MersV1, PubMed, Checkpoint, bibRecord, 001D29

Transition from a plasmid to a chromosomal mode of replication entails additional regulators.

Identifieur interne : 001D29 ( PubMed/Checkpoint ); précédent : 001D28; suivant : 001D30

Transition from a plasmid to a chromosomal mode of replication entails additional regulators.

Auteurs : Tatiana Venkova-Canova [États-Unis] ; Dhruba K. Chattoraj

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2011.

RBID : pubmed:21444815

Descripteurs français

KwdFr :
- Chromosomes de bactérie (génétique), Cycle cellulaire (génétique), Escherichia coli (génétique), Helicase (génétique), Helicase (métabolisme), Origine de réplication, Plasmides (génétique), Réplication de l'ADN, Séquence nucléotidique, Test de retard de migration électrophorétique, Transactivateurs (génétique), Transactivateurs (métabolisme), Vibrio cholerae (cytologie), Vibrio cholerae (génétique).
MESH :
- cytologie : Vibrio cholerae.
- génétique : Chromosomes de bactérie, Cycle cellulaire, Escherichia coli, Helicase, Plasmides, Transactivateurs, Vibrio cholerae.
- métabolisme : Helicase, Transactivateurs.
- Origine de réplication, Réplication de l'ADN, Séquence nucléotidique, Test de retard de migration électrophorétique.

English descriptors

KwdEn :
- Base Sequence, Cell Cycle (genetics), Chromosomes, Bacterial (genetics), DNA Helicases (genetics), DNA Helicases (metabolism), DNA Replication, Electrophoretic Mobility Shift Assay, Escherichia coli (genetics), Plasmids (genetics), Replication Origin, Trans-Activators (genetics), Trans-Activators (metabolism), Vibrio cholerae (cytology), Vibrio cholerae (genetics).
MESH :
- chemical , genetics : DNA Helicases, Trans-Activators.
- cytology : Vibrio cholerae.
- genetics : Cell Cycle, Chromosomes, Bacterial, Escherichia coli, Plasmids, Vibrio cholerae.
- chemical , metabolism : DNA Helicases, Trans-Activators.
- Base Sequence, DNA Replication, Electrophoretic Mobility Shift Assay, Replication Origin.

Abstract

Plasmid origins of replication are rare in bacterial chromosomes, except in multichromosome bacteria. The replication origin of Vibrio cholerae chromosome II (chrII) closely resembles iteron-bearing plasmid origins. Iterons are repeated initiator binding sites in plasmid origins and participate both in replication initiation and its control. The control is mediated primarily by coupling of iterons via the bound initiators ("handcuffing"), which causes steric hindrance to the origin. The control in chrII must be different, since the timing of its replication is cell cycle-specific, whereas in plasmids it is random. Here we show that chrII uses, in addition to iterons, another kind of initiator binding site, named 39-mers. The 39-mers confer stringent control by increasing handcuffing of iterons, presumably via initiator remodeling. Iterons, although potential inhibitors of replication themselves, restrain the 39-mer-mediated inhibition, possibly by direct coupling ("heterohandcuffing"). We propose that the presumptive transition of a plasmid to a chromosomal mode of control requires additional regulators to increase the stringency of control, and as will be discussed, to gain the capacity to modulate the effectiveness of the regulators at different stages of the cell cycle.

DOI: 10.1073/pnas.1013244108
PubMed: 21444815

Affiliations:

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Le document en format XML

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<term>DNA Helicases (metabolism)</term>
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<term>Electrophoretic Mobility Shift Assay</term>
<term>Escherichia coli (genetics)</term>
<term>Plasmids (genetics)</term>
<term>Replication Origin</term>
<term>Trans-Activators (genetics)</term>
<term>Trans-Activators (metabolism)</term>
<term>Vibrio cholerae (cytology)</term>
<term>Vibrio cholerae (genetics)</term>
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<term>Escherichia coli (génétique)</term>
<term>Helicase (génétique)</term>
<term>Helicase (métabolisme)</term>
<term>Origine de réplication</term>
<term>Plasmides (génétique)</term>
<term>Réplication de l'ADN</term>
<term>Séquence nucléotidique</term>
<term>Test de retard de migration électrophorétique</term>
<term>Transactivateurs (génétique)</term>
<term>Transactivateurs (métabolisme)</term>
<term>Vibrio cholerae (cytologie)</term>
<term>Vibrio cholerae (génétique)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA Helicases</term>
<term>Trans-Activators</term>
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<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Vibrio cholerae</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Vibrio cholerae</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Cycle</term>
<term>Chromosomes, Bacterial</term>
<term>Escherichia coli</term>
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<term>Vibrio cholerae</term>
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<term>Plasmides</term>
<term>Transactivateurs</term>
<term>Vibrio cholerae</term>
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<term>Réplication de l'ADN</term>
<term>Séquence nucléotidique</term>
<term>Test de retard de migration électrophorétique</term>
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<front><div type="abstract" xml:lang="en">Plasmid origins of replication are rare in bacterial chromosomes, except in multichromosome bacteria. The replication origin of Vibrio cholerae chromosome II (chrII) closely resembles iteron-bearing plasmid origins. Iterons are repeated initiator binding sites in plasmid origins and participate both in replication initiation and its control. The control is mediated primarily by coupling of iterons via the bound initiators ("handcuffing"), which causes steric hindrance to the origin. The control in chrII must be different, since the timing of its replication is cell cycle-specific, whereas in plasmids it is random. Here we show that chrII uses, in addition to iterons, another kind of initiator binding site, named 39-mers. The 39-mers confer stringent control by increasing handcuffing of iterons, presumably via initiator remodeling. Iterons, although potential inhibitors of replication themselves, restrain the 39-mer-mediated inhibition, possibly by direct coupling ("heterohandcuffing"). We propose that the presumptive transition of a plasmid to a chromosomal mode of control requires additional regulators to increase the stringency of control, and as will be discussed, to gain the capacity to modulate the effectiveness of the regulators at different stages of the cell cycle.</div>
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<Abstract><AbstractText>Plasmid origins of replication are rare in bacterial chromosomes, except in multichromosome bacteria. The replication origin of Vibrio cholerae chromosome II (chrII) closely resembles iteron-bearing plasmid origins. Iterons are repeated initiator binding sites in plasmid origins and participate both in replication initiation and its control. The control is mediated primarily by coupling of iterons via the bound initiators ("handcuffing"), which causes steric hindrance to the origin. The control in chrII must be different, since the timing of its replication is cell cycle-specific, whereas in plasmids it is random. Here we show that chrII uses, in addition to iterons, another kind of initiator binding site, named 39-mers. The 39-mers confer stringent control by increasing handcuffing of iterons, presumably via initiator remodeling. Iterons, although potential inhibitors of replication themselves, restrain the 39-mer-mediated inhibition, possibly by direct coupling ("heterohandcuffing"). We propose that the presumptive transition of a plasmid to a chromosomal mode of control requires additional regulators to increase the stringency of control, and as will be discussed, to gain the capacity to modulate the effectiveness of the regulators at different stages of the cell cycle.</AbstractText>
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Transition from a plasmid to a chromosomal mode of replication entails additional regulators.

Transition from a plasmid to a chromosomal mode of replication entails additional regulators.

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