Document Detail


Persistent telomere damage induces bypass of mitosis and tetraploidy.
MedLine Citation:
PMID:  20371347     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tetraploidization has been proposed as an intermediate step toward aneuploidy in human cancer but a general mechanism for the induction of tetraploidy during tumorigenesis is lacking. We report that tetraploidization occurs in p53-deficient cells experiencing a prolonged DNA damage signal due to persistent telomere dysfunction. Live-cell imaging revealed that these cells have an extended G2 due to ATM/ATR- and Chk1/Chk2-mediated inhibition of Cdk1/CyclinB and eventually bypass mitosis. Despite their lack of mitosis, the cells showed APC/Cdh1-dependent degradation of the replication inhibitor geminin, followed by accumulation of Cdt1, which is required for origin licensing. Cells then entered a second S phase resulting in whole-genome reduplication and tetraploidy. Upon restoration of telomere protection, these tetraploid cells resumed cell division cycles and proliferated. These observations suggest a general mechanism for the induction of tetraploidization in the early stages of tumorigenesis when telomere dysfunction can result from excessive telomere shortening.
Authors:
Teresa Davoli; Eros Lazzerini Denchi; Titia de Lange
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell     Volume:  141     ISSN:  1097-4172     ISO Abbreviation:  Cell     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-07     Completed Date:  2010-04-22     Revised Date:  2011-07-27    
Medline Journal Info:
Nlm Unique ID:  0413066     Medline TA:  Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  81-93     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
Affiliation:
Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
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MeSH Terms
Descriptor/Qualifier:
Aneuploidy
Animals
Cadherins / metabolism
Cell Cycle Proteins / metabolism
Cell Line
DNA Damage
Embryo, Mammalian / cytology
Humans
Mice
Mitosis*
Neoplasms / genetics*
Ploidies*
Telomere / genetics*
Ubiquitin-Protein Ligase Complexes / metabolism
Grant Support
ID/Acronym/Agency:
DP1 OD000379-05/OD/NIH HHS
Chemical
Reg. No./Substance:
0/Cadherins; 0/Cell Cycle Proteins; EC 6.3.2.19/Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19/anaphase-promoting complex
Comments/Corrections

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