scholarly journals A single-point mutation in HCF causes temperature-sensitive cell-cycle arrest and disrupts VP16 function.

1997 ◽  
Vol 11 (6) ◽  
pp. 726-737 ◽  
Author(s):  
H Goto ◽  
S Motomura ◽  
A C Wilson ◽  
R N Freiman ◽  
Y Nakabeppu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Point Mutation ◽  
Single Point ◽  
Single Point Mutation ◽  
Temperature Sensitive ◽  
Sensitive Cell ◽  
Cycle Arrest

A temperature-sensitive mutation affecting cilia regeneration, nuclear development, and the cell cycle of Tetrahymena thermophila is rescued by cytoplasmic exchange

1988 ◽  
Vol 8 (7) ◽  
pp. 2681-2689
Author(s):  
D G Pennock ◽  
T Thatcher ◽  
M A Gorovsky
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Tetrahymena Thermophila ◽  
Wild Type Cell ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Wild Type ◽  
Atp Production ◽  
Cycle Arrest ◽  
Temperature Sensitive Mutation

A temperature-sensitive mutation was isolated that blocks cilia regeneration and arrests growth in Tetrahymena thermophila. Protein and RNA synthesis and ATP production appeared to be largely unaffected at the restrictive temperature, suggesting that the mutation is specific for cilia regeneration and growth. At the restrictive temperature, mutant cells arrested at a specific point in the cell cycle, after macronuclear S phase and shortly before micronuclear mitosis. Arrested cells did not undergo nuclear divisions, DNA replication, or cytokinesis, so the mutation appears to cause true cell cycle arrest. Surprisingly, the mutation does not appear to affect micronuclear mitosis directly but rather some event(s) prior to micronuclear mitosis that must be completed before cells can complete the cell cycle. The cell cycle arrest was transiently complemented by wild-type cytoplasm exchanged during conjugation with a wild-type cell. Each starved, wild-type cell apparently contained enough rescuing factor to support an average of six cell divisions. Thus, this mutation affects assembly and/or function of at least one but not all of the microtubule-based structures in T. thermophila.

Abnormal integrity of the nucleolus associated with cell cycle arrest owing to the temperature-sensitive ubiquitin-activating enzyme E1

1995 ◽  
Vol 3 (2) ◽  
pp. 115-123 ◽  
Author(s):  
T. Sudha ◽  
H. Tsuji ◽  
M. Sameshima ◽  
Y. Matsuda ◽  
S. Kaneda ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Temperature Sensitive ◽  
Cycle Arrest

scholarly journals Removal of a Single α-Tubulin Gene Intron Suppresses Cell Cycle Arrest Phenotypes of Splicing Factor Mutations in Saccharomyces cerevisiae

2002 ◽  
Vol 22 (3) ◽  
pp. 801-815 ◽  
Author(s):  
C. Geoffrey Burns ◽  
Ryoma Ohi ◽  
Sapna Mehta ◽  
Eileen T. O’Toole ◽  
Mark Winey ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Cycle Control ◽  
Mrna Splicing ◽  
Temperature Sensitive ◽  
Cycle Arrest ◽  
Indirect Consequence ◽  
Tubulin Protein ◽  
Cell Cycle Block

ABSTRACT Genetic and biochemical studies of Schizosaccharomyces pombe and Saccharomyces cerevisiae have identified gene products that play essential functions in both pre-mRNA splicing and cell cycle control. Among these are the conserved, Myb-related CDC5 (also known as Cef1p in S. cerevisiae) proteins. The mechanism by which loss of CDC5/Cef1p function causes both splicing and cell cycle defects has been unclear. Here we provide evidence that cell cycle arrest in a new temperature-sensitive CEF1 mutant, cef1-13, is an indirect consequence of defects in pre-mRNA splicing. Although cef1-13 cells harbor global defects in pre-mRNA splicing discovered through intron microarray analysis, inefficient splicing of the α-tubulin-encoding TUB1 mRNA was considered as a potential cause of the cef1-13 cell cycle arrest because cef1-13 cells arrest uniformly at G2/M with many hallmarks of a defective microtubule cytoskeleton. Consistent with this possibility, cef1-13 cells possess reduced levels of total TUB1 mRNA and α-tubulin protein. Removing the intron from TUB1 in cef1-13 cells boosts TUB1 mRNA and α-tubulin expression to near wild-type levels and restores microtubule stability in the cef1-13 mutant. As a result, cef1-13 tub1Δi cells progress through mitosis and their cell cycle arrest phenotype is alleviated. Removing the TUB1 intron from two other splicing mutants that arrest at G2/M, prp17Δ and prp22-1 strains, permits nuclear division, but suppression of the cell cycle block is less efficient. Our data raise the possibility that although cell cycle arrest phenotypes in prp mutants can be explained by defects in pre-mRNA splicing, the transcript(s) whose inefficient splicing contributes to cell cycle arrest is likely to be prp mutant dependent.

scholarly journals Regulation of p53-mediated apoptosis and cell cycle arrest by Steel factor.

1995 ◽  
Vol 15 (12) ◽  
pp. 6953-6960 ◽  
Author(s):  
J L Abrahamson ◽  
J M Lee ◽  
A Bernstein
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
P53 Protein ◽  
Cell Types ◽  
Signalling Pathway ◽  
Temperature Sensitive ◽  
P53 Expression ◽  
Steel Factor ◽  
Cycle Arrest

Activation of the p53 protein can lead to apoptosis and cell cycle arrest. In contrast, activation of the signalling pathway controlled by the Kit receptor tyrosine kinase prevents apoptosis and promotes cell division of a number of different cell types in vivo. We have investigated the consequences of activating the Kit signalling pathway by its ligand Steel factor on these opposing functions of the p53 protein in Friend erythroleukemia cells. A temperature-sensitive p53 allele (Val-135) was introduced into the Friend erythroleukemia cell line (DP-16) which lacks endogenous p53 expression. At 38.5 degrees C, the Val-135 protein maintains a mutant conformation and has no effect on cell growth. At 32 degrees C, the mutant protein assumes wild-type properties and induces these cells to arrest in G1, terminally differentiate, and die by apoptosis. We demonstrate that Steel factor inhibits p53-mediated apoptosis and differentiation but has no effect on p53-mediated G1/S cell cycle arrest. These results demonstrate that Steel factor functions as a cell survival factor in part through the suppression of differentiation and apoptosis induced by p53 and suggest that cell cycle arrest and apoptosis may be separable functions of p53.

scholarly journals Functions of Fission Yeast Orp2 in DNA Replication and Checkpoint Control

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 599-607
Author(s):  
Joan Kiely ◽  
S B Haase ◽  
Paul Russell ◽  
Janet Leatherwood
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Cell Cycle Arrest ◽  
Fission Yeast ◽  
Replication Initiation ◽  
Initiation Factor ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Checkpoint Control ◽  
Cycle Arrest

Abstract orp2 is an essential gene of the fission yeast Schizosaccharomyces pombe with 22% identity to budding yeast ORC2. We isolated temperature-sensitive alleles of orp2 using a novel plasmid shuffle based on selection against thymidine kinase. Cells bearing the temperature-sensitive allele orp2-2 fail to complete DNA replication at a restrictive temperature and undergo cell cycle arrest. Cell cycle arrest depends on the checkpoint genes rad1 and rad3. Even when checkpoint functions are wild type, the orp2-2 mutation causes high rates of chromosome and plasmid loss. These phenotypes support the idea that Orp2 is a replication initiation factor. Selective spore germination allowed analysis of orp2 deletion mutants. These experiments showed that in the absence of orp2 function, cells proceed into mitosis despite a lack of DNA replication. This suggests either that the Orp2 protein is a part of the checkpoint machinery or more likely that DNA replication initiation is required to induce the replication checkpoint signal.

scholarly journals A temperature-sensitive mutation affecting cilia regeneration, nuclear development, and the cell cycle of Tetrahymena thermophila is rescued by cytoplasmic exchange.

1988 ◽  
Vol 8 (7) ◽  
pp. 2681-2689 ◽  
Author(s):  
D G Pennock ◽  
T Thatcher ◽  
M A Gorovsky
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Tetrahymena Thermophila ◽  
Wild Type Cell ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Wild Type ◽  
Atp Production ◽  
Cycle Arrest ◽  
Temperature Sensitive Mutation

A temperature-sensitive mutation was isolated that blocks cilia regeneration and arrests growth in Tetrahymena thermophila. Protein and RNA synthesis and ATP production appeared to be largely unaffected at the restrictive temperature, suggesting that the mutation is specific for cilia regeneration and growth. At the restrictive temperature, mutant cells arrested at a specific point in the cell cycle, after macronuclear S phase and shortly before micronuclear mitosis. Arrested cells did not undergo nuclear divisions, DNA replication, or cytokinesis, so the mutation appears to cause true cell cycle arrest. Surprisingly, the mutation does not appear to affect micronuclear mitosis directly but rather some event(s) prior to micronuclear mitosis that must be completed before cells can complete the cell cycle. The cell cycle arrest was transiently complemented by wild-type cytoplasm exchanged during conjugation with a wild-type cell. Each starved, wild-type cell apparently contained enough rescuing factor to support an average of six cell divisions. Thus, this mutation affects assembly and/or function of at least one but not all of the microtubule-based structures in T. thermophila.

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