Allele-specific suppression of dnaA (Ts) mutations by rpoB mutations in Escherichia coli

Atlung, Tove

doi:10.1007/bf00327932

Cited by 51 publications

(33 citation statements)

References 25 publications

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“…Except for the dnaA167 mutant, all the class 2 mutants have DnaA proteins that are irreversibly inactivated at the nonpermissive teiperature. In addition, suppression of the temperature sensitivity by the RNA polymerase mutation rpoB902 occurs in all class 1 mutants, whereas this is not the case for class 2 mutants, again with the exception of the dnaA167 mutant (1,4,12).…”

Section: Discussionmentioning

confidence: 93%

Coordination of chromosome replication initiation in Escherichia coli: effects of different dnaA alleles

et al. 1988

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Section: Discussionmentioning

confidence: 93%

Coordination of chromosome replication initiation in Escherichia coli: effects of different dnaA alleles

et al. 1988

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“…Mutations in rpoB and rpoC, which encode the ␤ and ␤Ј subunits of RNAP, respectively, have been shown to increase copy numbers of both the chromosome and chimeric plasmids (oriC plasmids) carrying both an oriC site and a ColE1-type replication origin (4,5). Further, specific rpoB mutations have been shown to suppress the temperature sensitivity phenotype of certain dnaA(Ts) mutations (6). Despite the evidence suggesting an involvement of RNAP, a specific transcription event required for initiation has not been identified.…”

Section: For Review)mentioning

confidence: 99%

The absence of effect of gid or mioC transcription on the initiation of chromosomal replication in Escherichia coli

Bates

Boye²,

Asai

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Despite the widely accepted view that transcription of gid and mioC is required for efficient initiation of cloned oriC, we show that these transcriptions have very little effect on initiation of chromosome replication at wild-type chromosomal oriC. Furthermore, neither gid nor mioC transcription is required in cells deficient in the histone-like proteins Fis or IHF. However, oriC that is sufficiently impaired for initiation by deletion of DnaA box R4 requires transcription of at least one of these genes. We conclude that transcription of mioC and especially gid is needed to activate oriC only under suboptimal conditions. We suggest that either the rifampicin-sensitive step of initiation is some other transcription occurring from promoter(s) within oriC, or the original inference of transcriptional activation derived from the rifampicin experiments is incorrect.Initiation of replication of the Escherichia coli chromosome occurs at a unique site, oriC. Initiation depends primarily on DnaA protein, which binds to five 9-bp repeats within oriC and facilitates duplex melting at three AϩT-rich 13-mers (see Fig. 1). DnaB helicase subsequently enters the opened duplex and leads to priming and chain elongation reactions resulting in bidirectional replication. oriC is a complex regulatory region containing recognition sites for many positive and negative regulatory proteins, including Fis, IHF, SeqA, and IciA, some or all of which are thought to help precisely regulate initiations occurring at oriC (see ref. 1 for review).Early physiology experiments by Lark (2) and Messer (3) first suggested that RNA polymerase (RNAP) is somehow involved in initiation at oriC. This was inferred from findings that rifampicin (an inhibitor of RNAP) inhibits a new round of DNA synthesis at a time when protein synthesis is no longer required. Genetic evidence as well suggests a role of RNAP in initiation. Mutations in rpoB and rpoC, which encode the ␤ and ␤Ј subunits of RNAP, respectively, have been shown to increase copy numbers of both the chromosome and chimeric plasmids (oriC plasmids) carrying both an oriC site and a ColE1-type replication origin (4, 5). Further, specific rpoB mutations have been shown to suppress the temperature sensitivity phenotype of certain dnaA(Ts) mutations (6). Despite the evidence suggesting an involvement of RNAP, a specific transcription event required for initiation has not been identified.Of promoters possibly involved in transcriptional activation of initiation, one likely candidate is the promoter of gidAB. The gid promoter (P gid ) is situated just counterclockwise of oriC ( Fig. 1) and transcription proceeds leftward away from oriC. oriC plasmids in which the gid promoter has been inactivated exhibit decreased transformation efficiency and stability as well as decreased replication in vitro (7,8). The twin-domain model of Liu and Wang (9) predicts that an actively transcribing RNAP generates local domains of increased negative supercoiling behind it and positive supercoiling in front of it. It...

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“…Involvement of the dnaA product in the transcription that is obligatory for the initiation of chromosome replication has been proposed on the basis of genetic evidence that the temperature-sensitive phenotype of some dnaA mutants is reversed by a rifampin resistance (Rif r ) mutation in the rpoB gene (4,5).…”

mentioning

confidence: 99%

Suppression of thermosensitive initiation of DNA replication in a dnaR mutant of Escherichia coli by a rifampin resistance mutation in the rpoB gene

Sakakibara

1995

J Bacteriol

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The thermosensitivity of the Escherichia coli dnaR130 mutant in initiation of DNA replication was suppressed by a spontaneous rifampin resistance mutation in rpoB, the gene for the ␤ subunit of RNA polymerase. Among the dnaR-suppressing rpoB alleles obtained was rpoB22, which was able to suppress the thermosensitivity of the dnaA46 or dnaA167 mutant, but not that of the dnaA5 mutant, in initiation of replication. Some dnaAsuppressing rpoB alleles obtained from rifampin-resistant derivatives of the dnaA mutants were able to suppress the dnaR defect. The dnaR mutant with the rpoB22 allele was deprived of thermoresistance by the dnaA5 mutation and of viability at low and high temperatures by the dnaA46 but not the dnaA167 mutation. The results show that the rpoB-mediated suppression of the dnaA or dnaR defect depends on the functions of both dnaA and dnaR products. I propose that the dnaR product has a key role in transcriptional activation of the replication origin for the dnaA-dependent initiation of DNA replication.

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Allele-specific suppression of dnaA (Ts) mutations by rpoB mutations in Escherichia coli

Cited by 51 publications

References 25 publications

Coordination of chromosome replication initiation in Escherichia coli: effects of different dnaA alleles

Coordination of chromosome replication initiation in Escherichia coli: effects of different dnaA alleles

The absence of effect of gid or mioC transcription on the initiation of chromosomal replication in Escherichia coli

Suppression of thermosensitive initiation of DNA replication in a dnaR mutant of Escherichia coli by a rifampin resistance mutation in the rpoB gene

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