In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.

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...

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Autores principales:	Laure Rousseau, Olivier Etienne, Telma Roque, Chantal Desmaze, Céline Haton, Marc-André Mouthon, Jacqueline Bernardino-Sgherri, Jeroen Essers, Roland Kanaar, François D Boussin
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f95c774b93764c7aa02cb09eb5f9819e
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spelling	oai:doaj.org-article:f95c774b93764c7aa02cb09eb5f9819e2021-11-18T07:17:10ZIn vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.1932-620310.1371/journal.pone.0037194https://doaj.org/article/f95c774b93764c7aa02cb09eb5f9819e2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22666344/?tool=EBIhttps://doaj.org/toc/1932-6203We 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 RousseauOlivier EtienneTelma RoqueChantal DesmazeCéline HatonMarc-André MouthonJacqueline Bernardino-SgherriJeroen EssersRoland KanaarFrançois D BoussinPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 5, p e37194 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Laure Rousseau Olivier Etienne Telma Roque Chantal Desmaze Céline Haton Marc-André Mouthon Jacqueline Bernardino-Sgherri Jeroen Essers Roland Kanaar François D Boussin In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
description	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.
format	article
author	Laure Rousseau Olivier Etienne Telma Roque Chantal Desmaze Céline Haton Marc-André Mouthon Jacqueline Bernardino-Sgherri Jeroen Essers Roland Kanaar François D Boussin
author_facet	Laure Rousseau Olivier Etienne Telma Roque Chantal Desmaze Céline Haton Marc-André Mouthon Jacqueline Bernardino-Sgherri Jeroen Essers Roland Kanaar François D Boussin
author_sort	Laure Rousseau
title	In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
title_short	In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
title_full	In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
title_fullStr	In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
title_full_unstemmed	In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.
title_sort	in vivo importance of homologous recombination dna repair for mouse neural stem and progenitor cells.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/f95c774b93764c7aa02cb09eb5f9819e
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In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells.

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