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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| creator | Rousseau, Laure Etienne, Olivier Roque, Telma Desmaze, Chantal Haton, Céline Mouthon, Marc-André Bernardino-Sgherri, Jacqueline Essers, Jeroen Kanaar, Roland Boussin, François D |
| 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. |
| doi_str_mv | 10.1371/journal.pone.0037194 |
| format | Article |
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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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0037194</identifier><identifier>PMID: 22666344</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Apoptosis - radiation effects ; Biology ; Biotechnology ; Brain ; Brain - cytology ; Brain - growth & development ; Brain - metabolism ; Brain - radiation effects ; Brain damage ; Cell cycle ; Cell Cycle - genetics ; Cell Cycle - radiation effects ; Cell Nucleus - genetics ; Cell Nucleus - radiation effects ; Cells (biology) ; Cortex ; Deoxyribonucleic acid ; Disruption ; DNA ; DNA damage ; DNA Damage - genetics ; DNA Helicases - deficiency ; DNA Helicases - metabolism ; DNA repair ; DNA Repair - genetics ; DNA Repair - radiation effects ; Female ; Genetic recombination ; Genomics ; Homologous recombination ; Homologous Recombination - radiation effects ; Homology ; Ionizing radiation ; Irradiated ; Irradiation ; Mice ; Neural stem cells ; Neural Stem Cells - cytology ; Neural Stem Cells - metabolism ; Neural Stem Cells - radiation effects ; Neuroglia - cytology ; Neuroglia - metabolism ; Neuroglia - radiation effects ; Nuclear Proteins - deficiency ; Nuclear Proteins - metabolism ; Pregnancy ; Radiation ; Radiation damage ; Radiation effects ; Repair ; Sensitivity enhancement ; Stem cells ; Time Factors ; Yeast</subject><ispartof>PloS one, 2012-05, Vol.7 (5), p.e37194-e37194</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Rousseau et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Rousseau et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-79da417644c6692ce7e46f277968d42448ae3a4360767a77ffef044fcc3e788d3</citedby><cites>FETCH-LOGICAL-c692t-79da417644c6692ce7e46f277968d42448ae3a4360767a77ffef044fcc3e788d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362579/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362579/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22666344$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rousseau, Laure</creatorcontrib><creatorcontrib>Etienne, Olivier</creatorcontrib><creatorcontrib>Roque, Telma</creatorcontrib><creatorcontrib>Desmaze, Chantal</creatorcontrib><creatorcontrib>Haton, Céline</creatorcontrib><creatorcontrib>Mouthon, Marc-André</creatorcontrib><creatorcontrib>Bernardino-Sgherri, Jacqueline</creatorcontrib><creatorcontrib>Essers, Jeroen</creatorcontrib><creatorcontrib>Kanaar, Roland</creatorcontrib><creatorcontrib>Boussin, François D</creatorcontrib><title>In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><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.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - radiation effects</subject><subject>Biology</subject><subject>Biotechnology</subject><subject>Brain</subject><subject>Brain - cytology</subject><subject>Brain - growth & development</subject><subject>Brain - metabolism</subject><subject>Brain - radiation effects</subject><subject>Brain damage</subject><subject>Cell cycle</subject><subject>Cell Cycle - genetics</subject><subject>Cell Cycle - radiation effects</subject><subject>Cell Nucleus - genetics</subject><subject>Cell Nucleus - radiation effects</subject><subject>Cells (biology)</subject><subject>Cortex</subject><subject>Deoxyribonucleic acid</subject><subject>Disruption</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Damage - genetics</subject><subject>DNA Helicases - deficiency</subject><subject>DNA Helicases - metabolism</subject><subject>DNA repair</subject><subject>DNA Repair - genetics</subject><subject>DNA Repair - radiation effects</subject><subject>Female</subject><subject>Genetic recombination</subject><subject>Genomics</subject><subject>Homologous recombination</subject><subject>Homologous Recombination - radiation effects</subject><subject>Homology</subject><subject>Ionizing radiation</subject><subject>Irradiated</subject><subject>Irradiation</subject><subject>Mice</subject><subject>Neural stem cells</subject><subject>Neural Stem Cells - cytology</subject><subject>Neural Stem Cells - metabolism</subject><subject>Neural Stem Cells - radiation effects</subject><subject>Neuroglia - cytology</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - radiation effects</subject><subject>Nuclear Proteins - deficiency</subject><subject>Nuclear Proteins - metabolism</subject><subject>Pregnancy</subject><subject>Radiation</subject><subject>Radiation damage</subject><subject>Radiation effects</subject><subject>Repair</subject><subject>Sensitivity enhancement</subject><subject>Stem cells</subject><subject>Time Factors</subject><subject>Yeast</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QLgujFjEmTSZobYVi_BhYX_LoNmfSkk6FNatIO-u9Nne4ylb2QXrS8ec6b5O05WfYUoyUmHL_Z-yE41Sw772CJUJIEvZedY0GKBSsQuX_yfZY9inGP0IqUjD3MzoqCMUYoPc-qjcsP9uBz23Y-9MppyL3Jd771ja_9EPMA2rdb61RvvcvffV4npVM25MaHvE0E5A6GoJo89tDmylV5F3wNzvYJ0NA08XH2wKgmwpPpfZF9__D-2-WnxdX1x83l-mqhmSj6BReVopgzSjVLggYOlJmCc8HKihaUlgqIooQhzrji3BgwiFKjNQFelhW5yJ4ffbvGRzkFFCUmxQphgQuSiM2RqLzayy7YVoXf0isr_wo-1FKF3uoGpBErzTndCpJOpLlSqNBbJGC7MqLEApLX22m3YdtCpcH1KYWZ6XzF2Z2s_UESwooVF8ng1WQQ_M8BYi9bG8fAlIOUq8QIlyXDZDWe-8U_6N23m6hapQtYZ3zaV4-mck05R4jigiZqeQeVngpaq1M3GZv0WcHrWUFievjV12qIUW6-fvl_9vrHnH15wu5ANf0u-mYYGy3OQXoEdfAxBjC3IWMkx2G4SUOOwyCnYUhlz05_0G3RTfeTPwoVBAA</recordid><startdate>20120529</startdate><enddate>20120529</enddate><creator>Rousseau, Laure</creator><creator>Etienne, Olivier</creator><creator>Roque, Telma</creator><creator>Desmaze, Chantal</creator><creator>Haton, Céline</creator><creator>Mouthon, Marc-André</creator><creator>Bernardino-Sgherri, Jacqueline</creator><creator>Essers, Jeroen</creator><creator>Kanaar, Roland</creator><creator>Boussin, François D</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120529</creationdate><title>In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells</title><author>Rousseau, Laure ; Etienne, Olivier ; Roque, Telma ; Desmaze, Chantal ; Haton, Céline ; Mouthon, Marc-André ; Bernardino-Sgherri, Jacqueline ; Essers, Jeroen ; Kanaar, Roland ; Boussin, François D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-79da417644c6692ce7e46f277968d42448ae3a4360767a77ffef044fcc3e788d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - 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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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22666344</pmid><doi>10.1371/journal.pone.0037194</doi><tpages>e37194</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
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| issn | 1932-6203 1932-6203 |
| language | eng |
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| subjects | Animals Apoptosis Apoptosis - genetics Apoptosis - radiation effects Biology Biotechnology Brain Brain - cytology Brain - growth & development Brain - metabolism Brain - radiation effects Brain damage Cell cycle Cell Cycle - genetics Cell Cycle - radiation effects Cell Nucleus - genetics Cell Nucleus - radiation effects Cells (biology) Cortex Deoxyribonucleic acid Disruption DNA DNA damage DNA Damage - genetics DNA Helicases - deficiency DNA Helicases - metabolism DNA repair DNA Repair - genetics DNA Repair - radiation effects Female Genetic recombination Genomics Homologous recombination Homologous Recombination - radiation effects Homology Ionizing radiation Irradiated Irradiation Mice Neural stem cells Neural Stem Cells - cytology Neural Stem Cells - metabolism Neural Stem Cells - radiation effects Neuroglia - cytology Neuroglia - metabolism Neuroglia - radiation effects Nuclear Proteins - deficiency Nuclear Proteins - metabolism Pregnancy Radiation Radiation damage Radiation effects Repair Sensitivity enhancement Stem cells Time Factors Yeast |
| title | In vivo importance of homologous recombination DNA repair for mouse neural stem and progenitor cells |
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