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Co-operative autoregulation of a replication protein gene.

Identifieur interne : 002972 ( PubMed/Curation ); précédent : 002971; suivant : 002973

Co-operative autoregulation of a replication protein gene.

Auteurs : A E Gammie ; J H Crosa

Source :

RBID : pubmed:1809840

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English descriptors

Abstract

In this work we present the localization and characterization of the repl promoter (Prepl) and show aspects of the regulation. Comparison of Prepl with other autoregulated replication protein gene promoters revealed similarities, but Prepl differs from some of these characterized promoters in not being regulated by the heat-shock RNA polymerase. Primer extension analysis showed that Prepl is contained within five helically aligned 18 base pair repeats, or 18-mers of the previously defined minimal origin. In addition, we find that Prepl is autoregulated by a trans-acting product encoded in the REPI region. Purified Repl protein binds to the 18-mer region of the origin, suggesting that the repl gene is autoregulated by the protein product. The autoregulation appears to be co-operative since decreasing the 18-mer binding site region results in a concomitant non-linear loss of autorepression. The deletion derivatives show a decreased ability to bind the Repl protein when compared with origin DNA containing all of the binding region. The diminished capacity of the various deletion derivatives to bind Repl in vitro correlates with the loss of autorepression seen in vivo.

DOI: 10.1111/j.1365-2958.1991.tb01861.x
PubMed: 1809840

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A E Gammie
<affiliation>
<nlm:affiliation>Department of Microbiology and Immunology, Oregon Health Sciences University, Portland 97201.</nlm:affiliation>
<wicri:noCountry code="subField">Portland 97201</wicri:noCountry>
</affiliation>

Le document en format XML

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<term>Bacterial Proteins (genetics)</term>
<term>Base Sequence</term>
<term>DNA Mutational Analysis</term>
<term>DNA Replication (genetics)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>Gene Expression Regulation, Bacterial</term>
<term>Molecular Sequence Data</term>
<term>Plasmids (genetics)</term>
<term>Promoter Regions, Genetic (genetics)</term>
<term>Replicon (genetics)</term>
<term>Repressor Proteins (genetics)</term>
<term>Sequence Homology, Nucleic Acid</term>
<term>Trans-Activators</term>
<term>Transcriptional Activation</term>
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<keywords scheme="KwdFr" xml:lang="fr">
<term>Activation de la transcription</term>
<term>Analyse de mutations d'ADN</term>
<term>Données de séquences moléculaires</term>
<term>Plasmides (génétique)</term>
<term>Protéines bactériennes (génétique)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de répression (génétique)</term>
<term>Régions promotrices (génétique) (génétique)</term>
<term>Régulation de l'expression des gènes bactériens</term>
<term>Réplication de l'ADN (génétique)</term>
<term>Réplicon (génétique)</term>
<term>Similitude de séquences d'acides nucléiques</term>
<term>Séquence nucléotidique</term>
<term>Transactivateurs</term>
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<term>Bacterial Proteins</term>
<term>DNA-Binding Proteins</term>
<term>Repressor Proteins</term>
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<term>DNA Replication</term>
<term>Plasmids</term>
<term>Promoter Regions, Genetic</term>
<term>Replicon</term>
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<term>Plasmides</term>
<term>Protéines bactériennes</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines de répression</term>
<term>Régions promotrices (génétique)</term>
<term>Réplication de l'ADN</term>
<term>Réplicon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Base Sequence</term>
<term>DNA Mutational Analysis</term>
<term>Gene Expression Regulation, Bacterial</term>
<term>Molecular Sequence Data</term>
<term>Sequence Homology, Nucleic Acid</term>
<term>Trans-Activators</term>
<term>Transcriptional Activation</term>
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<term>Activation de la transcription</term>
<term>Analyse de mutations d'ADN</term>
<term>Données de séquences moléculaires</term>
<term>Régulation de l'expression des gènes bactériens</term>
<term>Similitude de séquences d'acides nucléiques</term>
<term>Séquence nucléotidique</term>
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<front>
<div type="abstract" xml:lang="en">In this work we present the localization and characterization of the repl promoter (Prepl) and show aspects of the regulation. Comparison of Prepl with other autoregulated replication protein gene promoters revealed similarities, but Prepl differs from some of these characterized promoters in not being regulated by the heat-shock RNA polymerase. Primer extension analysis showed that Prepl is contained within five helically aligned 18 base pair repeats, or 18-mers of the previously defined minimal origin. In addition, we find that Prepl is autoregulated by a trans-acting product encoded in the REPI region. Purified Repl protein binds to the 18-mer region of the origin, suggesting that the repl gene is autoregulated by the protein product. The autoregulation appears to be co-operative since decreasing the 18-mer binding site region results in a concomitant non-linear loss of autorepression. The deletion derivatives show a decreased ability to bind the Repl protein when compared with origin DNA containing all of the binding region. The diminished capacity of the various deletion derivatives to bind Repl in vitro correlates with the loss of autorepression seen in vivo.</div>
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<Abstract>
<AbstractText>In this work we present the localization and characterization of the repl promoter (Prepl) and show aspects of the regulation. Comparison of Prepl with other autoregulated replication protein gene promoters revealed similarities, but Prepl differs from some of these characterized promoters in not being regulated by the heat-shock RNA polymerase. Primer extension analysis showed that Prepl is contained within five helically aligned 18 base pair repeats, or 18-mers of the previously defined minimal origin. In addition, we find that Prepl is autoregulated by a trans-acting product encoded in the REPI region. Purified Repl protein binds to the 18-mer region of the origin, suggesting that the repl gene is autoregulated by the protein product. The autoregulation appears to be co-operative since decreasing the 18-mer binding site region results in a concomitant non-linear loss of autorepression. The deletion derivatives show a decreased ability to bind the Repl protein when compared with origin DNA containing all of the binding region. The diminished capacity of the various deletion derivatives to bind Repl in vitro correlates with the loss of autorepression seen in vivo.</AbstractText>
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