Microtubule-dependent cell cycle regulation is implicated in the G2 phase of Hydra cells

1988 ◽  
Vol 91 (3) ◽  
pp. 347-359
Author(s):  
S. Dubel ◽  
M. Little
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Immunofluorescent Staining ◽  
Cycle Arrest ◽  
Low Concentrations ◽  
Dependent Cell ◽  
G2 Phase ◽  
Phase Visualization ◽  
Cycle Regulation ◽  
First Time

Interstitial cells of Hydra attenuata, from which nerve cells and nematocytes (stinging cells) differentiate, were arrested in either metaphase or G2 by different concentrations of the microtubule-depolymerizing agent nocodazole. At a concentration of 1.4 nM-nocodazole, a large number of cells were arrested in metaphase. However, at concentrations of 2 nM-nocodazole and above most of the cells were arrested at a distinct point in G2 several hours before mitosis. After removal of the 2 nM-nocodazole block, 75% of the cells entered the next cell cycle about 10 h later. To our knowledge this is the first time that cells have been synchronized by arresting them in the G2 phase. Visualization of Hydra microtubules with a tubulin monoclonal antibody and immunofluorescent staining showed that the very low concentrations of nocodazole used for cell cycle arrest were indeed affecting microtubule structures. Spindles and stem cell microtubules disappeared at 0.8-1 nM-nocodazole, followed by nerve microtubules (about 2 nM), cnidocil microtubules (10 nM) and finally by nematocyte microtubules (34 nM). Taken together, these data strongly indicate a microtubule-dependent mechanism of cell cycle regulation in the G2 phase.

Abstract W P198: Sphingomyelin Synthases Regulate Neuronal Cell Proliferation and Cell Cycle Progression

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Umadevi V Wesley ◽  
Daniel Tremmel ◽  
Robert Dempsey
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Cycle Progression ◽  
Cycle Arrest ◽  
Cycle Regulation ◽  
Cerebral Artery Occlusion

Introduction: The molecular mechanisms of cerebral ischemia damage and protection are not completely understood, but a number of reports implicate the contribution of lipid metabolism and cell-cycle regulating proteins in stroke out come. We have previously shown that tricyclodecan-9-yl-xanthogenate (D609) resulted in increased ceramide levels after transient middle cerebral artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR). We hypothesized that D609 induced cell cycle arrest probably by inhibiting sphingomyelin synthase (SMS). In this study, we examined the direct effects of SMS on cell cycle progression and proliferation of neuroblast cells. Methods: Ischemia was induced by middle cerebral artery occlusion (MCAO) and reperfusion. Expression levels were measured by western blot analysis, RT-PCR, and Immunofluorescence staining. SMS1 and 2 expressions were silenced by stable transfection with SMS1/2-targeted shRNA. Cell cycle analysis was performed using Flow cytometry. Data were analyzed using MODFIT cell cycle analysis program. Cell proliferation rate was measured by MTT assay. Results: We have identified that the expression of SMS1is significantly up-regulated in the ischemic hemisphere following MCAO. Neuro-2a cells transfected with SMS specific ShRNA acquired more neuronal like phenotype and exhibited decreased proliferation rate. Also, silencing of both SMS1 and 2 induced cell-cycle arrest as shown by significantly increased percentage of cells in G0/G1 and decreased proportion of cells in S-phase as compared to control cells. This was accompanied by up-regulation of cyclin-dependent kinase (Cdk) inhibitors p21 and decreased levels of phophorylated AKT levels. Furthermore, loss of SMS inhibited the migratory potential of Neuro 2a cells. Summary: Up-regulation of SMS under ischemic/reperfusion conditions suggests that this enzyme potentially contributes to cell cycle regulation and may contribute to maintaining neuronal cell population. Further studies may open up a new direction for identifying the molecular mechanisms of cell cycle regulation and protection following ischemic stroke

scholarly journals Absence of p53-dependent cell cycle regulation in pluripotent mouse cell lines

Oncogene ◽  
1998 ◽  
Vol 16 (23) ◽  
pp. 3003-3011 ◽  
Author(s):  
Prabha K Schmidt-Kastner ◽  
Karen Jardine ◽  
Michelle Cormier ◽  
Michael W McBurney
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Cell Cycle Regulation ◽  
Mouse Cell ◽  
Dependent Cell ◽  
Cycle Regulation

scholarly journals A role for ATP Citrate Lyase in cell cycle regulation during myeloid differentiation

2019 ◽  
Author(s):  
Jess Rhee ◽  
Lauren A. Solomon ◽  
Rodney P. DeKoter
Keyword(s):  
Cell Cycle ◽  
Fatty Acid ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Acid Synthesis ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Cycle Arrest ◽  
Citrate Lyase ◽  
Cycle Regulation

AbstractDifferentiation of myeloid progenitor cells into macrophages is accompanied by increased PU.1 concentration and increasing cell cycle length, culminating in cell cycle arrest. Induction of PU.1 expression in a cultured myeloid cell line expressing low PU.1 concentration results in decreased levels of mRNA encoding ATP-Citrate Lyase (ACL) and cell cycle arrest. ACL is an essential enzyme for generating acetyl-CoA, a key metabolite for the first step in fatty acid synthesis as well as for histone acetylation. We hypothesized that ACL may play a role in cell cycle regulation in the myeloid lineage. In this study, we found that acetyl-CoA or acetate supplementation was sufficient to rescue cell cycle progression in cultured BN cells treated with an ACL inhibitor or induced for PU.1 expression. Acetyl-CoA supplementation was also sufficient to rescue cell cycle progression in BN cells treated with a fatty acid synthase (FASN) inhibitor. We demonstrated that acetyl-CoA was utilized in both fatty acid synthesis and histone acetylation pathways to promote proliferation. Finally, we found that Acly mRNA transcript levels decrease during normal macrophage differentiation from bone marrow precursors. Our results suggest that regulation of ACL activity is a potentially important point of control for cell cycle regulation in the myeloid lineage.

scholarly journals FAR1 and the G1 phase specificity of cell cycle arrest by mating factor in Saccharomyces cerevisiae.

1995 ◽  
Vol 15 (5) ◽  
pp. 2509-2516 ◽  
Author(s):  
J D McKinney ◽  
F R Cross
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
G1 Phase ◽  
Cycle Arrest ◽  
Gal1 Promoter ◽  
G1 Phase Arrest ◽  
Terminal Amino ◽  
Cycle Regulation ◽  
Mating Factor

Significant accumulation of Far1p is restricted to the G1 phase of the Saccharomyces cerevisiae cell cycle. Here we demonstrate yeast cell cycle regulation of Far1p proteolysis. Deletions within the 50 N-terminal amino acids of Far1p increase stability and reduce cell cycle regulation of Far1p abundance. Whereas wild-type Far1p specifically and exclusively promotes G1 phase arrest in response to mating factor, stabilized Far1p promoted arrest both during and after G1. The loss of the G1 specificity of Far1p action requires elimination of FAR1 transcriptional regulation (by means of the GAL1 promoter) as well as N-terminal truncation. Thus, the cell cycle specificity of mating factor arrest may be largely due to cell cycle regulation of FAR1 transcription and protein stability.

scholarly journals Inducing controlled cell cycle arrest and re-entry during asexual proliferation ofPlasmodium falciparummalaria parasites

2018 ◽  
Author(s):  
Riëtte van Biljon ◽  
Jandeli Niemand ◽  
Roelof van Wyk ◽  
Katherine Clark ◽  
Bianca Verlinden ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Cycle Regulation ◽  
Malaria Parasites ◽  
New Approach ◽  
Mitotic Kinases ◽  
Cycle Arrest ◽  
Cycle Regulation ◽  
Early Phases

ABSTRACTThe life cycle of the malaria parasitePlasmodium falciparumis tightly regulated, oscillating between stages of intense proliferation and quiescence. Cyclic 48-hour asexual replication ofPlasmodiumis markedly different from cell division in higher eukaryotes, and mechanistically poorly understood. Here, we report tight synchronisation of malaria parasites during the early phases of the cell cycle by exposure to DL-α-difluoromethylornithine (DFMO), which results in the depletion of polyamines. This induces an inescapable cell cycle arrest in G1(~15 hours post-invasion) by blocking G1/S transition. Cell cycle-arrested parasites enter a quiescent G0-like state but, upon addition of exogenous polyamines, re-initiate their cell cycle in a coordinated fashion. This ability to halt malaria parasites at a specific point in their cell cycle, and to subsequently trigger re-entry into the cell cycle, provides a valuable framework to investigate cell cycle regulation in these parasites. We therefore used gene expression analyses to show that re-entry into the cell cycle involves expression of Ca2+-sensitive (cdpk4andpk2)and mitotic kinases (nimaandark2),with deregulation of the pre-replicative complex associated with expression ofpk2. Changes in gene expression could be driven through transcription factors MYB1 and two ApiAP2 family members. This new approach to parasite synchronisation therefore expands our currently limited toolkit to investigate cell cycle regulation in malaria parasites.

Expression profiles of miRNAs and involvement of miR-100 and miR-34 in regulation of cell cycle arrest in Artemia

2015 ◽  
Vol 470 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Ling-Ling Zhao ◽  
Feng Jin ◽  
Xiang Ye ◽  
Lin Zhu ◽  
Jin-Shu Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Expression Profiles ◽  
Regulatory Mechanisms ◽  
Cycle Progression ◽  
Cycle Arrest ◽  
Regulation Of Cell Cycle ◽  
Cycle Regulation

We established an expression profile of miRNA for cell cycle arrest in Artemia and found that miR-100 and miR-34 promote and prevent cell cycle progression respectively. The regulatory mechanisms of these two miRNAs provide insights into cell cycle regulation.

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