  
John W. Ainsworth
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Doubling Time ◽  
Tritiated Thymidine ◽  
Cell Counts ◽  
The Mean ◽  
Gap Phase ◽  
Potorous Tridactylus ◽  
Stimulation Of

The phases of the cell cycle of Potorous tridactylus (PtK2) cells were determined in vitro by analysis of labeled mitoses for 37-½ hours after a tritiated thymidine pulse. The mean duration of DNA synthesis (tS) was 8 h. The mean duration of the gap phase before appearance of labeled mitoses was 5 h. Whereas the duration of the cell cycle (tC) based on analysis of labeled mitoses was 30 h, the doubling time (tD) derived from cell counts in the same cultures was only about 23 h. The analysis of the indices of labeled nuclei and mitoses suggests a stimulation of cells at the time of pulse labeling, which was maximal after beginning of the gap phase before DNA-synthesis, and possibly caused the observed difference between tC and tD.

Maytansine-Induced Mitotic Arrest in Human Lymphoblasts

1977 ◽  
Vol 35 ◽  
pp. 460-461
Author(s):  
Tai-Te Chao ◽  
John Sullivan ◽  
Awtar Krishan
Keyword(s):  
Electron Microscopy ◽  
Cell Cycle ◽  
Transmission Electron Microscopy ◽  
Tubulin Polymerization ◽  
Vinca Alkaloids ◽  
Antimitotic Activity ◽  
Transmission Electron ◽  
Flow Microfluorometry ◽  
Brain Tubulin

Maytansine, a novel ansa macrolide (1), has potent anti-tumor and antimitotic activity (2, 3). It blocks cell cycle traverse in mitosis with resultant accumulation of metaphase cells (4). Inhibition of brain tubulin polymerization in vitro by maytansine has also been reported (3). The C-mitotic effect of this drug is similar to that of the well known Vinca- alkaloids, vinblastine and vincristine. This study was carried out to examine the effects of maytansine on the cell cycle traverse and the fine struc- I ture of human lymphoblasts.Log-phase cultures of CCRF-CEM human lymphoblasts were exposed to maytansine concentrations from 10-6 M to 10-10 M for 18 hrs. Aliquots of cells were removed for cell cycle analysis by flow microfluorometry (FMF) (5) and also processed for transmission electron microscopy (TEM). FMF analysis of cells treated with 10-8 M maytansine showed a reduction in the number of G1 cells and a corresponding build-up of cells with G2/M DNA content.

Fibronexus-Like Adhesion Sites are Present at the Invasive Zones of Human Epidermoid Carcinomas

1982 ◽  
Vol 40 ◽  
pp. 106-109
Author(s):  
Irwin I. Singer
Keyword(s):  
Cell Cycle ◽  
Serum Concentration ◽  
Substrate Binding ◽  
High Serum ◽  
Adhesion Sites ◽  
Substrate Adhesion ◽  
Focal Contacts ◽  
Adhesion Complex ◽  
Low Serum

Our previous results indicate that two types of fibronectin-cytoskeletal associations may be formed at the fibroblast surface: dorsal matrixbinding fibronexuses generated in high serum (5% FBS) cultures, and ventral substrate-adhering units formed in low serum (0.3% FBS) cultures. The substrate-adhering fibronexus consists of at least vinculin (VN) and actin in its cytoplasmic leg, and fibronectin (FN) as one of its major extracellular components. This substrate-adhesion complex is localized in focal contacts, the sites of closest substratum approach visualized with interference reflection microscopy, which appear to be the major points of cell-tosubstrate adhesion. In fibroblasts, the latter substrate-binding complex is characteristic of cultures that are arrested at the G1 phase of the cell cycle due to the low serum concentration in their medium. These arrested fibroblasts are very well spread, flattened, and immobile.

Immunocytochemical studies on the behavior of RuBisCO and LHCP II during the cell cycle of synchronized Euglena gracilis

1990 ◽  
Vol 48 (3) ◽  
pp. 662-663
Author(s):  
Tetsuaki Osafune ◽  
Shuji Sumida ◽  
Tomoko Ehara ◽  
Eiji Hase ◽  
Jerome A. Schiff
Keyword(s):  
Cell Cycle ◽  
Immunoelectron Microscopy ◽  
Growth Phase ◽  
Euglena Gracilis ◽  
Dark Period ◽  
Light Period ◽  
Carboxylase Activity ◽  
Immunocytochemical Studies ◽  
Lhcp Ii

Changes in the morphology of pyrenoid and the distribution of RuBisCO in the chloroplast of Euglena gracilis were followed by immunoelectron microscopy during the cell cycle in a light (14 h)- dark (10 h) synchronized culture under photoautotrophic conditions. The imrnunoreactive proteins wereconcentrated in the pyrenoid, and less densely distributed in the stroma during the light period (growth phase, Fig. 1-2), but the pyrenoid disappeared during the dark period (division phase), and RuBisCO was dispersed throughout the stroma. Toward the end of the division phase, the pyrenoid began to form in the center of the stroma, and RuBisCO is again concentrated in that pyrenoid region. From a comparison of photosynthetic CO2-fixation with the total carboxylase activity of RuBisCO extracted from Euglena cells in the growth phase, it is suggested that the carboxylase in the pyrenoid functions in CO2-fixation in photosynthesis.

Effect of Chrysanthemum flavonoids on growth and cell cycle regulators of gastric cancer cell

2010 ◽  
Vol 34 (8) ◽  
pp. S50-S50
Author(s):  
Xiaoyan Pan ◽  
Xinmei Zhou ◽  
Guangtao Xu ◽  
Lingfen Miao ◽  
Shuoru Zhu
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cell Cycle Regulators
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