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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-15T18:34:27Z</responseDate> <request identifier=oai:HAL:inserm-00849779v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:inserm-00849779v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:INSERM</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:IRSET-TNGC</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:IRSET-4</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Suppression of genetic recombination in the pseudoautosomal region and at subtelomeres in mice with a hypomorphic Spo11 allele.</title> <creator>Smagulova, Fatima</creator> <creator>Brick, Kevin</creator> <creator>Pu, Yongmei</creator> <creator>Sengupta, Uttara</creator> <creator>Camerini-Otero, Daniel, </creator> <creator>Petukhova, Galina</creator> <contributor>Department of Biochemistry and Molecular Biology ; Uniformed Services University of the Health Sciences</contributor> <contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Genetics and Biochemistry Branch ; National Institute of Health (NIH) - National Institute of Diabetes, Digestive and Kidney Diseases</contributor> <contributor>This research was supported by the NIH grant 1R01GM084104-01A1 from NIGMS (G.V.P.); grants FS71HU, R071HU and CS71HU from USUHS (G.V.P.) and by the NIDDK Intramural Research Program (RDCO).</contributor> <description>International audience</description> <source>ISSN: 1471-2164</source> <source>BMC Genomics</source> <publisher>BioMed Central</publisher> <identifier>inserm-00849779</identifier> <identifier>http://www.hal.inserm.fr/inserm-00849779</identifier> <identifier>http://www.hal.inserm.fr/inserm-00849779/document</identifier> <identifier>http://www.hal.inserm.fr/inserm-00849779/file/1471-2164-14-493.pdf</identifier> <source>http://www.hal.inserm.fr/inserm-00849779</source> <source>BMC Genomics, BioMed Central, 2013, 14 (1), pp.493. 〈10.1186/1471-2164-14-493〉</source> <identifier>DOI : 10.1186/1471-2164-14-493</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1186/1471-2164-14-493</relation> <identifier>PUBMED : 23870400</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/23870400</relation> <language>en</language> <subject lang=en>Homologous recombination</subject> <subject lang=en>Recombination hotspots</subject> <subject lang=en>SPO11</subject> <subject lang=en>Subtelomeres</subject> <subject lang=en>Double stranded DNA breaks</subject> <subject>[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN]</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>BACKGROUND: Homologous recombination is the key process that generates genetic diversity and drives evolution. SPO11 protein triggers recombination by introducing DNA double stranded breaks at discreet areas of the genome called recombination hotspots. The hotspot locations are largely determined by the DNA binding specificity of the PRDM9 protein in human, mice and most other mammals. In budding yeast Saccharomyces cerevisae, which lacks a Prdm9 gene, meiotic breaks are formed opportunistically in the regions of accessible chromatin, primarily at gene promoters. The genome-wide distribution of hotspots in this organism can be altered by tethering Spo11 protein to Gal4 recognition sequences in the strain expressing Spo11 attached to the DNA binding domain of the Gal4 transcription factor. To establish whether similar re-targeting of meiotic breaks can be achieved in PRDM9-containing organisms we have generated a Gal4BD-Spo11 mouse that expresses SPO11 protein joined to the DNA binding domain of yeast Gal4. RESULTS: We have mapped the genome-wide distribution of the recombination initiation sites in the Gal4BD-Spo11 mice. More than two hundred of the hotspots in these mice were novel and were likely defined by Gal4BD, as the Gal4 consensus motif was clustered around the centers in these hotspots. Surprisingly, meiotic DNA breaks in the Gal4BD-Spo11 mice were significantly depleted near the ends of chromosomes. The effect is particularly striking at the pseudoautosomal region of the X and Y chromosomes -- normally the hottest region in the genome. CONCLUSIONS: Our data suggest that specific, yet-unidentified factors influence the initiation of meiotic recombination at subtelomeric chromosomal regions.</description> <date>2013-07-22</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>