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Cell Cycle Process (cell + cycle_process)
Selected AbstractsCharacteristics of microcystin production in the cell cycle of Microcystis viridisENVIRONMENTAL TOXICOLOGY, Issue 1 2004Keishi Kameyama Abstract The correlation between the content of three microcystins (types LR, RR and YR) and the cell cycle of an axenic strain of Microcystis viridis, NIES-102, was investigated under conditions of high (16 mg L,1) and low (1.0 mg L,1) nitrate (NO3 -N) concentrations. Each phase of the cell cycle was identified using a flow cytometer equipped with a 488-nm argon laser using SYTOX Green dye, which binds specifically to nucleic acids and can be exited by the wavelength (Ex/Em: 504/523 nm on DNA). Microcystin concentration showed a positive linear correlation with DNA concentration. The microcystin content of the cells changed remarkably as the cell cycle process proceeded, with maximum content in the G2/M phase and minimum content in the G0/G1 phase. Under a condition of high NO3 -N concentration, the ratio of the total content in the G0/G1 phase to that in the G2/M phase was about 6:1. In contrast, for the two batch cultures the total content was 1.3-fold greater in the G2/M phase. The compositions of the three microcystins also changed along with the cell cycle process, although there was little difference in composition that was related to NO3 -N concentration. Therefore, there were distinctive compositions specific to each phase of the cycle, and the cell cycle of the M. viridis strain was more strongly responsible for both the quantity and the types of microcystin production than was the effect of NO3 -N concentration. © 2004 Wiley Periodicals, Inc. Environ Toxicol 19: 20,25, 2004. [source] Cell cycle execution point analysis of ORC function and characterization of the checkpoint response to ORC inactivation in Saccharomyces cerevisiaeGENES TO CELLS, Issue 6 2006Daniel G. Gibson Chromosomal replication initiates through the assembly of a prereplicative complex (pre-RC) at individual replication origins in the G1-phase, followed by activation of these complexes in the S-phase. In Saccharomyces cerevisiae, the origin recognition complex (ORC) binds replication origins throughout the cell cycle and participates in pre-RC assembly. Whether the ORC plays an additional role subsequent to pre-RC assembly in replication initiation or any other essential cell cycle process is not clear. To study the function of the ORC during defined cell cycle periods, we performed cell cycle execution point analyses with strains containing a conditional mutation in the ORC1, ORC2 or ORC5 subunit of ORC. We found that the ORC is essential for replication initiation, but is dispensable for replication elongation or later cell cycle events. Defective initiation in ORC mutant cells results in incomplete replication and mitotic arrest enforced by the DNA damage and spindle assembly checkpoint pathways. The involvement of the spindle assembly checkpoint implies a defect in kinetochore-spindle attachment or sister chromatid cohesion due to incomplete replication and/or DNA damage. Remarkably, under semipermissive conditions for ORC1 function, the spindle checkpoint alone suffices to block proliferation, suggesting this checkpoint is highly sensitive to replication initiation defects. We discuss the potential significance of these overlapping checkpoints and the impact of our findings on previously postulated role(s) of ORCs in other cell cycle functions. [source] Elevation of cyclin D1 following trimethyltin induced hippocampal neurodegenerationJOURNAL OF NEUROCHEMISTRY, Issue 2002R. N. Wine Previous work has suggested that a major contributor to neuronal cell death is the aberrant induction of the cell cycle process, as indicated by an up-regulation of cyclin D. In order to examine the temporal and spatial relationship of cyclin D in a model of acute neurodegeneration, the hippocampal toxicant, trimethyltin (TMT; 2.0 mg/kg), was administered to 21-day old CD,1 male mice and the level and cellular localization of cyclin D1 examined. Within 24 h following TMT, dentate granule cells of the hippocampus showed evidence of neuronal necrosis resulting in severe cell loss over a 3-day period. The pyramidal cell layer was spared with only sparse punctate neuronal necrosis. Microglia response was seen at 72 h with ameboid microglia present in the dentate and ramified microglia present in the pyramidal cell layer, contributing to the elevation seen in TNF-alpha mRNA levels. A transient elevation was seen in mRNA levels for cyclin D1 over 48,72 h post-TMT. Immunohistochemistry demonstrated a transient increase in staining for cyclin D1 in CA1 pyramidal neurons as early as 24 h. Punctate staining occurred in neurons throughout the dentate at 48 h. BrdU positive cells were present along the inner blades of the dentate in control animals. Following TMT exposure, an increase was seen in both the number of neurons stained and a diffusion of the staining pattern into the full dentate region. Thus, in TMT-induced neurodegeneration, cyclin D1 is not expressed in the vulnerable neurons but rather in neurons spared from degeneration. This expression pattern appears to not be linked to an increase in the cellular processes for proliferation as the majority of BrdU positive cells were present in the region of neuronal damage. [source] Cell proliferation and cell cycle control: a mini reviewINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 12 2004C.H. Golias Summary Tumourigenesis is the result of cell cycle disorganisation, leading to an uncontrolled cellular proliferation. Specific cellular processes-mechanisms that control cell cycle progression and checkpoint traversation through the intermitotic phases are deregulated. Normally, these events are highly conserved due to the existence of conservatory mechanisms and molecules such as cell cycle genes and their products: cyclins, cyclin dependent kinases (Cdks), Cdk inhibitors (CKI) and extra cellular factors (i.e. growth factors). Revolutionary techniques using laser cytometry and commercial software are available to quantify and evaluate cell cycle processes and cellular growth. S-phase fraction measurements, including ploidy values, using histograms and estimation of indices such as the mitotic index and tumour-doubling time indices, provide adequate information to the clinician to evaluate tumour aggressiveness, prognosis and the strategies for radiotherapy and chemotherapy in experimental researches. [source] | ||||||||||