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.

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 Involvement of calcineurin‐dependent degradation of Yap1p in Ca 2+ ‐induced G 2 cell‐cycle regulation in Saccharomyces cerevisiae

EMBO Reports ◽  
2006 ◽  
Vol 7 (5) ◽  
pp. 519-524 ◽  
Author(s):  
Hiroshi Yokoyama ◽  
Masaki Mizunuma ◽  
Michiyo Okamoto ◽  
Josuke Yamamoto ◽  
Dai Hirata ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cycle Regulation

scholarly journals Involvement of S-adenosylmethionine in G1 cell-cycle regulation in Saccharomyces cerevisiae

2004 ◽  
Vol 101 (16) ◽  
pp. 6086-6091 ◽  
Author(s):  
M. Mizunuma ◽  
K. Miyamura ◽  
D. Hirata ◽  
H. Yokoyama ◽  
T. Miyakawa
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cycle Regulation

scholarly journals Ste12 and Mcm1 regulate cell cycle-dependent transcription of FAR1.

1996 ◽  
Vol 16 (6) ◽  
pp. 2830-2837 ◽  
Author(s):  
L J Oehlen ◽  
J D McKinney ◽  
F R Cross
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Transcriptional Activation ◽  
G1 Phase ◽  
Protein Accumulation ◽  
Transcriptional Activation Domain ◽  
Cycle Arrest ◽  
Gal1 Promoter ◽  
Combinatorial Control ◽  
Cycle Dependent

The transcripts of many genes involved in Saccharomyces cerevisiae mating were found to fluctuate during the cell cycle. In the absence of a functional Ste12 transcription factor, both the levels and the cell cycle pattern of expression of these genes were affected. FUS1 and AGA1 levels, which are maximally expressed only in G1-phase cells, were strongly reduced in ste12- cells. The cell cycle transcription pattern for FAR1 was changed in ste12- cells: the gene was still significantly expressed in G2/M, but transcript levels were strongly reduced in G1 phase, resulting in a lack of Far1 protein accumulation. G2/M transcription of FAR1 was dependent on the transcription factor Mcm1, and expression of a gene with Mcm1 fused to a strong transcriptional activation domain resulted in increased levels of FAR1 transcription. The pattern of cell cycle-regulated transcription of FAR1 could involve combinatorial control of Ste12 and Mcm1. Forced G1 expression of FAR1 from the GAL1 promoter resorted the ability to arrest in response to pheromone in ste12-cells. This indicates that transcription of FAR1 in the G1 phase is essential for accumulation of the protein and for pheromone-induced cell cycle arrest.

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 Cell-size regulation in budding yeast does not depend on linear accumulation of Whi5

2020 ◽  
Vol 117 (25) ◽  
pp. 14243-14250 ◽  
Author(s):  
Felix Barber ◽  
Ariel Amir ◽  
Andrew W. Murray
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Cell Cycle Regulation ◽  
Budding Yeast ◽  
Size Control ◽  
Size Distributions ◽  
Wild Type ◽  
Gal1 Promoter ◽  
The Mean ◽  
Cycle Regulation

Cells must couple cell-cycle progress to their growth rate to restrict the spread of cell sizes present throughout a population. Linear, rather than exponential, accumulation of Whi5, was proposed to provide this coordination by causing a higher Whi5 concentration in cells born at a smaller size. We tested this model using the inducibleGAL1promoter to make the Whi5 concentration independent of cell size. At an expression level that equalizes the mean cell size with that of wild-type cells, the size distributions of cells with galactose-induced Whi5 expression and wild-type cells are indistinguishable. Fluorescence microscopy confirms that the endogenous andGAL1promoters produce different relationships between Whi5 concentration and cell volume without diminishing size control in the G1 phase. We also expressed Cln3 from the GAL1 promoter, finding that the spread in cell sizes for an asynchronous population is unaffected by this perturbation. Our findings indicate that size control in budding yeast does not fundamentally originate from the linear accumulation of Whi5, contradicting a previous claim and demonstrating the need for further models of cell-cycle regulation to explain how cell size controls passage through Start.

scholarly journals Cell cycle regulation of thymidine kinase: residues near the carboxyl terminus are essential for the specific degradation of the enzyme at mitosis.

1991 ◽  
Vol 11 (5) ◽  
pp. 2538-2546 ◽  
Author(s):  
M G Kauffman ◽  
T J Kelly
Keyword(s):  
Cell Cycle ◽  
Amino Acids ◽  
Thymidine Kinase ◽  
Cell Cycle Regulation ◽  
Carboxyl Terminus ◽  
G1 Phase ◽  
Cycle Phase ◽  
M Phase ◽  
Specific Degradation ◽  
Cycle Regulation

The level of human thymidine kinase (TK) polypeptide is subject to cell cycle regulation. The enzyme is barely detectable in G1 phase but increases 10- to 20-fold by M phase. The low level of human TK in G1 phase is due primarily to the specific degradation of the protein during cell division. Substitution of heterologous promoters, removal of the introns, and deletion of all of the 3' untranslated region from the human TK gene do not affect cell cycle regulation of the enzyme. However, deletion of the carboxyl-terminal 40 amino acids or fusion of beta-galactosidase to the carboxyl terminus of human TK completely abolishes cell cycle regulation and stabilizes the protein throughout the cell cycle. These alterations do not significantly alter the specific enzymatic activity of TK. Changing the carboxyl terminus or deletion of the last 10 amino acids does not alter cell cycle regulation. These data demonstrate that residues near the carboxyl terminus of TK are essential for the cell cycle phase-specific degradation of the enzyme.

scholarly journals Cell Cycle Regulation of the Saccharomyces cerevisiae Polo-Like Kinase Cdc5p

1998 ◽  
Vol 18 (12) ◽  
pp. 7360-7370 ◽  
Author(s):  
Liang Cheng ◽  
Linda Hunke ◽  
Christopher F. J. Hardy
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Kinase Activity ◽  
Anaphase Promoting Complex ◽  
Mitotic Kinases ◽  
Polo Kinase ◽  
Evolutionarily Conserved ◽  
M Phase ◽  
Cycle Regulation

ABSTRACT Progression through and completion of mitosis require the actions of the evolutionarily conserved Polo kinase. We have determined that the levels of Cdc5p, a Saccharomyces cerevisiae member of the Polo family of mitotic kinases, are cell cycle regulated. Cdc5p accumulates in the nuclei of G2/M-phase cells, and its levels decline dramatically as cells progress through anaphase and begin telophase. We report that Cdc5p levels are sensitive to mutations in key components of the anaphase-promoting complex (APC). We have determined that Cdc5p-associated kinase activity is restricted to G2/M and that this activity is posttranslationally regulated. These results further link the actions of the APC to the completion of mitosis and suggest possible roles for Cdc5p during progression through and completion of mitosis.

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