TEL1 from Saccharomyces cerevisiae suppresses chromosome aberrations induced by ionizing radiation in ataxia-telangiectasia cells without affecting cell cycle checkpoints

2001 ◽  
Vol 40 (4) ◽  
pp. 309-315 ◽  
Author(s):  
J.-P. Cao ◽  
M. S. Meyn ◽  
F. Eckardt-Schupp ◽  
E. Fritz
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Ionizing Radiation ◽  
Chromosome Aberrations ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Checkpoints

scholarly journals Defect in Multiple Cell Cycle Checkpoints in Ataxia-Telangiectasia Postirradiation

1996 ◽  
Vol 271 (34) ◽  
pp. 20486-20493 ◽  
Author(s):  
Heather Beamish ◽  
Richard Williams ◽  
Philip Chen ◽  
Martin F. Lavin
Keyword(s):  
Cell Cycle ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Checkpoints ◽  
Multiple Cell

scholarly journals Regulation of Mitotic Exit by Cell Cycle Checkpoints: Lessons From Saccharomyces cerevisiae

Genes ◽  
2020 ◽  
Vol 11 (2) ◽  
pp. 195 ◽  
Author(s):  
Laura Matellán ◽  
Fernando Monje-Casas
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Genome Stability ◽  
Molecular Mechanisms ◽  
Model Organism ◽  
Mitotic Exit ◽  
Cell Cycle Checkpoints ◽  
Dna Integrity ◽  
Intracellular Signals ◽  
Dividing Cells

In order to preserve genome integrity and their ploidy, cells must ensure that the duplicated genome has been faithfully replicated and evenly distributed before they complete their division by mitosis. To this end, cells have developed highly elaborated checkpoints that halt mitotic progression when problems in DNA integrity or chromosome segregation arise, providing them with time to fix these issues before advancing further into the cell cycle. Remarkably, exit from mitosis constitutes a key cell cycle transition that is targeted by the main mitotic checkpoints, despite these surveillance mechanisms being activated by specific intracellular signals and acting at different stages of cell division. Focusing primarily on research carried out using Saccharomyces cerevisiae as a model organism, the aim of this review is to provide a general overview of the molecular mechanisms by which the major cell cycle checkpoints control mitotic exit and to highlight the importance of the proper regulation of this process for the maintenance of genome stability during the distribution of the duplicated chromosomes between the dividing cells.

scholarly journals Postreplication Repair and PCNA Modification in Schizosaccharomyces pombe

2006 ◽  
Vol 17 (7) ◽  
pp. 2976-2985 ◽  
Author(s):  
Jonathan Frampton ◽  
Anja Irmisch ◽  
Catherine M. Green ◽  
Andrea Neiss ◽  
Michelle Trickey ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Ionizing Radiation ◽  
Schizosaccharomyces Pombe ◽  
Uv Irradiation ◽  
Proliferating Cell Nuclear Antigen ◽  
S Phase ◽  
Cell Cycle Checkpoints ◽  
Nuclear Antigen ◽  
Proliferating Cell

Ubiquitination of proliferating cell nuclear antigen (PCNA) plays a crucial role in regulating replication past DNA damage in eukaryotes, but the detailed mechanisms appear to vary in different organisms. We have examined the modification of PCNA in Schizosaccharomyces pombe. We find that, in response to UV irradiation, PCNA is mono- and poly-ubiquitinated in a manner similar to that in Saccharomyces cerevisiae. However in undamaged Schizosaccharomyces pombe cells, PCNA is ubiquitinated in S phase, whereas in S. cerevisiae it is sumoylated. Furthermore we find that, unlike in S. cerevisiae, mutants defective in ubiquitination of PCNA are also sensitive to ionizing radiation, and PCNA is ubiquitinated after exposure of cells to ionizing radiation, in a manner similar to the response to UV-irradiation. We show that PCNA modification and cell cycle checkpoints represent two independent signals in response to DNA damage. Finally, we unexpectedly find that PCNA is ubiquitinated in response to DNA damage when cells are arrested in G2.

A multifaceted role for ATM in genome maintenance

2003 ◽  
Vol 5 (16) ◽  
pp. 1-21 ◽  
Author(s):  
Tej K. Pandita
Keyword(s):  
Cell Cycle ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Control ◽  
Cell Cycle Checkpoints ◽  
Telomere Maintenance ◽  
Loss Of Function ◽  
Genome Maintenance ◽  
Ataxia Telangiectasia Mutated ◽  
Gonadal Atrophy ◽  
Mitogenic Signal Transduction

The pleiotropic nature of the clinical phenotypes of patients with ataxia-telangiectasia (A-T) – which encompass cerebellar degeneration (leading to ataxia), gonadal atrophy, and cancer predisposition – suggests multiple functions of the gene responsible for the disease. The ataxia-telangiectasia mutated gene product (ATM), whose loss of function is responsible for ataxia-telangiectasia, is a protein kinase that interacts with several substrates and is implicated in mitogenic signal transduction, chromosome condensation, meiotic recombination, cell-cycle control and telomere maintenance. This review focuses on the critical roles that ATM appears to play in cell-cycle checkpoints, DNA repair, telomere metabolism and oxidative stress, indicating how defects in these processes might lead to ataxia-telangiectasia.

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