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Replication regulation of Vibrio cholerae chromosome II involves initiator binding to the origin both as monomer and as dimer

Identifieur interne : 002212 ( Main/Exploration ); précédent : 002211; suivant : 002213

Replication 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. Chattoraj

Source :

RBID : PMC:3401445

Descripteurs français

English descriptors

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.


Url:
DOI: 10.1093/nar/gks260
PubMed: 22447451
PubMed Central: 3401445


Affiliations:


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Le document en format XML

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<name sortKey="Jha, Jyoti K" sort="Jha, Jyoti K" uniqKey="Jha J" first="Jyoti K." last="Jha">Jyoti K. Jha</name>
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<title level="j">Nucleic Acids Research</title>
<idno type="ISSN">0305-1048</idno>
<idno type="eISSN">1362-4962</idno>
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<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>
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<term>ADN bactérien ()</term>
<term>ADN bactérien (métabolisme)</term>
<term>Chaperons moléculaires (métabolisme)</term>
<term>Chromosomes de bactérie ()</term>
<term>Chromosomes de bactérie (métabolisme)</term>
<term>Dimérisation</term>
<term>Liaison aux protéines</term>
<term>Mutation</term>
<term>Origine de réplication</term>
<term>Protéines bactériennes ()</term>
<term>Protéines bactériennes (génétique)</term>
<term>Protéines bactériennes (métabolisme)</term>
<term>Protéines de liaison à l'ADN ()</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de liaison à l'ADN (métabolisme)</term>
<term>Réplication de l'ADN</term>
<term>Sites de fixation</term>
<term>Vibrio cholerae (génétique)</term>
<term>Vibrio cholerae (métabolisme)</term>
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<term>Bacterial Proteins</term>
<term>DNA, Bacterial</term>
<term>DNA-Binding Proteins</term>
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<term>Bacterial Proteins</term>
<term>DNA-Binding Proteins</term>
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<term>Bacterial Proteins</term>
<term>DNA, Bacterial</term>
<term>DNA-Binding Proteins</term>
<term>Molecular Chaperones</term>
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<term>Chromosomes, Bacterial</term>
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<term>Vibrio cholerae</term>
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<term>Protéines bactériennes</term>
<term>Protéines de liaison à l'ADN</term>
<term>Vibrio cholerae</term>
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<term>Chromosomes, Bacterial</term>
<term>Vibrio cholerae</term>
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<term>ADN bactérien</term>
<term>Chaperons moléculaires</term>
<term>Chromosomes de bactérie</term>
<term>Protéines bactériennes</term>
<term>Protéines de liaison à l'ADN</term>
<term>Vibrio cholerae</term>
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<term>Binding Sites</term>
<term>DNA Replication</term>
<term>Dimerization</term>
<term>Mutation</term>
<term>Protein Binding</term>
<term>Replication Origin</term>
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<term>Mutation</term>
<term>Origine de réplication</term>
<term>Protéines bactériennes</term>
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<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>
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