Replication regulation of Vibrio cholerae chromosome II involves initiator binding to the origin both as monomer and as dimer.
Identifieur interne : 001D92 ( PubMed/Corpus ); précédent : 001D91; suivant : 001D93Replication 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 [ 1362-4962 ] ; 2012.
English descriptors
- KwdEn :
- Bacterial Proteins (chemistry), Bacterial Proteins (genetics), Bacterial Proteins (metabolism), Binding Sites, Chromosomes, Bacterial (chemistry), Chromosomes, Bacterial (metabolism), DNA Replication, DNA, Bacterial (chemistry), DNA, Bacterial (metabolism), DNA-Binding Proteins (chemistry), DNA-Binding Proteins (genetics), DNA-Binding Proteins (metabolism), Dimerization, Molecular Chaperones (metabolism), Mutation, Protein Binding, Replication Origin, Vibrio cholerae (genetics), Vibrio cholerae (metabolism).
- MESH :
- chemical , chemistry : Bacterial Proteins, DNA, Bacterial, DNA-Binding Proteins.
- chemical , genetics : Bacterial Proteins, DNA-Binding Proteins.
- chemical , metabolism : Bacterial Proteins, DNA, Bacterial, DNA-Binding Proteins, Molecular Chaperones.
- chemistry : Chromosomes, Bacterial.
- genetics : Vibrio cholerae.
- metabolism : Chromosomes, Bacterial, Vibrio cholerae.
- Binding Sites, DNA Replication, Dimerization, Mutation, Protein Binding, Replication Origin.
Abstract
The origin region of Vibrio cholerae 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. In vitro, 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 in vivo. The chaperones preferentially improved dimer binding in vitro, further suggesting the importance of dimer binding in the control of chrII replication.
DOI: 10.1093/nar/gks260
PubMed: 22447451
Links to Exploration step
pubmed:22447451Le document en format XML
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Chattoraj</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22447451</idno><idno type="pmid">22447451</idno><idno type="doi">10.1093/nar/gks260</idno><idno type="wicri:Area/PubMed/Corpus">001D92</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001D92</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Replication regulation of Vibrio cholerae 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><affiliation><nlm:affiliation>Laboratory of Biochemistry and Molecular Biology, NCI, 37 Convent Drive, NIH, Bethesda, MD 20892-4260, USA.</nlm:affiliation></affiliation></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="eISSN">1362-4962</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bacterial Proteins (chemistry)</term><term>Bacterial Proteins (genetics)</term><term>Bacterial Proteins (metabolism)</term><term>Binding Sites</term><term>Chromosomes, Bacterial (chemistry)</term><term>Chromosomes, Bacterial (metabolism)</term><term>DNA Replication</term><term>DNA, Bacterial (chemistry)</term><term>DNA, Bacterial (metabolism)</term><term>DNA-Binding Proteins (chemistry)</term><term>DNA-Binding Proteins (genetics)</term><term>DNA-Binding Proteins (metabolism)</term><term>Dimerization</term><term>Molecular Chaperones (metabolism)</term><term>Mutation</term><term>Protein Binding</term><term>Replication Origin</term><term>Vibrio cholerae (genetics)</term><term>Vibrio cholerae (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Bacterial Proteins</term><term>DNA, Bacterial</term><term>DNA-Binding Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bacterial Proteins</term><term>DNA-Binding Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bacterial Proteins</term><term>DNA, Bacterial</term><term>DNA-Binding Proteins</term><term>Molecular Chaperones</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Chromosomes, Bacterial</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Vibrio cholerae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Chromosomes, Bacterial</term><term>Vibrio cholerae</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Binding Sites</term><term>DNA Replication</term><term>Dimerization</term><term>Mutation</term><term>Protein Binding</term><term>Replication Origin</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The origin region of Vibrio cholerae 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. In vitro, 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 in vivo. The chaperones preferentially improved dimer binding in vitro, further suggesting the importance of dimer binding in the control of chrII replication.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22447451</PMID><DateCompleted><Year>2012</Year><Month>10</Month><Day>22</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1362-4962</ISSN><JournalIssue CitedMedium="Internet"><Volume>40</Volume><Issue>13</Issue><PubDate><Year>2012</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Nucleic acids research</Title><ISOAbbreviation>Nucleic Acids Res.</ISOAbbreviation></Journal><ArticleTitle>Replication regulation of Vibrio cholerae chromosome II involves initiator binding to the origin both as monomer and as dimer.</ArticleTitle><Pagination><MedlinePgn>6026-38</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/nar/gks260</ELocationID><Abstract><AbstractText>The origin region of Vibrio cholerae 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. In vitro, 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 in vivo. The chaperones preferentially improved dimer binding in vitro, further suggesting the importance of dimer binding in the control of chrII replication.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jha</LastName><ForeName>Jyoti K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Laboratory of Biochemistry and Molecular Biology, NCI, 37 Convent Drive, NIH, Bethesda, MD 20892-4260, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Demarre</LastName><ForeName>Gaëlle</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Venkova-Canova</LastName><ForeName>Tatiana</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Chattoraj</LastName><ForeName>Dhruba K</ForeName><Initials>DK</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>03</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nucleic Acids Res</MedlineTA><NlmUniqueID>0411011</NlmUniqueID><ISSNLinking>0305-1048</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004269">DNA, Bacterial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018832">Molecular Chaperones</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001665" MajorTopicYN="N">Binding Sites</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002876" MajorTopicYN="N">Chromosomes, Bacterial</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004261" MajorTopicYN="Y">DNA Replication</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004269" MajorTopicYN="N">DNA, Bacterial</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019281" MajorTopicYN="N">Dimerization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018832" MajorTopicYN="N">Molecular Chaperones</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018741" 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