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
Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 521-534
Author(s):  
Peter M Garber ◽  
Jasper Rine

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.


2004 ◽  
Vol 112 (5) ◽  
pp. 760-770 ◽  
Author(s):  
Katharine H. Wrighton ◽  
Cecilia M. Prêle ◽  
Andrew Sunters ◽  
W. Andrew Yeudall

2013 ◽  
Vol 15 (9) ◽  
Author(s):  
Kumud Kant Awasthi ◽  
Anjali Awasthi ◽  
Narender Kumar ◽  
Partha Roy ◽  
Kamlendra Awasthi ◽  
...  

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

Open Biology ◽  
2014 ◽  
Vol 4 (3) ◽  
pp. 140008 ◽  
Author(s):  
Thomas Turner ◽  
Thomas Caspari

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.


Author(s):  
Mariana I Testoni ◽  
Alejandro D Bolzán ◽  
Martha S Bianchi ◽  
Néstor O Bianchi
Keyword(s):  

Mutagenesis ◽  
1990 ◽  
Vol 5 (3) ◽  
pp. 279-284 ◽  
Author(s):  
Roderick A. F. MacLeod ◽  
Anne F. Christie ◽  
Nina D. Costa ◽  
Peter E. Bryant

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