Document Detail


P element excision and repair by non-homologous end joining occurs in both G1 and G2 of the cell cycle.
MedLine Citation:
PMID:  15590325     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
P element excision generates a DNA double-strand break at the transposon donor site. Genetic studies have demonstrated a strong bias toward repair of P element-induced DNA breaks by homologous recombination with the sister chromatid, suggesting that P element excision occurs after DNA replication, in G2 of the cell cycle. We developed methods to arrest Drosophila tissue culture cells and assay P element excision in either G1- or G2-arrested cells. Dacapo or tribbles transgene expression arrests cells in either G2 or G2, respectively. RNA-mediated gene interference (RNAi) directed against cyclin E or cyclin A arrests cells in G1 or G2, respectively. P element excision occurs efficiently in both G1- and G2-arrested cells, suggesting that cell cycle regulation of P element transposase does not occur in our somatic cell system. DNA double-strand break repair occurs by two predominant mechanisms: homologous recombination (HR) and non-homologous end joining (NHEJ). HR is thought to be restricted to the post-replicative, G2, phase of the cell cycle, while NHEJ may occur throughout the cell cycle. Our results indicate that NHEJ repair of an extrachromasomal plasmid substrate occurs at least as efficiently in G2-arrested cells as in asynchronous cells or in G1-arrested cells.
Authors:
Brian T Weinert; Bosun Min; Donald C Rio
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  DNA repair     Volume:  4     ISSN:  1568-7864     ISO Abbreviation:  DNA Repair (Amst.)     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2004-12-13     Completed Date:  2005-05-05     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  101139138     Medline TA:  DNA Repair (Amst)     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  171-81     Citation Subset:  IM    
Affiliation:
Department of Molecular and Cell Biology, Center for Integrative Genomics, University of California, Berkeley, 16 Barker Hall, CA 94720-3204, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Cycle Proteins / physiology
DNA
DNA Damage
DNA Repair*
DNA Replication
DNA Transposable Elements / genetics*
Drosophila Proteins / physiology
Drosophila melanogaster / genetics*
G1 Phase / genetics*
G2 Phase / genetics*
Nuclear Proteins / physiology
Plasmids
Protein-Serine-Threonine Kinases / physiology
Recombination, Genetic*
Transgenes / physiology*
Grant Support
ID/Acronym/Agency:
R01GM48862/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/DNA Transposable Elements; 0/Dacapo protein, Drosophila; 0/Drosophila Proteins; 0/Nuclear Proteins; 0/tribbles protein, Drosophila; 9007-49-2/DNA; EC 2.7.11.1/Protein-Serine-Threonine Kinases

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