Replication regulation of Vibrio cholerae chromosome II involves initiator binding to the origin both as monomer and as dimer
Identifieur interne : 001282 ( Pmc/Checkpoint ); précédent : 001281; suivant : 001283Replication regulation of Vibrio cholerae chromosome II involves initiator binding to the origin both as monomer and as dimer
Auteurs : Jyoti K. Jha ; Gaëlle Demarre ; Tatiana Venkova-Canova ; Dhruba K. ChattorajSource :
- Nucleic Acids Research [ 0305-1048 ] ; 2012.
Abstract
The origin region of
Url:
DOI: 10.1093/nar/gks260
PubMed: 22447451
PubMed Central: 3401445
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Replication regulation of <italic>Vibrio cholerae</italic> chromosome II involves initiator binding to the origin both as monomer and as dimer</title><author><name sortKey="Jha, Jyoti K" sort="Jha, Jyoti K" uniqKey="Jha J" first="Jyoti K." last="Jha">Jyoti K. Jha</name></author><author><name sortKey="Demarre, Gaelle" sort="Demarre, Gaelle" uniqKey="Demarre G" first="Gaëlle" last="Demarre">Gaëlle Demarre</name></author><author><name sortKey="Venkova Canova, Tatiana" sort="Venkova Canova, Tatiana" uniqKey="Venkova Canova T" first="Tatiana" last="Venkova-Canova">Tatiana Venkova-Canova</name></author><author><name sortKey="Chattoraj, Dhruba K" sort="Chattoraj, Dhruba K" uniqKey="Chattoraj D" first="Dhruba K." last="Chattoraj">Dhruba K. Chattoraj</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22447451</idno><idno type="pmc">3401445</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401445</idno><idno type="RBID">PMC:3401445</idno><idno type="doi">10.1093/nar/gks260</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000F50</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000F50</idno><idno type="wicri:Area/Pmc/Curation">000F50</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000F50</idno><idno type="wicri:Area/Pmc/Checkpoint">001282</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">001282</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Replication regulation of <italic>Vibrio cholerae</italic> chromosome II involves initiator binding to the origin both as monomer and as dimer</title><author><name sortKey="Jha, Jyoti K" sort="Jha, Jyoti K" uniqKey="Jha J" first="Jyoti K." last="Jha">Jyoti K. Jha</name></author><author><name sortKey="Demarre, Gaelle" sort="Demarre, Gaelle" uniqKey="Demarre G" first="Gaëlle" last="Demarre">Gaëlle Demarre</name></author><author><name sortKey="Venkova Canova, Tatiana" sort="Venkova Canova, Tatiana" uniqKey="Venkova Canova T" first="Tatiana" last="Venkova-Canova">Tatiana Venkova-Canova</name></author><author><name sortKey="Chattoraj, Dhruba K" sort="Chattoraj, Dhruba K" uniqKey="Chattoraj D" first="Dhruba K." last="Chattoraj">Dhruba K. Chattoraj</name></author></analytic><series><title level="j">Nucleic Acids Research</title><idno type="ISSN">0305-1048</idno><idno type="eISSN">1362-4962</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The origin region of <italic>Vibrio cholerae</italic> chromosome II (chrII) resembles plasmid origins that have repeated initiator-binding sites (iterons). Iterons are essential for initiation as well as preventing over-initiation of plasmid replication. In chrII, iterons are also essential for initiation but over-initiation is prevented by sites called 39-mers. Both iterons and 39-mers are binding sites of the chrII specific initiator, RctB. Here, we have isolated RctB mutants that permit over-initiation in the presence of 39-mers. Characterization of two of the mutants showed that both are defective in 39-mer binding, which helps to explain their over-initiation phenotype. <italic>In vitro</italic>, RctB bound to 39-mers as monomers, and to iterons as both monomers and dimers. Monomer binding to iterons increased in both the mutants, suggesting that monomers are likely to be the initiators. We suggest that dimers might be competitive inhibitors of monomer binding to iterons and thus help control replication negatively. ChrII replication was found to be dependent on chaperones DnaJ and DnaK <italic>in vivo</italic>. The chaperones preferentially improved dimer binding <italic>in vitro</italic>, further suggesting the importance of dimer binding in the control of chrII replication.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Jacob, F" uniqKey="Jacob F">F Jacob</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dodson, M" uniqKey="Dodson M">M Dodson</name></author><author><name sortKey="Echols, H" uniqKey="Echols H">H Echols</name></author><author><name sortKey="Wickner, S" uniqKey="Wickner S">S Wickner</name></author><author><name sortKey="Alfano, C" uniqKey="Alfano C">C Alfano</name></author><author><name sortKey="Mensa Wilmot, K" uniqKey="Mensa Wilmot K">K Mensa-Wilmot</name></author><author><name sortKey="Gomes, B" uniqKey="Gomes B">B Gomes</name></author><author><name sortKey="Lebowitz, J" uniqKey="Lebowitz J">J LeBowitz</name></author><author><name sortKey="Roberts, Jd" uniqKey="Roberts J">JD 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Nucleic Acids Res</journal-id><journal-id journal-id-type="iso-abbrev">Nucleic Acids Res</journal-id><journal-id journal-id-type="publisher-id">nar</journal-id><journal-id journal-id-type="hwp">nar</journal-id><journal-title-group><journal-title>Nucleic Acids Research</journal-title></journal-title-group><issn pub-type="ppub">0305-1048</issn><issn pub-type="epub">1362-4962</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22447451</article-id><article-id pub-id-type="pmc">3401445</article-id><article-id pub-id-type="doi">10.1093/nar/gks260</article-id><article-id pub-id-type="publisher-id">gks260</article-id><article-categories><subj-group subj-group-type="heading"><subject>Genome Integrity, Repair and Replication</subject></subj-group></article-categories><title-group><article-title>Replication regulation of <italic>Vibrio cholerae</italic> chromosome II involves initiator binding to the origin both as monomer and as dimer</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Jha</surname><given-names>Jyoti K.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Demarre</surname><given-names>Gaëlle</given-names></name></contrib><contrib contrib-type="author"><name><surname>Venkova-Canova</surname><given-names>Tatiana</given-names></name></contrib><contrib contrib-type="author"><name><surname>Chattoraj</surname><given-names>Dhruba K.</given-names></name><xref ref-type="corresp" rid="gks260-COR1">*</xref></contrib></contrib-group><aff id="gks260-AFF1">Laboratory of Biochemistry and Molecular Biology, NCI, 37 Convent Drive, Room 6044, NIH, Bethesda, MD 20892-4260, USA</aff><author-notes><corresp id="gks260-COR1">*To whom correspondence should be addressed. Tel: <phone>+1 301 496 9194</phone>; Fax: <fax>+1 301 480 1493</fax>; Email: <email>chattoraj@nih.gov</email></corresp><fn><p>Present address: Gaëlle Demarre, CNRS – Centre de Génétique Moléculaire – UPR 2167, Gif-sur-Yvette, France.</p></fn></author-notes><pmc-comment>For NAR both ppub and collection dates generated for PMC processing 1/27/05 beck</pmc-comment>
<pub-date pub-type="collection"><month>7</month><year>2012</year></pub-date><pub-date pub-type="ppub"><month>7</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>24</day><month>3</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>24</day><month>3</month><year>2012</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>40</volume><issue>13</issue><fpage>6026</fpage><lpage>6038</lpage><history><date date-type="received"><day>16</day><month>1</month><year>2012</year></date><date date-type="rev-recd"><day>18</day><month>2</month><year>2012</year></date><date date-type="accepted"><day>8</day><month>3</month><year>2012</year></date></history><permissions><copyright-statement>Published by Oxford University Press 2012.</copyright-statement><copyright-year>2012</copyright-year><license license-type="creative-commons" xlink:href="http://creativecommons.org/licenses/by-nc/3.0"><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0">http://creativecommons.org/licenses/by-nc/3.0</ext-link>), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>The origin region of <italic>Vibrio cholerae</italic> chromosome II (chrII) resembles plasmid origins that have repeated initiator-binding sites (iterons). Iterons are essential for initiation as well as preventing over-initiation of plasmid replication. In chrII, iterons are also essential for initiation but over-initiation is prevented by sites called 39-mers. Both iterons and 39-mers are binding sites of the chrII specific initiator, RctB. Here, we have isolated RctB mutants that permit over-initiation in the presence of 39-mers. Characterization of two of the mutants showed that both are defective in 39-mer binding, which helps to explain their over-initiation phenotype. <italic>In vitro</italic>, RctB bound to 39-mers as monomers, and to iterons as both monomers and dimers. Monomer binding to iterons increased in both the mutants, suggesting that monomers are likely to be the initiators. We suggest that dimers might be competitive inhibitors of monomer binding to iterons and thus help control replication negatively. ChrII replication was found to be dependent on chaperones DnaJ and DnaK <italic>in vivo</italic>. The chaperones preferentially improved dimer binding <italic>in vitro</italic>, further suggesting the importance of dimer binding in the control of chrII replication.</p></abstract><counts><page-count count="13"></page-count></counts></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Chattoraj, Dhruba K" sort="Chattoraj, Dhruba K" uniqKey="Chattoraj D" first="Dhruba K." last="Chattoraj">Dhruba K. Chattoraj</name><name sortKey="Demarre, Gaelle" sort="Demarre, Gaelle" uniqKey="Demarre G" first="Gaëlle" last="Demarre">Gaëlle Demarre</name><name sortKey="Jha, Jyoti K" sort="Jha, Jyoti K" uniqKey="Jha J" first="Jyoti K." last="Jha">Jyoti K. Jha</name><name sortKey="Venkova Canova, Tatiana" sort="Venkova Canova, Tatiana" uniqKey="Venkova Canova T" first="Tatiana" last="Venkova-Canova">Tatiana Venkova-Canova</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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