The target of the negative regulator of pMB1 replication overlaps with part of the repressor coding sequence

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Abstract

Plasmid mutants (svir), insensitive to inhibition by the repressor of initiation of pMB1 replication, have been selected by exploiting their ability to support λ growth in the presence of λ repressor and inhibitor of plasmid replication. The alteration in the mechanism that controls plasmid replication causes a change in the plasmid copy number. svir mutants are dominant, as expected for mutants in the target of a repressor, but at the same time they are unable to synthesise a repressor active on the wild-type target. This lack of cross interaction between svir mutants and a co-resident wild-type plasmid results in their compatibility. These findings are explained by postulating that the target of the inhibitor of pMB1 replication coincides with part of the DNA segment that codes for the inhibitor itself. As a consequence single base pair changes in the target result in altered repressor molecules.

Original languageEnglish
Pages (from-to)40-45
Number of pages6
JournalMGG Molecular & General Genetics
Volume184
Issue number1
DOIs
Publication statusPublished - Nov 1981

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Plasmids
Repressor Proteins
Base Pairing
DNA
Growth

ASJC Scopus subject areas

  • Genetics

Cite this

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title = "The target of the negative regulator of pMB1 replication overlaps with part of the repressor coding sequence",
abstract = "Plasmid mutants (svir), insensitive to inhibition by the repressor of initiation of pMB1 replication, have been selected by exploiting their ability to support λ growth in the presence of λ repressor and inhibitor of plasmid replication. The alteration in the mechanism that controls plasmid replication causes a change in the plasmid copy number. svir mutants are dominant, as expected for mutants in the target of a repressor, but at the same time they are unable to synthesise a repressor active on the wild-type target. This lack of cross interaction between svir mutants and a co-resident wild-type plasmid results in their compatibility. These findings are explained by postulating that the target of the inhibitor of pMB1 replication coincides with part of the DNA segment that codes for the inhibitor itself. As a consequence single base pair changes in the target result in altered repressor molecules.",
author = "Gianni Cesareni",
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T1 - The target of the negative regulator of pMB1 replication overlaps with part of the repressor coding sequence

AU - Cesareni, Gianni

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N2 - Plasmid mutants (svir), insensitive to inhibition by the repressor of initiation of pMB1 replication, have been selected by exploiting their ability to support λ growth in the presence of λ repressor and inhibitor of plasmid replication. The alteration in the mechanism that controls plasmid replication causes a change in the plasmid copy number. svir mutants are dominant, as expected for mutants in the target of a repressor, but at the same time they are unable to synthesise a repressor active on the wild-type target. This lack of cross interaction between svir mutants and a co-resident wild-type plasmid results in their compatibility. These findings are explained by postulating that the target of the inhibitor of pMB1 replication coincides with part of the DNA segment that codes for the inhibitor itself. As a consequence single base pair changes in the target result in altered repressor molecules.

AB - Plasmid mutants (svir), insensitive to inhibition by the repressor of initiation of pMB1 replication, have been selected by exploiting their ability to support λ growth in the presence of λ repressor and inhibitor of plasmid replication. The alteration in the mechanism that controls plasmid replication causes a change in the plasmid copy number. svir mutants are dominant, as expected for mutants in the target of a repressor, but at the same time they are unable to synthesise a repressor active on the wild-type target. This lack of cross interaction between svir mutants and a co-resident wild-type plasmid results in their compatibility. These findings are explained by postulating that the target of the inhibitor of pMB1 replication coincides with part of the DNA segment that codes for the inhibitor itself. As a consequence single base pair changes in the target result in altered repressor molecules.

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