scholarly journals The Schizosaccharomyces pombe cdc14 gene is required for septum formation and can also inhibit nuclear division.

1993 ◽  
Vol 4 (5) ◽  
pp. 531-539 ◽  
Author(s):  
C Fankhauser ◽  
V Simanis
Keyword(s):  
Cell Cycle ◽  
Amino Acids ◽  
Cell Division ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Arrest ◽  
Null Allele ◽  
Nuclear Division ◽  
Septum Formation ◽  
Cycle Arrest ◽  
Mitotic Inhibitor

A conditional heat-sensitive mutation in the cdc14 gene of the fission yeast Schizosaccharomyces pombe results in failure to form a septum. Cells become highly elongated and multinucleate as growth and nuclear division continue in the absence of cell division. This article describes the cloning of the cdc14 gene and the identification of its product, a protein of 240 amino acids, p28cdc14. A null allele of the cdc14 gene shows that the gene is essential for septum formation and completion of the cell-division cycle. Overexpression of the gene product, p28cdc14, causes cell-cycle arrest in late G2 before mitosis. Cells leaking past the block activate p34cdc2 kinase and show condensed chromosomes, but the normal rearrangements of the microtubules and microfilaments that are associated with the transition from interphase to mitosis do not occur. Overexpression of p28cdc14 in mutants, in which the timing of mitosis is altered, suggests that these effects may be mediated upstream of the mitotic inhibitor wee1. These data are consistent with the idea that p28cdc14 may play a role in both the initiation of mitosis and septum formation and, by doing so, be part of the mechanism that coordinates these two cell-cycle events.

scholarly journals Anticancer potential of nitric oxide (NO) in neuroblastoma treatment

RSC Advances ◽  
2021 ◽  
Vol 11 (16) ◽  
pp. 9112-9120
Author(s):  
Jenna L. Gordon ◽  
Kristin J. Hinsen ◽  
Melissa M. Reynolds ◽  
Tyler A. Smith ◽  
Haley O. Tucker ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Cell Division ◽  
Cell Viability ◽  
Cell Cycle Arrest ◽  
Neuroblastoma Cells ◽  
Cycle Arrest

S-Nitrosoglutathione (GSNO) reduces cell viability, inhibits cell division, and induces cell cycle arrest and apoptosis in neuroblastoma cells.

Oxygen uptake during the cell cycle of the fission yeast Schizosaccharomyces pombe

1978 ◽  
Vol 33 (1) ◽  
pp. 399-411
Author(s):  
J. Creanor
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Oxygen Uptake ◽  
Dna Synthesis ◽  
Schizosaccharomyces Pombe ◽  
Fission Yeast ◽  
Nuclear Division ◽  
Synchronous Culture ◽  
Synchronous Cultures ◽  
The Many

Oxygen uptake was measured in synchronous cultures of the fission yeast Schizosaccharomyces pombe. The rate of oxygen uptake was found to increase in a step-wise manner at the beginning of the cycle and again in the middle of the cycle. The increases in rate were such that overall, oxygen uptake doubled in rate once per cell cycle. Addition of inhibitors of DNA synthesis or nuclear division to a synchronous culture did not affect the uptake of oxygen. In an induced synchronous culture, in which DNA synthesis, cell division, and nuclear division, but not ‘growth’ were synchronized, oxygen uptake increased continuously in rate and did not show the step-wise rises which were shown in the selection-synchronized culture. These results were compared with previous measurements of oxygen uptake in yeast and an explanation is suggested for the many different patterns which have been reported.

MicroRNA-1225-5p acts as a tumor-suppressor in laryngeal cancer via targeting CDC14B

2019 ◽  
Vol 400 (2) ◽  
pp. 237-246 ◽  
Author(s):  
Peng Sun ◽  
Dan Zhang ◽  
Haiping Huang ◽  
Yafeng Yu ◽  
Zhendong Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Division ◽  
Cell Cycle Arrest ◽  
Molecular Mechanisms ◽  
Normal Tissues ◽  
Cycle Arrest ◽  
Enhanced Expression ◽  
Insight Into

Abstract This study aimed to investigate the role of miRNA-1225-5p (miR-1225) in laryngeal carcinoma (LC). We found that the expression of miR-1225 was suppressed in human LC samples, while CDC14B (cell division cycle 14B) expression was reinforced in comparison with surrounding normal tissues. We also demonstrated that enhanced expression of miR-1225 impaired the proliferation and survival of LC cells, and resulted in G1/S cell cycle arrest. In contrast, reduced expression of miR-1225 promoted cell survival. Moreover, miR-1225 resulted in G1/S cell cycle arrest and enhanced cell death. Further, miR-1225 targets CDC14B 3′-UTR and recovery of CDC14B expression counteracted the suppressive influence of miR-1225 on LC cells. Thus, these findings offer insight into the biological and molecular mechanisms behind the development of LC.

Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway

1990 ◽  
Vol 10 (12) ◽  
pp. 6482-6490
Author(s):  
F R Cross
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Arrest ◽  
S Phase ◽  
Signalling Pathway ◽  
Phase Cell ◽  
Glucose Medium ◽  
Coding Sequence ◽  
Cycle Arrest

Null mutations in three genes encoding cyclin-like proteins (CLN1, CLN2, and CLN3) in Saccharomyces cerevisiae cause cell cycle arrest in G1 (cln arrest). In cln1 cln2 cln3 strains bearing plasmids containing the CLN3 (also called WHI1 or DAF1) coding sequence under the transcriptional control of a galactose-regulated promoter, shift from galactose to glucose medium (shutting off synthesis of CLN3 mRNA) allowed completion of cell cycles in progress but caused arrest in the ensuing unbudded G1 phase. Cell growth was not inhibited in arrested cells. Cell division occurred in glucose medium even if cells were arrested in S phase during the initial 2 h of glucose treatment, suggesting that CLN function may not be required in the cell cycle after S phase. However, when the coding sequence of the hyperactive C-terminal truncation allele CLN3-2 (formerly DAF1-1) was placed under GAL control, cells went through multiple cycles before arresting after a shift from galactose to glucose. These results suggest that the C terminus of the wild-type protein confers functional instability. cln-arrested cells are mating competent. However, cln arrest is distinct from constitutive activation of the mating-factor signalling pathway because cln-arrested cells were dependent on the addition of pheromone both for mating and for induction of an alpha-factor-induced transcript, FUS1, and because MATa/MAT alpha (pheromone-nonresponsive) strains were capable of cln arrest in G1 (although a residual capacity for cell division before arrest was observed in MATa/MAT alpha strains). These results are consistent with a specific CLN requirement for START transit.

scholarly journals Sulforaphane-induced G2/M Phase Cell Cycle Arrest Involves Checkpoint Kinase 2-mediated Phosphorylation of Cell Division Cycle 25C

2004 ◽  
Vol 279 (24) ◽  
pp. 25813-25822 ◽  
Author(s):  
Shivendra V. Singh ◽  
Anna Herman-Antosiewicz ◽  
Ajita V. Singh ◽  
Karen L. Lew ◽  
Sanjay K. Srivastava ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Arrest ◽  
Cell Division Cycle ◽  
Phase Cell ◽  
Checkpoint Kinase ◽  
Cycle Arrest ◽  
Checkpoint Kinase 2 ◽  
M Phase

scholarly journals Loss of Oncogenic H-ras-Induced Cell Cycle Arrest and p38 Mitogen-Activated Protein Kinase Activation by Disruption of Gadd45a

2003 ◽  
Vol 23 (11) ◽  
pp. 3859-3871 ◽  
Author(s):  
Dmitry V. Bulavin ◽  
Oleg Kovalsky ◽  
M. Christine Hollander ◽  
Albert J. Fornace
Keyword(s):  
Cell Cycle ◽  
Amino Acids ◽  
Protein Kinase ◽  
Cell Cycle Arrest ◽  
P38 Mapk ◽  
Mitogen Activated Protein Kinase ◽  
Mapk Activation ◽  
Cycle Arrest ◽  
Mitogen Activated Protein ◽  
P53 Activation

ABSTRACT The activation of p53 is a guardian mechanism to protect primary cells from malignant transformation; however, the details of the activation of p53 by oncogenic stress are still incomplete. In this report we show that in Gadd45a −/− mouse embryo fibroblasts (MEF), overexpression of H-ras activates extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) but not p38 kinase, and this correlates with the loss of H-ras-induced cell cycle arrest (premature senescence). Inhibition of p38 mitogen-activated protein kinase (MAPK) activation correlated with the deregulation of p53 activation, and both a p38 MAPK chemical inhibitor and the expression of a dominant-negative p38α inhibited p53 activation in the presence of H-ras in wild-type MEF. p38, but not ERK or JNK, was found in a complex with Gadd45 proteins. The region of interaction was mapped to amino acids 71 to 96, and the central portion (amino acids 71 to 124) of Gadd45a was required for p38 MAPK activation in the presence of H-ras. Our results indicate that this Gadd45/p38 pathway plays an important role in preventing oncogene-induced growth at least in part by regulating the p53 tumor suppressor.

scholarly journals A RAD9-dependent cell cycle arrest in response to unresolved recombination intermediates in Saccharomyces cerevisiae

2019 ◽  
Author(s):  
Hardeep Kaur ◽  
GN Krishnaprasad ◽  
Michael Lichten
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Damage ◽  
Cell Division ◽  
Cell Cycle Arrest ◽  
Mitotic Cell ◽  
Cycle Arrest ◽  
Associated Lesions

AbstractIn Saccharomyces cerevisiae, the conserved Sgs1-Top3-Rmi1 helicase-decatenase regulates homologous recombination by limiting accumulation of recombination intermediates that are precursors of crossovers. In vitro studies have suggested that the dissolution of double-Holliday junction joint molecules by Sgs1-driven convergent junction migration and Top3-Rmi1 mediated strand decatenation could be responsible for this. To ask if dissolution occurs in vivo, we conditionally depleted Sgs1 and/or Rmi1 during return to growth, a procedure where recombination intermediates formed during meiosis are resolved when cells resume the mitotic cell cycle. Sgs1 depletion during return to growth delayed joint molecule resolution, but ultimately most were resolved and cells divided normally. In contrast, Rmi1 depletion resulted in delayed and incomplete joint molecule resolution, and most cells did not divide. rad9Δ mutation restored cell division in Rmi1-depleted cells, indicating that the DNA damage checkpoint caused this cell cycle arrest. Restored cell division in rad9Δ, Rmi1-depleted cells frequently produced anucleate cells, consistent with the suggestion that persistent recombination intermediates prevented chromosome segregation. Our findings indicate that Sgs1-Top3-Rmi1 acts in vivo, as it does in vitro, to promote recombination intermediate resolution by dissolution. They also indicate that, in the absence of Top3-Rmi1 activity, unresolved recombination intermediates persist and activate the DNA damage response, which is usually thought to be activated by much earlier DNA damage-associated lesions.

Vertebrate p34cdc2 phosphorylation site mutants: effects upon cell cycle progression in the fission yeast Schizosaccharomyces pombe

1992 ◽  
Vol 102 (1) ◽  
pp. 43-53 ◽  
Author(s):  
W. Krek ◽  
J. Marks ◽  
N. Schmitz ◽  
E.A. Nigg ◽  
V. Simanis
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Arrest ◽  
Fission Yeast ◽  
Cell Cycle Progression ◽  
Atp Binding ◽  
In Vitro Mutagenesis ◽  
Cycle Progression ◽  
Cycle Arrest ◽  
P34 Cdc2

We have used the fission yeast Schizosaccharomyces pombe to analyse the effects of in vitro mutagenesis of the four known phosphorylation sites in the chicken p34(cdc2) protein, Thr 14, Tyr 15, Thr 161 and Ser 277, upon cell cycle progression. We have studied both the effect of overexpression of mutant proteins in a cdc2+ background and assayed their ability to rescue null and temperature-sensitive alleles of cdc2. Mutations of Thr 14 and Tyr 15 within the ATP binding domain of p34(cdc2) that mimic constitutive phosphorylation cause dominant negative cell cycle arrest when overexpressed. In contrast, some substitutions that simulate permanent dephosphorylation of the corresponding sites advance dephosphorylation of the corresponding sites advance mitosis. These data confirm the model that p34(cdc2) function is negatively regulated by phosphorylation of residues in the ATP binding site. Mutagenesis of the conserved residue Thr 161 functionally inactivates p34(cdc2), and our data suggest that both phosphorylation and dephosphorylation events at Thr 161 are required for progression through the cell cycle. Mutations at the fourth site of phosphorylation. Ser 277, lead to cold-sensitive cell cycle arrest, in minimal but not rich growth medium, suggesting that this site is involved in monitoring the nutritional status of the cell.

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