Document Detail

In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
MedLine Citation:
PMID:  22666344     Owner:  NLM     Status:  MEDLINE    
We characterized the in vivo importance of the homologous recombination factor RAD54 for the developing mouse brain cortex in normal conditions or after ionizing radiation exposure. Contrary to numerous homologous recombination genes, Rad54 disruption did not impact the cortical development without exogenous stress, but it dramatically enhanced the radiation sensitivity of neural stem and progenitor cells. This resulted in the death of all cells irradiated during S or G2, whereas the viability of cells irradiated in G1 or G0 was not affected by Rad54 disruption. Apoptosis occurred after long arrests at intra-S and G2/M checkpoints. This concerned every type of neural stem and progenitor cells, showing that the importance of Rad54 for radiation response was linked to the cell cycle phase at the time of irradiation and not to the differentiation state. In the developing brain, RAD54-dependent homologous recombination appeared absolutely required for the repair of damages induced by ionizing radiation during S and G2 phases, but not for the repair of endogenous damages in normal conditions. Altogether our data support the existence of RAD54-dependent and -independent homologous recombination pathways.
Laure Rousseau; Olivier Etienne; Telma Roque; Chantal Desmaze; Céline Haton; Marc-André Mouthon; Jacqueline Bernardino-Sgherri; Jeroen Essers; Roland Kanaar; François D Boussin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-05-29
Journal Detail:
Title:  PloS one     Volume:  7     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2012  
Date Detail:
Created Date:  2012-06-05     Completed Date:  2012-10-29     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e37194     Citation Subset:  IM    
Laboratoire de Radiopathologie, SCSR, iRCM, DSV, CEA, Fontenay-aux-Roses, France.
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MeSH Terms
Apoptosis / genetics,  radiation effects
Brain / cytology,  growth & development,  metabolism,  radiation effects
Cell Cycle / genetics,  radiation effects
Cell Nucleus / genetics,  radiation effects
DNA Damage / genetics
DNA Helicases / deficiency,  metabolism
DNA Repair / genetics*,  radiation effects
Homologous Recombination* / radiation effects
Neural Stem Cells / cytology,  metabolism*,  radiation effects
Neuroglia / cytology,  metabolism,  radiation effects
Nuclear Proteins / deficiency,  metabolism
Time Factors
Reg. No./Substance:
0/Nuclear Proteins; EC 3.6.1.-/DNA Helicases; EC 3.6.4.-/Rad54l protein, mouse

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