DNA replication of the resistance plasmid R100 and its control

Ohtsubo, Hideomi; Ryder, Thomas B.; Maeda, Yoshimi; Armstrong, Karen; Ohtsubo, Eiichi

doi:10.1016/0065-227x(86)90018-3

Cited by 38 publications

(38 citation statements)

References 30 publications

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“…Plasmid pHO100 (Fig. 1), which is 7,052 base pairs in length, is a hybrid between R100 miniplasmids pSMl and pMB8 (21). The replication system of pMB8 is related to that of ColEl, which cannot replicate in the polA mutant strain.…”

Section: Resultsmentioning

confidence: 99%

“…The mutants of pHO100 used were pHO100-B4, pHO100-B5, pHOl10-B24, pHO100-B27, pHO100-B37, pHO100-B46, and pHO100-E217. They have been constructed previously by the linker mutagenesis technique (21). pYK2, another pHO100 derivative, was constructed by combining pHO100-B24 and pHO100-B4 to eliminate the ori region (Y. Kawai and E. Ohtsubo, unpublished data).…”

Section: Methodsmentioning

confidence: 99%

“…We show here that pemK encodes a factor which stabilizes the plasmid by killing the host cells and that pemI inhibits the stabilization. The nucleotide sequence in the pem region shows two open reading frames (ORF2 and ORF3) that have been shown to be organized into an operon (2,21). We assume that ORF3 corresponds to pemK and that ORF2 corresponds to peml, which might control the killing function of pemK.…”

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Two genes, pemK and pemI, responsible for stable maintenance of resistance plasmid R100

1988

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Plasmid R100 was found to have two genes, designated pemK and pemI, that were responsible for its stable inheritance during cell division. They are located near the region that is essential for autonomous replication. Under conditions that inhibit replication of R100 derivatives, the plasmid containing these pem genes gave only a few segregants in viable cells and increased the number of nonviable cells in the population, suggesting that a product from the pem region stabilized the plasmid by killing plasmid-free segregants. Inactivation of one of the two translational open reading frames in the pem region caused the loss of the killing function, and thus, the open reading frame is a gene designated pemK, which encodes the killing factor. The coexistence of the pem+ plasmid with a high-copy-number plasmid carrying the other open reading frame inhibited stabilization, and thus, the second open reading frame is a gene designated peml, which encodes the inhibitor which might control the killing function of pemK. It is likely that the two open reading frames were transcribed from a promoter. There were no significant homologies in DNA sequences between the pem gene of R100 and the genes previously shown to be responsible for the stable inheritance of the other plasmids.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Two genes, pemK and pemI, responsible for stable maintenance of resistance plasmid R100

1988

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“…Bacterial cells were plated on an L-plate containing 50 mg/mL kanamycin and the total numbers of transformants of P3478 and of DH5a were counted. The ampicillin-resistance plasmid pHO100 (Ohtsubo et al 1986) was also electroporated into P3478 and DH5a to lean the efficiency of electroporation into each of the E. coli strains. The transposition frequency was calculated as a value per donor molecule, by dividing the number of transformants of P3478 with the number of transformants of DH5a and multiplying with the electroporation efficiency.…”

Section: Assay Of Transposition Productsmentioning

confidence: 99%

A cell‐free system of Tn3 transposition and transposition immunity

1996

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“…Most of IncFII plasmids contain multiple replicons, which are composed of the master IncFII replicon together with one or more other replicons such as IncFIA (rep1A) [2], IncFIB (rep1B) [3], and that (repB) belonging to an uncharacterized incompatibility group [4]; by contrast, there are some IncFII plasmids, such as R100 (accession number AP000342) [5] and R1 [6], which contain the sole IncFII replicon. IncFII plasmids with multiple replicons can overcome the incompatibility barrier with incoming plasmids [1].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Structure genomics of two chimera plasmids p675920-1 and p675920-2 coexisting in a multi-drug resistant Klebsiella pneumoniae isolate

Feng¹,

Yin²,

Zhan³

et al. 2018

Oncotarget

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This study dealt with detailed genomic characterization of two multidrug resistant (MDR) plasmids p675920-1 and p675920-2 from a single clinical Klebsiella pneumoniae isolate 675920. p675920-1 was essentially a hybrid of the IncFII plasmid pHN7A8 and the IncR plasmid pKPC-LK30, and functioned as an IncFII plasmid with inactivation of the IncR replication gene. The backbone of p675920-2 was a hybrid of a novel replicon, three maintenance regions (22.0-, 2.7-, 2.6-kb in length, respectively) as found in pKPYL2, p10164-3 and pK1HV, respectively, and the entire 25.9-kb conjugal transfer region of pKPYL2. p675920-1 and p675920-2 carried a large number of resistance genes, which contributed to resistance to at least seven classes of antibiotics (β-lactams, quinolones, aminoglycosides, fosfomycins, sulphonamides, trimethoprims, and tetracyclines) and one kind of heavy mental (mercury). All of these resistance genes are associated with mobile elements such as insertion sequences, insertion sequence-based transposition units, and transposons, which constituted a total of three novel MDR regions, two in p675920-1 and another in p675920-2. Coexistence of two MDR plasmids p675920-1 and p675920-2 made K. pneumoniae 675920 tend to become extensively drug-resistant.

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DNA replication of the resistance plasmid R100 and its control

Cited by 38 publications

References 30 publications

Two genes, pemK and pemI, responsible for stable maintenance of resistance plasmid R100

Two genes, pemK and pemI, responsible for stable maintenance of resistance plasmid R100

A cell‐free system of Tn3 transposition and transposition immunity

WITHDRAWN: Structure genomics of two chimera plasmids p675920-1 and p675920-2 coexisting in a multi-drug resistant Klebsiella pneumoniae isolate

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