Are there DNA damage checkpoints inE. coli?

BioEssays ◽  
1995 ◽  
Vol 17 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Bryn A. Bridges
Keyword(s):  
Dna Damage ◽  
Dna Damage Checkpoints

Overlapping Roles of the Spindle Assembly and DNA Damage Checkpoints in the Cell-Cycle Response to Altered Chromosomes in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 521-534
Author(s):  
Peter M Garber ◽  
Jasper Rine
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Spindle Checkpoint ◽  
Dna Lesions ◽  
Replication Proteins ◽  
Replication Checkpoint ◽  
Dna Damage Checkpoints ◽  
Dna Replication Checkpoint ◽  
Mcm Proteins ◽  
Stalled Replication Forks

Abstract The MAD2-dependent spindle checkpoint blocks anaphase until all chromosomes have achieved successful bipolar attachment to the mitotic spindle. The DNA damage and DNA replication checkpoints block anaphase in response to DNA lesions that may include single-stranded DNA and stalled replication forks. Many of the same conditions that activate the DNA damage and DNA replication checkpoints also activated the spindle checkpoint. The mad2Δ mutation partially relieved the arrest responses of cells to mutations affecting the replication proteins Mcm3p and Pol1p. Thus a previously unrecognized aspect of spindle checkpoint function may be to protect cells from defects in DNA replication. Furthermore, in cells lacking either the DNA damage or the DNA replication checkpoints, the spindle checkpoint contributed to the arrest responses of cells to the DNA-damaging agent methyl methanesulfonate, the replication inhibitor hydroxyurea, and mutations affecting Mcm2p and Orc2p. Thus the spindle checkpoint was sensitive to a wider range of chromosomal perturbations than previously recognized. Finally, the DNA replication checkpoint did not contribute to the arrests of cells in response to mutations affecting ORC, Mcm proteins, or DNA polymerase δ. Thus the specificity of this checkpoint may be more limited than previously recognized.

scholarly journals Aberrant p53 alters DNA damage checkpoints in response to cisplatin: Downregulation of CDK expression and activity

2004 ◽  
Vol 112 (5) ◽  
pp. 760-770 ◽  
Author(s):  
Katharine H. Wrighton ◽  
Cecilia M. Prêle ◽  
Andrew Sunters ◽  
W. Andrew Yeudall
Keyword(s):  
Dna Damage ◽  
Dna Damage Checkpoints ◽  
Expression And Activity

DNA damage checkpoints in nasopharyngeal carcinoma

Oral Oncology ◽  
2014 ◽  
Vol 50 (5) ◽  
pp. 339-344 ◽  
Author(s):  
Randy Y.C. Poon
Keyword(s):  
Dna Damage ◽  
Nasopharyngeal Carcinoma ◽  
Dna Damage Checkpoints

scholarly journals When heat casts a spell on the DNA damage checkpoints

Open Biology ◽  
2014 ◽  
Vol 4 (3) ◽  
pp. 140008 ◽  
Author(s):  
Thomas Turner ◽  
Thomas Caspari
Keyword(s):  
Dna Damage ◽  
Ataxia Telangiectasia ◽  
Current Knowledge ◽  
Dna Damage Checkpoint ◽  
Ataxia Telangiectasia Mutated ◽  
Patron Saint ◽  
Checkpoint Kinases ◽  
Dna Damage Checkpoints ◽  
Heat Response ◽  
Elevated Body Temperature

Peregrine Laziosi (1265–1345), an Italian priest, became the patron saint of cancer patients when the tumour in his left leg miraculously disappeared after he developed a fever. Elevated body temperature can cause tumours to regress and sensitizes cancer cells to agents that break DNA. Why hyperthermia blocks the repair of broken chromosomes by changing the way that the DNA damage checkpoint kinases ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) are activated is an unanswered question. This review discusses the current knowledge of how heat affects the ATR–Chk1 and ATM–Chk2 kinase networks, and provides a possible explanation of why homeothermal organisms such as humans still possess this ancient heat response.

Activation of DNA Damage Checkpoints in CHO Cells Requires a Certain Level of DNA Damage

2001 ◽  
Vol 287 (3) ◽  
pp. 775-780 ◽  
Author(s):  
Man-Rong Jiang ◽  
Ying Yang ◽  
Jia-Rui Wu
Keyword(s):  
Dna Damage ◽  
Cho Cells ◽  
Dna Damage Checkpoints

scholarly journals Maintenance of Double-Stranded Telomeric Repeats as the Critical Determinant for Cell Viability in Yeast Cells Lacking Ku

2002 ◽  
Vol 22 (7) ◽  
pp. 2182-2193 ◽  
Author(s):  
Serge Gravel ◽  
Raymund J. Wellinger
Keyword(s):  
Dna Damage ◽  
Elevated Temperatures ◽  
Telomeric Repeat ◽  
Telomere Maintenance ◽  
Yeast Cells ◽  
Chromosomal Dna ◽  
End Joining ◽  
Telomeric Repeats ◽  
Critical Determinant ◽  
Dna Damage Checkpoints

ABSTRACT The Saccharomyces cerevisiae Ku complex, while important for nonhomologous DNA end joining, is also necessary for maintaining wild-type telomere length and a normal chromosomal DNA end structure. Yeast cells lacking Ku can grow at 23°C but are unable to do so at elevated temperatures due to an activation of DNA damage checkpoints. To gain insights into the mechanisms affected by temperature in such strains, we isolated and characterized a new allele of the YKU70 gene, yku70-30ts . By several criteria, the Yku70-30p protein is functional at 23°C and nonfunctional at 37°C. The analyses of telomeric repeat maintenance as well as the terminal DNA end structure in strains harboring this allele alone or in strains with a combination of other mutations affecting telomere maintenance show that the altered DNA end structure in yeast cells lacking Ku is not generated in a telomerase-dependent fashion. Moreover, the single-stranded G-rich DNA on such telomeres is not detected by DNA damage checkpoints to arrest cell growth, provided that there are sufficient double-stranded telomeric repeats present. The results also demonstrate that mutations in genes negatively affecting G-strand synthesis (e.g., RIF1) or C-strand synthesis (e.g., the DNA polymerase α gene) allow for the maintenance of longer telomeric repeat tracts in cells lacking Ku. Finally, extending telomeric repeat tracts in such cells at least temporarily suppresses checkpoint activation and growth defects at higher temperatures. Thus, we hypothesize that an aspect of the coordinated synthesis of double-stranded telomeric repeats is sensitive to elevated temperatures.

scholarly journals Obtusilactone A and (−)-sesamin induce apoptosis in human lung cancer cells by inhibiting mitochondrial Lon protease and activating DNA damage checkpoints

2010 ◽  
Vol 101 (12) ◽  
pp. 2612-2620 ◽  
Author(s):  
Hui-Min Wang ◽  
Kuo-Chen Cheng ◽  
Cheng-Jung Lin ◽  
Shu-Wei Hsu ◽  
Wei-Cheng Fang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lon Protease ◽  
Dna Damage Checkpoints ◽  
Human Lung Cancer Cells

scholarly journals DNA damage checkpoints in mammals

Mutagenesis ◽  
2005 ◽  
Vol 21 (1) ◽  
pp. 3-9 ◽  
Author(s):  
Hiroyuki Niida ◽  
Makoto Nakanishi
Keyword(s):  
Dna Damage ◽  
Dna Damage Checkpoints
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