<i>sbmC</i>, a stationary‐phase induced SOS <i>Escherichia coli</i> gene, whose product protects cells from the DNA replication inhibitor microcin B17

Baquero, M; Bouzon, Madeleine; Varea, Julio; Moreno, Felipe

doi:10.1111/j.1365-2958.1995.mmi_18020301.x

Cited by 74 publications

(56 citation statements)

References 31 publications

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“…Thus, amplification of gyrI and mdfA may prevent MMC from interacting with DNA, its macromolecular target. Amplification of gyrI has previously been shown to protect cells from the action of microcin B17, a DNA-cleaving agent (6). This compound causes double-stranded DNA breaks in vivo and in vitro only in concert with DNA gyrase (39).…”

Section: Discussionmentioning

confidence: 99%

In Vivo Titration of Mitomycin C Action by Four Escherichia coli Genomic Regions on Multicopy Plasmids

2001

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Mitomycin C (MMC), a DNA-damaging agent, is a potent inducer of the bacterial SOS response; surprisingly, it has not been used to select resistant mutants from wild-type Escherichia coli. MMC resistance is caused by the presence of any of four distinct E. coli genes (mdfA, gyrl, rob, and sdiA) on high-copy-number vectors. mdfA encodes a membrane efflux pump whose overexpression results in broad-spectrum chemical resistance. The gyrI (also called sbmC) gene product inhibits DNA gyrase activity in vitro, while the rob protein appears to function in transcriptional activation of efflux pumps. SdiA is a transcriptional activator of ftsQAZ genes involved in cell division.Mitomycin C (MMC), an antitumor agent isolated from Streptomyces cultures, is used in chemotherapy (30). It interacts with DNA by intercalation and adduct formation (37). These actions trigger the SOS response, the concerted induction of several DNA repair, and recombination activities controlled by the lexA-specified repressor in Escherichia coli (42). This interaction has been studied by in vitro and in vivo methods. The breadth of the SOS regulatory circuit has been approximated by screening a collection of Escherichia coli promoter-lacZYA gene fusions for those which displayed increased ␤-galactosidase activity in the presence of low levels of MMC (19). Similarly, two-dimensional electrophoretic separation of E. coli polypeptides induced by a DNA cleaving treatment has been catalogued (38). The expression of at least 29 genes is induced by DNA damage; 18 of these are regulated by the SOS response, while 11 are lexA independent (42).Global regulatory circuits do not act in isolation (29). Rather, a stress treatment may induce many regulons, as has been observed by both two-dimensional protein separation methodology in studies of Salmonella enterica serovar Typhimurium (13) and gene fusion-based analyses of E. coli (7) after hydrogen peroxide treatment. The concerted action of all such induced regulons describes the responses to the stress caused by an individual chemical treatment. Such interactions may also be suggested by the analysis of pleiotropic mutants (20) resistant to DNA-damaging agents.Despite the clinical, molecular biological, and historical importance of MMC-DNA interactions, the selection of MMCresistant mutants has been limited to a single pseudoreversion study (24,26). Further genetic studies might enhance our understanding of the cellular interactions with MMC. Demanding overexpression of a gene product is a classic means of overcoming chemical toxicity (20). Such selections were used to define the regulatory circuit controlling his operon expression in Salmonella serovar Typhimurium (32). This selection system was later exploited to select gene amplification events in bacteria (4). Similar selections with PALA, N-(phosphonacetyl)-L-aspartate, and methotrexate led to amplification of specific genes encoding enzymes targeted by the inhibitors in mammalian cells (34,41). With the construction of yeast genomic DNA libraries in high-...

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Section: Discussionmentioning

confidence: 99%

In Vivo Titration of Mitomycin C Action by Four Escherichia coli Genomic Regions on Multicopy Plasmids

2001

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“…9 In E.coli, the expression of sbmC is induced by DNA-damaging agents, possesses a quasicanonical LexA box and much like umuDC, the expression of sbmC is RecA and LexA dependent. 9 Thus, upregulation of umuD, lexA, dinP and sbmC by all nine FQs is likely LexA dependent. Figure 1b shows some of the more responsive clones as well as those related to the SOS response.…”

Section: Fq-responsive Promoters Involved In Stress Responsementioning

confidence: 99%

“…8 ) The sbmC gene was originally Salmonella responses to fluoroquinolones G Yim et al identified by its ability to confer resistance to MccB17 at high copy number. 9 MccB17 is a peptide antibiotic that induces double-stranded breaks in DNA in a DNA gyrase-dependent manner. 9 In E.coli, the expression of sbmC is induced by DNA-damaging agents, possesses a quasicanonical LexA box and much like umuDC, the expression of sbmC is RecA and LexA dependent.…”

Section: Fq-responsive Promoters Involved In Stress Responsementioning

confidence: 99%

“…9 MccB17 is a peptide antibiotic that induces double-stranded breaks in DNA in a DNA gyrase-dependent manner. 9 In E.coli, the expression of sbmC is induced by DNA-damaging agents, possesses a quasicanonical LexA box and much like umuDC, the expression of sbmC is RecA and LexA dependent. 9 Thus, upregulation of umuD, lexA, dinP and sbmC by all nine FQs is likely LexA dependent.…”

Section: Fq-responsive Promoters Involved In Stress Responsementioning

confidence: 99%

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Modulation of Salmonella gene expression by subinhibitory concentrations of quinolones

et al. 2010

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Approximately 2.7% of a collection of Salmonella enterica var. Typhimurium promoter-lux reporter strains showed altered transcriptional patterns when exposed to low concentrations of nine different fluoroquinolones (FQs). Even at the subinhibitory concentrations employed, all nine FQs upregulated genes involved in the SOS response, umuD, lexA, sbmC and dinP. In addition, transcriptional regulators, genes putatively associated with membrane integrity (spr), virulence (sicA) and metabolism (plsB) were affected. Using the Ames test with Salmonella strain TA102, increased mutagenicity was demonstrated in response to all the FQs tested: ciprofloxacin, moxifloxacin, levofloxacin and gatifloxacin. Transcriptional effects were largely specific to the FQ antimicrobials. Such responses are consistent with the primary mechanism of action of this class of inhibitor, namely, the introduction of DNA damage. This work provides support for the notion that small molecules can have functions other than growth inhibition that may affect the establishment and maintenance of community dynamics in complex environments.

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“…Independently, Baquero et al (26) reported that the gyrI gene (identical to the sbmC gene) belongs to the SOS regulon. The inactivation of GyrI causes cells to be more sensitive to microcin B17, whereas its overexpression yields microcin B17-resistant cells (26).…”

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confidence: 99%

Characterization of the Interaction between DNA Gyrase Inhibitor and DNA Gyrase of Escherichia coli

Nakanishi¹,

Imajoh‐Ohmi²,

Hanaoka³

2002

Journal of Biological Chemistry

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Escherichia coli DNA gyrase is comprised of two subunits, GyrA and GyrB. Previous studies have shown that GyrI, a regulatory factor of DNA gyrase activity, inhibits the supercoiling activity of DNA gyrase and that both overexpression and antisense expression of the gyrI gene suppress cell proliferation. Here we have analyzed the interaction of GyrI with DNA gyrase using two approaches. First, immunoprecipitation experiments revealed that GyrI interacts preferentially with the holoenzyme in an ATP-independent manner, although a weak interaction was also detected between GyrI and the individual GyrA and GyrB subunits. Second, surface plasmon resonance experiments indicated that GyrI binds to the gyrase holoenzyme with higher affinity than to either the GyrA or GyrB subunit alone. Unlike quinolone antibiotics, GyrI was not effective in stabilizing the cleavable complex consisting of gyrase and DNA. Further, we identified an 8-residue synthetic peptide, corresponding to amino acids 89 ITGGQYAV 96 of GyrI, which inhibits gyrase activity in an in vitro supercoiling assay. Surface plasmon resonance analysis of the ITG-GQYAV-containing peptide-gyrase interaction indicated a high association constant for this interaction. These results suggest that amino acids 89 -96 of GyrI are essential for its interaction with, and inhibition of, DNA gyrase.

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sbmC, a stationary‐phase induced SOS Escherichia coli gene, whose product protects cells from the DNA replication inhibitor microcin B17

Cited by 74 publications

References 31 publications

In Vivo Titration of Mitomycin C Action by Four Escherichia coli Genomic Regions on Multicopy Plasmids

In Vivo Titration of Mitomycin C Action by Four Escherichia coli Genomic Regions on Multicopy Plasmids

Modulation of Salmonella gene expression by subinhibitory concentrations of quinolones

Characterization of the Interaction between DNA Gyrase Inhibitor and DNA Gyrase of Escherichia coli

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