Incompatibility and INCFII Plasmid Replication Control

Rownd, Robert H.; Womble, David D.; Dong, Xinnian; Luckow, Verne A.; Wu, Ru Ping

doi:10.1007/978-1-4613-2447-8_26

Cited by 24 publications

(68 citation statements)

References 33 publications

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“…Recently, in vitro transcription experiments have shown that there is a structural rearrangement of ColEl preprimer RNA during the early stages of its synthesis (15,44). The binding of RNA-I to RNA-II may prevent the formation of a secondary structure required for initiation of replication (15), which may be similar to the mechanism proposed for the interaction of RNA-E with the repAl mRNA in the case of IncFII plasmid NR1 (28).…”

Section: Resultsmentioning

confidence: 76%

“…The target site for RNA-E has been shown to be the complementary RNA sequences within the leader regions of the repAl mRNAs (12,39). The sites of initial interaction between the :RNAs appear to be 6-base single-stranded loops present in both RNA-E and repAl mRNA (24,25,28,39). Several incompatibility (Inc-) and plasmid copy number (Cop-) mutants of NR1 have base substitutions that alter the RNA-E and the repAl mRNA * Corresponding author.…”

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confidence: 99%

“…Plasmid pRR12 is a copy mutant of NR1 that has a single base substitution in the 6-base incompatibility target loop, which weakens the interaction between RNA-E and repAl mRNA without changing their rates of synthesis (42). Copy mutant pRR21 contains a base substitution in Pc, resulting in a 10-fold stimulation of constitutive RNA-CX transcription (28,40). Copy mutant pRR39 has transposon Tn3 inserted in Pc, which inactivates the promoter and prevents RNA-CX transcription (3,40,42).…”

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confidence: 99%

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Transcriptional pausing in a region important for plasmid NR1 replication control

1987

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The results of in vitro single-round transcription experiments indicated that RNA polymerase pauses during transcription of the leader region that precedes the repAl gene of IncFII plasmid NR1. Transcription initiated at either of the two transcription promoter sites of the repAl gene, which encodes the essential replication initiation protein of NR1, was observed to pause in this region. Pausing was specifically enhanced by addition of NusA protein, an Escherichia coli transcription accessory factor. Northern blot RNA-DNA hybridization analysis of repAl mRNA synthesized in vivo revealed RNA species that had lengths equivalent to those of the in vitro-paused intermediates. The steady-state rate of in vivo repAl mRNA transcription downstream from the pause sites (measured by quantitative hybridization of pulse-labeled RNA to DNA probes complementary to different segments of repAl mRNA) was not appreciably affected, which suggests that the pause sites do not promote premature termination of transcription. The pause sites were located between the target sequence within the leader region of the mRNA that interacts with a 91-base countertranscript and the beginning of the repAl coding sequence. Because the countertranscript is an inhibitor of translation of repAl mRNA, transcriptional pausing in this region may be an important feature of the regulation of RepAl synthesis, which is the mechanism by which plasmid NR1 controls its replication.

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Section: Resultsmentioning

confidence: 76%

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confidence: 99%

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confidence: 99%

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Transcriptional pausing in a region important for plasmid NR1 replication control

1987

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“…IncFll plasmid NR1 (8,34,42,57) is a transmissible, multiple-antibiotic-resistant (R) plasmid with a size of 94.5 kilobase pairs (kb) and a low copy number of about 2 per bacterial chromosome (43,44,59). Plasmid pRR12 (31) is an Inc-Cop-mutant of NR1 that contains a single-base-pair substitution in the incRNA gene that regulates the translation of the mRNA for the repAl gene (40,41,44,53,54), which encodes the replication initiation protein of the plasmid (37,40,45).…”

Section: Methodsmentioning

confidence: 99%

DnaA protein is not essential for replication of IncFII plasmid NR1

1989

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By transformation of dnaA null mutant host cells that are suppressed either by an rnh mutation or by chromosomal integration of a mini-R1 plasmid, it was shown that replication of miniplasmids composed of the NR1 minimal replicon had no absolute dependence upon DnaA protein. In addition, the suppression of the dnaA null mutation by the integrated mini-R1, which is an IncFII relative of NR1, was found to be sensitive to the expression of IncFII-specific plasmid incompatibility. This suggests that the integrative suppression by mini-R1 is under the control of the normal IncFII plasmid replication circuitry. Although NR1 replication had no absolute requirement for DnaA, the copy numbers of NR1-derived miniplasmids were lower in dnaA null mutants, and the plasmids exhibited a much reduced stability of inheritance during subculture in the absence of selection. This suggests that DnaA protein may participate in IncFII plasmid replication in some auxiliary way, such as by increasing the efficiency of formation of an open initiation complex at the plasmid replication origin. Such an auxiliary role for DnaA in IncFII replication would be different from that for replication of most other plasmids examined, for which DnaA has been found to be either essential or unimportant.

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“…For IncFII plasmid NR1, a 95-kb self-transmissible antibiotic resistance plasmid with a copy number of approximately two per chromosome in Escherichia coli (36,49), those two functions are mediated by the repA replicon (25,34,48) and the stability (stb) locus (25,27,28,41,42), respectively. Miniplasmids that incorporate repA and stb are replicated and inherited with characteristics essentially similar to those of the 95-kb parental plasmid (25,41).…”

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Insertion and deletion mutations in the repA4 region of the IncFII plasmid NR1 cause unstable inheritance

et al. 1993

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For a bacterial plasmid to be inherited in a stable manner, its replication during the cell division cycle and the partitioning of plasmid replicas to daughter cells during cell division both must be carefully regulated and coordinated. For IncFII plasmid NR1, a 95-kb self-transmissible antibiotic resistance plasmid with a copy number of approximately two per chromosome in Escherichia coli (36, 49), those two functions are mediated by the repA replicon (25,34,48) and the stability (stb) locus (25, 27, 28, 41, 42), respectively.

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Incompatibility and INCFII Plasmid Replication Control

Cited by 24 publications

References 33 publications

Transcriptional pausing in a region important for plasmid NR1 replication control

Transcriptional pausing in a region important for plasmid NR1 replication control

DnaA protein is not essential for replication of IncFII plasmid NR1

Insertion and deletion mutations in the repA4 region of the IncFII plasmid NR1 cause unstable inheritance

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