scholarly journals Early Cell Cycle Box-Mediated Transcription ofCLN3 and SWI4 Contributes to the Proper Timing of the G1-to-S Transition in Budding Yeast

2001 ◽  
Vol 21 (13) ◽  
pp. 4140-4148 ◽  
Author(s):  
Vivian L. MacKay ◽  
Bernard Mai ◽  
Laurie Waters ◽  
Linda L. Breeden
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Cell Volume ◽  
Budding Yeast ◽  
S Phase ◽  
Proper Timing ◽  
Cdc28 Kinase ◽  
Rate Limiting

ABSTRACT The Cln3-Cdc28 kinase is required to activate the Swi4-Swi6 transcription complex which induces CLN1 andCLN2 transcription in late G1 and drives the transition to S. Cln3 and Swi4 are both rate limiting for G1 progression, and they are coordinately transcribed to peak at the M/G1 boundary. Early cell cycle box (ECB) elements, which confer M/G1-specific transcription, have been found in both promoters, and elimination of all ECB elements from the CLN3 promoter causes both a loss of periodicity and Cln3-deficient phenotypes, which include an extended G1interval and increased cell volume. Mutants lacking the ECB elements in both the CLN3 and SWI4 promoters have low and deregulated levels of CLN transcripts, and the G1-to-S transition for these mutants is delayed and highly variable. These observations support the view that the coordinated rise of Cln3 and Swi4 levels mediated by ECB-dependent transcription controls the timing of the G1-to-S phase transition.

scholarly journals Higher order genomic organization and regulatory compartmentalization for cell cycle control at the G1/S-phase transition

2018 ◽  
Vol 233 (10) ◽  
pp. 6406-6413 ◽  
Author(s):  
Prachi N. Ghule ◽  
David J. Seward ◽  
Andrew J. Fritz ◽  
Joseph R. Boyd ◽  
Andre J. van Wijnen ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Genomic Organization ◽  
Cell Cycle Control ◽  
Higher Order ◽  
S Phase

Glucose and glutamine metabolism control by APC and SCF during the G1-to-S phase transition of the cell cycle

2014 ◽  
Vol 70 (2) ◽  
pp. 569-581 ◽  
Author(s):  
Irving Omar Estévez-García ◽  
Verónica Cordoba-Gonzalez ◽  
Eleazar Lara-Padilla ◽  
Abel Fuentes-Toledo ◽  
Ramcés Falfán-Valencia ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
S Phase ◽  
Glutamine Metabolism

scholarly journals A-myb is expressed in bovine vascular smooth muscle cells during the late G1-to-S phase transition and cooperates with c-myc to mediate progression to S phase.

1997 ◽  
Vol 17 (5) ◽  
pp. 2448-2457 ◽  
Author(s):  
D J Marhamati ◽  
R E Bellas ◽  
M Arsura ◽  
K E Kypreos ◽  
G E Sonenshein
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
S Phase ◽  
Cdna Clones ◽  
Transactivation Domain ◽  
Rna Levels

The Myb family of transcription factors is defined by homology within the DNA binding domain and includes c-Myb, A-Myb, and B-Myb. The protein products of the myb genes all bind the Myb-binding site (MBS) [YG(A/G)C(A/C/G)GTT(G/A)]. A-myb has been found to display a limited pattern of expression. Here we report that bovine aortic smooth muscle cells (SMCs) express A-myb. Sequence analysis of isolated bovine A-myb cDNA clones spanning the entire coding region indicated extensive homology with the human gene, including the putative transactivation domain. Expression of A-myb was cell cycle dependent; levels of A-myb RNA increased in the late G1-to-S phase transition following serum stimulation of serum-deprived quiescent SMC cultures and peaked in S phase. Nuclear run-on analysis revealed that an increased rate of transcription can account for most of the increase in A-myb RNA levels. Treatment of SMC cultures with 5,6-dichlorobenzimidazole riboside, a selective inhibitor of RNA polymerase II, indicated an approximate 4-h half-life for A-myb mRNA during the S phase of the cell cycle. Expression of A-myb by SMCs was stimulated by basic fibroblast growth factor, in a cell density-dependent fashion. Cotransfection of a human A-myb expression vector activated a multimerized MBS element-driven reporter construct approximately 30-fold in SMCs. The activity of c-myb and c-myc promoters, which both contain multiple MBS elements, were similarly transactivated, approximately 30- and 50-fold, respectively, upon cotransfection with human A-myb. Lastly, A-myb RNA levels could be increased by a combination of phorbol ester plus insulin-like growth factor 1. To test the role of myb family members in progression through the cell cycle, we comicroinjected c-myc and myb expression vectors into serum-deprived quiescent SMCs. The combination of c-myc and either A-myb or c-myb but not B-myb synergistically led to entry into S phase, whereas microinjection of any vector alone had little effect on S phase entry. Thus, these results suggest that A-myb is a potent transactivator in bovine SMCs and that its expression induces progression into S phase of the cell cycle.

scholarly journals Ran1 functions to control the Cdc10/Sct1 complex through Puc1.

1997 ◽  
Vol 8 (6) ◽  
pp. 1117-1128 ◽  
Author(s):  
M Caligiuri ◽  
T Connolly ◽  
D Beach
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Protein Kinase ◽  
Cell Fate ◽  
Biochemical Analysis ◽  
Control Cell ◽  
S Phase ◽  
Present Evidence ◽  
Phosphorylation State

We have undertaken a biochemical analysis of the regulation of the G1/S-phase transition and commitment to the cell cycle in the fission yeast Schizosaccharomyces pombe. The execution of Start requires the activity of the Cdc2 protein kinase and the Sct1/Cdc10 transcription complex. Progression through G1 also requires the Ran1 protein kinase whose inactivation leads to activation of the meiotic pathway under conditions normally inhibitory to this process. We have found that in addition to Cdc2, Sct1/Cdc10 complex formation requires Ran1. We demonstrate that the Puc1 cyclin associates with Ran1 and Cdc10 in vivo and that the Ran1 protein kinase functions to control the association between Puc1 and Cdc10. In addition, we present evidence that the phosphorylation state of Cdc10 is altered upon inactivation of Ran1. These results provide biochemical evidence that demonstrate one mechanism by which the Ran1 protein kinase serves to control cell fate through Cdc10 and Puc1.

Regulation of intracellular pH during the G1/S-phase transition of the neuroblastoma cell cycle

1988 ◽  
Vol 174 (2) ◽  
pp. 521-524 ◽  
Author(s):  
Johannes Boonstra ◽  
Leon G.J. Tertoolen ◽  
Christine L. Mummery ◽  
Siegfried W. de Laat
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Intracellular Ph ◽  
Neuroblastoma Cell ◽  
S Phase

scholarly journals p27kip1 controls H-Ras/MAPK activation and cell cycle entry via modulation of MT stability

2015 ◽  
Vol 112 (45) ◽  
pp. 13916-13921 ◽  
Author(s):  
Linda Fabris ◽  
Stefania Berton ◽  
Ilenia Pellizzari ◽  
Ilenia Segatto ◽  
Sara D’Andrea ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Signaling Pathway ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
S Phase ◽  
Point Of View ◽  
Cell Cycle Entry ◽  
Pathway Activation ◽  
Direct Binding

The cyclin-dependent kinase (CDK) inhibitor p27kip1 is a critical regulator of the G1/S-phase transition of the cell cycle and also regulates microtubule (MT) stability. This latter function is exerted by modulating the activity of stathmin, an MT-destabilizing protein, and by direct binding to MTs. We recently demonstrated that increased proliferation in p27kip1-null mice is reverted by concomitant deletion of stathmin in p27kip1/stathmin double-KO mice, suggesting that a CDK-independent function of p27kip1 contributes to the control of cell proliferation. Whether the regulation of MT stability by p27kip1 impinges on signaling pathway activation and contributes to the decision to enter the cell cycle is largely unknown. Here, we report that faster cell cycle entry of p27kip1-null cells was impaired by the concomitant deletion of stathmin. Using gene expression profiling coupled with bioinformatic analyses, we show that p27kip1 and stathmin conjunctly control activation of the MAPK pathway. From a molecular point of view, we observed that p27kip1, by controlling MT stability, impinges on H-Ras trafficking and ubiquitination levels, eventually restraining its full activation. Our study identifies a regulatory axis controlling the G1/S-phase transition, relying on the regulation of MT stability by p27kip1 and finely controlling the spatiotemporal activation of the Ras-MAPK signaling pathway.

scholarly journals Protein phosphatase 2A (PP2A) promotes anaphase entry after DNA replication stress in budding yeast

2021 ◽  
Author(s):  
Cory Haluska ◽  
Fengzhi Jin ◽  
Yanchang Wang
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Dna Synthesis ◽  
Protein Phosphatase ◽  
Budding Yeast ◽  
Replication Stress ◽  
S Phase ◽  
Viability Loss ◽  
Phosphatase 2A ◽  
Dna Replication Stress

DNA replication stress activates the S-phase checkpoint that arrests the cell cycle, but it is poorly understood how cells recover from this arrest. Cyclin-dependent kinase (CDK) and Protein Phosphatase 2A (PP2A) are key cell cycle regulators, and Cdc55 is a regulatory subunit of PP2A in budding yeast. We found that yeast cells lacking functional PP2ACdc55 showed slow growth in the presence of hydroxyurea (HU), a DNA synthesis inhibitor, without obvious viability loss. Moreover, PP2A mutants exhibited delayed anaphase entry and sustained levels of anaphase inhibitor Pds1 after HU treatment. A DNA damage checkpoint Chk1 phosphorylates and stabilizes Pds1. We showed that chk1Δ and mutation of the Chk1 phosphorylation sites in Pds1 largely restored efficient anaphase entry in PP2A mutants after HU treatment. In addition, deletion of SWE1 that encodes the inhibitory kinase for CDK or mutation of the Swe1 phosphorylation site in CDK ( cdc28F19) also suppressed the anaphase entry delay in PP2A mutants after HU treatment. Our genetic data suggest that Swe1/CDK acts upstream of Pds1. Surprisingly, cdc55Δ showed significant suppression to the viability loss of S-phase checkpoint mutants during DNA synthesis block. Together, our results uncover a PP2A-Swe1-CDK-Chk1-Pds1 axis that promotes recovery from DNA replication stress.

scholarly journals Retinoblastoma 1 (RB1) modulates the proliferation of chicken preadipocytes

2018 ◽  
Author(s):  
Yu-Xiang Wang ◽  
Hai-Xia Wang ◽  
Wei Na ◽  
Fei-Yue Qin ◽  
Zhi-Wei Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Phase Transition ◽  
Cell Cycle ◽  
Gene Expression Analysis ◽  
Mammalian Species ◽  
S Phase ◽  
Pcr Analysis ◽  
Quantitative Real Time Pcr ◽  
Ki 67

AbstractRetinoblastoma 1 (RB1) has been extensively studied in mammalian species, but its function in avian species is unclear. The objective of this study was to reveal the role of chicken RB1 (Gallus gallus RB1, gRB1) in the proliferation of preadipocytes. In the current study, quantitative real-time PCR analysis showed that the expression levels of gRB1 transiently increased during the proliferation of preadipocytes. The MTT assay showed that gRB1 overexpression suppressed preadipocyte proliferation, and gRB1 interference promoted preadipocyte proliferation. Additionally, cell-cycle analysis indicated that gRB1 may play a crucial role in the G1/S transition. Consistently, gene expression analysis showed that gRB1 knockdown promoted marker of proliferation Ki-67 (MKi67) expression at 96 h (P < 0.05), and that overexpression of gRB1 reduced MKi67 expression at 72 h (P < 0.05). Together, our study demonstrated that gRB1 inhibited preadipocyte proliferation at least in part by inhibiting the G1 to S phase transition.

scholarly journals Stimulation of Cyclin-Dependent Kinase Activity and G1- to S-Phase Transition in Human Lymphocytes by the Human T-Cell Leukemia/Lymphotropic Virus Type 1 Tax Protein

1998 ◽  
Vol 72 (1) ◽  
pp. 633-640 ◽  
Author(s):  
Iris Schmitt ◽  
Oliver Rosin ◽  
Peter Rohwer ◽  
Manfred Gossen ◽  
Ralph Grassmann
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
T Cells ◽  
T Cell ◽  
Virus Type ◽  
S Phase ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Human T Cell

ABSTRACT The human T-cell leukemia/lymphotropic virus type 1 (HTLV-1) induces a malignant lymphocytic disease. The HTLV-1 transactivator protein, Tax, is believed to be crucial for the development of the disease since it is transforming in vitro and induces tumors in transgenic animals. Although the transcriptional modulation of viral and cellular gene expression by Tax has been analyzed thoroughly, it has remained unclear how the Tax functions act on the cell cycle of primary T cells. To investigate the mechanism of Tax-mediated T-cell stimulation, we transduced primary human cord blood T cells with a conditional, tetracycline repressor-based tax expression system. Permanent Tax expression results in an abnormal proliferation of T cells which closely resemble HTLV-1-infected lymphocytes. Suppression of Tax synthesis stopped lymphocyte growth and caused cell cycle arrest in the G1 phase. Upon reinduction oftax expression, the arrested cells entered the S phase. This showed that Tax has mitogenic activity, which is required for stimulating the G1- to S-phase transition of immortalized lymphocytes. In mammalian cells, the G1-phase progression is controlled by the serial activation of several cyclin-dependent kinases (Cdks), starting with Cdk4 and Cdk6. In the presence of Tax, both Cdk4 and Cdk6 were activated. The suppression of Tax synthesis, however, resulted in a significant reduction of the Cdk4 and Cdk6 activities but did not influence the expression of Cdk4, Cdk6, or cognate D-type cyclin proteins. These data suggest that Tax induces Cdk4 and Cdk6 activity in primary human T lymphocytes; this Cdk activation is likely to account for the mitogenic Tax effect and for the abnormal T-cell proliferation of HTLV-1-infected lymphocytes.

scholarly journals Fission yeast cell cycle mutants and the logic of eukaryotic cell cycle control

2020 ◽  
Vol 31 (26) ◽  
pp. 2871-2873
Author(s):  
Paul Nurse
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Fission Yeast ◽  
Cell Cycle Control ◽  
Eukaryotic Cell ◽  
S Phase ◽  
Cyclin Dependent Kinases ◽  
Starting Point ◽  
Rate Limiting ◽  
Working Out

Cell cycle mutants in the budding and fission yeasts have played critical roles in working out how the eukaryotic cell cycle operates and is controlled. The starting point was Lee Hartwell’s 1970s landmark papers describing the first cell division cycle (CDC) mutants in budding yeast. These mutants were blocked at different cell cycle stages and so were unable to complete the cell cycle, thus defining genes necessary for successful cell division. Inspired by Hartwell’s work, I isolated CDC mutants in the very distantly related fission yeast. This started a program of searches for mutants in fission yeast that revealed a range of phenotypes informative about eukaryotic cell cycle control. These included mutants defining genes that were rate-limiting for the onset of mitosis and of the S-phase, that were responsible for there being only one S-phase in each cell cycle, and that ensured that mitosis only took place when S-phase was properly completed. This is a brief account of the discovery of these mutants and how they led to the identification of cyclin-dependent kinases as core to these cell cycle controls.

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