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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>2018-01-15T18:33:27Z</responseDate> <request identifier=oai:HAL:hal-00873672v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-00873672v1</identifier> <datestamp>2018-01-11</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:AGROCAMPUS-OUEST</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:CNRS</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:UNAM</setSpec> <setSpec>collection:IGDR</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:UNIV-TLSE3</setSpec> <setSpec>collection:INSERM</setSpec> <setSpec>collection:INRA</setSpec> <setSpec>collection:IGDR-CR</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:AGREENIUM</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> <setSpec>collection:IRSET-EHESP</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Staphylococcus aureus-induced G2/M phase transition delay in host epithelial cells increases bacterial infective efficiency.</title> <creator>Alekseeva, Ludmila</creator> <creator>Rault, Lucie</creator> <creator>Almeida, Sintia</creator> <creator>Legembre, Patrick</creator> <creator>Edmond, Valérie</creator> <creator>Azevedo, Vasco</creator> <creator>Miyoshi, Anderson</creator> <creator>Even, Sergine</creator> <creator>Taieb, Frédéric</creator> <creator>Arlot-Bonnemains, Yannick</creator> <creator>Le Loir, Yves</creator> <creator>Berkova, Nadia</creator> <contributor>Science et Technologie du Lait et de l'Oeuf (STLO) ; Institut National de la Recherche Agronomique (INRA) - AGROCAMPUS OUEST</contributor> <contributor>Department of General Biology ; Federal University of Minas Gerais</contributor> <contributor>Récepteur de mort et échappement tumoral ; 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 ) - 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>Centre de physiopathologie de Toulouse Purpan (CPTP) ; Université Paul Sabatier - Toulouse 3 (UPS) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)</contributor> <contributor>Cancer du rein : bases moléculaires de la tumorogenèse ; Institut de Génétique et Développement de Rennes (IGDR) ; Université de Rennes 1 (UR1) - Centre National de la Recherche Scientifique (CNRS) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université de Rennes 1 (UR1) - Centre National de la Recherche Scientifique (CNRS) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <description>International audience</description> <source>ISSN: 1932-6203</source> <source>PLoS ONE</source> <publisher>Public Library of Science</publisher> <identifier>hal-00873672</identifier> <identifier>https://hal.archives-ouvertes.fr/hal-00873672</identifier> <identifier>https://hal.archives-ouvertes.fr/hal-00873672/document</identifier> <identifier>https://hal.archives-ouvertes.fr/hal-00873672/file/Staphylococcus_aureus-Induced.accepted.pdf</identifier> <source>https://hal.archives-ouvertes.fr/hal-00873672</source> <source>PLoS ONE, Public Library of Science, 2013, 8 (5), pp.e63279. 〈10.1371/journal.pone.0063279〉</source> <identifier>DOI : 10.1371/journal.pone.0063279</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0063279</relation> <identifier>PUBMED : 23717407</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/23717407</relation> <language>en</language> <subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Staphylococcus aureus is a highly versatile, opportunistic pathogen and the etiological agent of a wide range of infections in humans and warm-blooded animals. The epithelial surface is its principal site of colonization and infection. In this work, we investigated the cytopathic effect of S. aureus strains from human and animal origins and their ability to affect the host cell cycle in human HeLa and bovine MAC-T epithelial cell lines. S. aureus invasion slowed down cell proliferation and induced a cytopathic effect, resulting in the enlargement of host cells. A dramatic decrease in the number of mitotic cells was observed in the infected cultures. Flow cytometry analysis revealed an S. aureus-induced delay in the G2/M phase transition in synchronous HeLa cells. This delay required the presence of live S. aureus since the addition of the heat-killed bacteria did not alter the cell cycle. The results of Western blot experiments showed that the G2/M transition delay was associated with the accumulation of inactive cyclin-dependent kinase Cdk1, a key inducer of mitosis entry, and with the accumulation of unphosphorylated histone H3, which was correlated with a reduction of the mitotic cell number. Analysis of S. aureus proliferation in asynchronous, G1- and G2-phase-enriched HeLa cells showed that the G2 phase was preferential for bacterial infective efficiency, suggesting that the G2 phase delay may be used by S. aureus for propagation within the host. Taken together, our results divulge the potential of S. aureus in the subversion of key cellular processes such as cell cycle progression, and shed light on the biological significance of S. aureus-induced host cell cycle alteration.</description> <date>2013</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>