| Pot1 and cell cycle progression cooperate in telomere length regulation. | |
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MedLine Citation:
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PMID: 18066078 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Removal of the vertebrate telomere protein Pot1 results in a DNA damage response and cell cycle arrest. Here we show that loss of chicken Pot1 causes Chk1 activation, and inhibition of Chk1 signaling prevents the cell cycle arrest. However, arrest still occurs after disruption of ATM, which encodes another DNA damage response protein. These results indicate that Pot1 is required to prevent a telomere checkpoint mediated by another such protein, ATR, that is most likely triggered by the G-overhang. We also show that removal of Pot1 causes exceptionally rapid telomere growth upon arrest in late S/G2 of the cell cycle. However, release of the arrest slows both telomere growth and G-overhang elongation. Thus, Pot1 seems to regulate telomere length and G-overhang processing both through direct interaction with the telomere and by preventing a late S/G2 delay in the cell cycle. Our results reveal that cell cycle progression is an important component of telomere length regulation. |
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Authors:
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Dmitri Churikov; Carolyn M Price |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2007-12-09 |
Journal Detail:
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Title: Nature structural & molecular biology Volume: 15 ISSN: 1545-9985 ISO Abbreviation: Nat. Struct. Mol. Biol. Publication Date: 2008 Jan |
Date Detail:
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Created Date: 2008-01-07 Completed Date: 2008-03-11 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 101186374 Medline TA: Nat Struct Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 79-84 Citation Subset: IM |
Affiliation:
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Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, PO Box 0524, Cincinnati, Ohio 45267-0524, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Androstadienes
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pharmacology Caffeine / pharmacology Carbazoles / pharmacology Cell Cycle / drug effects, physiology* Cell Cycle Proteins / genetics, metabolism Cell Line DNA-Binding Proteins / deficiency, genetics, metabolism Enzyme Inhibitors / pharmacology Flow Cytometry G2 Phase Humans Indoles / pharmacology Kinetics Protein-Serine-Threonine Kinases / deficiency, genetics, metabolism S Phase Tamoxifen / pharmacology Telomere / chemistry, physiology* Telomere-Binding Proteins / deficiency, genetics, physiology* Tumor Suppressor Proteins / deficiency, genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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GM041803/GM/NIGMS NIH HHS; R01 GM041803-17/GM/NIGMS NIH HHS; R01 GM041803-21/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Androstadienes; 0/Carbazoles; 0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/Enzyme Inhibitors; 0/Indoles; 0/POT1 protein, human; 0/Telomere-Binding Proteins; 0/Tumor Suppressor Proteins; 10540-29-1/Tamoxifen; 136194-77-9/Go 6976; 19545-26-7/wortmannin; 58-08-2/Caffeine; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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