Genome-wide analysis of E.coli response to mitomycin (MMC) treatment in wild type and recN mutant
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli str. K-12 substr. MG1655
PROVIDER: GSE74882 | GEO | 2016/04/01
SECONDARY ACCESSION(S): PRJNA301720
REPOSITORIES: GEO
Similar Datasets
Project description:We report the role of recN in the induction of the sos response Examination of gene profiling at two time points after addition of mitomycin (MMC) at 10µg/ml
2016-04-01 | E-GEOD-74882 | biostudies-arrayexpress
Project description:The SOS response is a conserved pathway that is activated under certain stress conditions and is regulated by the repressor LexA and the activator RecA. The food-borne pathogen Listeria monocytogenes contains RecA and LexA homologs, but their roles in Listeria have not been established. In this study, we identified the SOS regulon in L. monocytogenes by comparing the transcription profiles of the wild-type strain and the ΔrecA mutant strain after exposure to the DNA damaging agent mitomycinC (MMC). The SOS response is an inducible pathway involved in DNA repair, restart of stalled replication forks, and in induction of genetic variation in stressed and stationary phase cells. It is regulated by LexA and RecA. LexA is an autoregulatory repressor which binds to a consensus sequence in the promoter region of the SOS response genes, thereby repressing transcription. A consensus LexA binding motif for L. monocytogenes has not been identified thus far. Generally, the SOS response is induced under circumstances in which single stranded DNA accumulates in the cell. This results in activation of RecA, which in turn stimulates cleavage of LexA, and ultimately in the induction of the SOS response. Keywords: stress response, loop design, SOS response, mitomycin c, listeria monocytogenes, RecA, LexA
2009-11-25 | GSE12634 | GEO
Project description:The SOS response is a conserved pathway that is activated under certain stress conditions and is regulated by the repressor LexA and the activator RecA. The food-borne pathogen Listeria monocytogenes contains RecA and LexA homologs, but their roles in Listeria have not been established. In this study, we identified the SOS regulon in L. monocytogenes by comparing the transcription profiles of the wild-type strain and the ÎrecA mutant strain after exposure to the DNA damaging agent mitomycinC (MMC). The SOS response is an inducible pathway involved in DNA repair, restart of stalled replication forks, and in induction of genetic variation in stressed and stationary phase cells. It is regulated by LexA and RecA. LexA is an autoregulatory repressor which binds to a consensus sequence in the promoter region of the SOS response genes, thereby repressing transcription. A consensus LexA binding motif for L. monocytogenes has not been identified thus far. Generally, the SOS response is induced under circumstances in which single stranded DNA accumulates in the cell. This results in activation of RecA, which in turn stimulates cleavage of LexA, and ultimately in the induction of the SOS response. Keywords: stress response, loop design, SOS response, mitomycin c, listeria monocytogenes, RecA, LexA Triple loop design of 3 independent experiments (series A, B, and C) using Wt strain and recA mutant (activator of the SOS response). Sampling was done before (t=0) and 1 hour after (t=60) exposure to mitomycin C (MMC) for both the wild-type strain and the recA mutant strain. One series therefore contains 4 samples and the complete experiments consists of 12 samples. Each of the 3 series was designed in a loop (wt, t=0 =>wt, t=60 => recA, t=60 => recA, t=0 => wt, t=0). These 3 loops were connected using series B as the central loop. Series B was connected to series A as follows: wt, t=0 (B) => recA, t=0 (A) and wt, t=60 (B) => recA, t=60 (A). Series B was connected to series C as follows: recA, t=0 (B) => wt, t=0 (C) and recA, t=60 (B) => wt, t=60 (C).
2010-05-19 | E-GEOD-12634 | biostudies-arrayexpress
Project description:Transcriptional profiling of E.coli SE15 comparing wild type E.coli SE15 with Autoindecur 2 synthesis gene LuxS mutnat E.coli SE15. E.coli SE15 is isolated from indwelling catheter of urinary tract infected patient. Examine change of quorum sensing related gene by deleting autoinducer 2 synthesis gene LuxS in E.coli
2013-08-02 | GSE49474 | GEO
Project description:RNA-seq was used to analysis of mazEF toxin-antitoxin system mediated post-transcriptional inhibition through its endoribonuclease activity. DNA damage agents ,such as MMC, activates the mazEF system leading to cells growth arrest. In the present study, results reveal that a larger number of genes involved in amino acid and carbohydrate metabolism, ion transport and transcription was down-regulated in the wild-type compared with the mazEF-dr mutant.
2017-04-11 | GSE97563 | GEO
Project description:Changes in gene expression after treatment of E. coli cultures with mitomycin C were assessed using gene array technology. Unexpectedly, a large number of genes (nearly 30% of all genes) displayed significant changes in their expression level. Analysis and classification of expression profiles of the corresponding genes allowed us to assign this large number of genes into a dozen to two dozen small clusters of genes with similar expression profiles. This assignment allowed us to describe systematically the changes in the level of gene expression in response to DNA damage. Among the damage-induced genes more than a hundred are novel. From those genes involved in DNA metabolism that have not been previously shown to be induced by DNA damage, for example, the mutS gene involved in mismatch repair is especially noteworthy. In addition to the SOS response, we observed the induction of other stress response pathways such as those of oxidative stress and osmotic protection. Among the genes that are down-regulated in response to DNA damage are numerous protein biosynthesis genes. Analysis of the gene expression data highlighted the essential involvement of sigmaS regulated genes and the general stress response network in the response to DNA damage. Keywords = DNA damage, recA, SOS Keywords: other
2002-02-26 | GSE33 | GEO
Project description:ObjectivesTo compare the urinary pH, recurrence-free survival (RFS), and safety of adjuvant intravesical therapy in patients with non-muscle-invasive bladder cancer (NMIBC) receiving mitomycin C (MMC) therapy and MMC + cytosine arabinoside (Ara-C) therapy.Patients and methodsA total of 165 patients with NMIBC from six hospitals were randomly allocated to two groups: weekly instillation of MMC + Ara-C (30 mg/30 mL + 200 mg/10 mL) for 6 weeks and the same instillation schedule of MMC (30 mg/40 mL). The primary outcome was RFS, and secondary outcomes were urinary pH and toxicity in the two groups.ResultsA total of 81 and 87 patients were randomised into the MMC and MMC + Ara-C groups, respectively. Overall, the RFS in the MMC + Ara-C group was significantly longer (P = 0.018) than that in the MMC group. A similar significant difference was detected in patients with intermediate-risk NMIBC, but not in those with high-risk NMIBC. The mean (SD) urinary pH was significantly higher in the MMC + Ara-C group than in the MMC group, at 6.56 (0.61) vs 5.78 (0.64) (P < 0.001), and the frequency of a urinary pH of >7.0 in the MMC and MMC + Ara-C groups was 6.3% and 26.7%, respectively (P < 0.001). Multivariate analysis models including clinicopathological features and second transurethral resection demonstrated that increased urinary pH was associated with better outcomes (hazard ratio 0.18, 95% confidential interval 0.18-0.038; P < 0.001). In all, there were 14 and 10 adverse events in the MMC and MMC + Ara-C groups, respectively, without a significant difference (P = 0.113).ConclusionsOur randomised clinical trial suggested that intravesical therapy with MMC and Ara-C is useful and safe for patients with intermediate-risk NMIBC. Increase in urinary pH with Ara-C is speculated as a mechanism for increased anti-cancer effects.
| S-EPMC9290455 | biostudies-literature
Project description:Changes in gene expression after treatment of E. coli cultures with mitomycin C were assessed using gene array technology. Unexpectedly, a large number of genes (nearly 30% of all genes) displayed significant changes in their expression level. Analysis and classification of expression profiles of the corresponding genes allowed us to assign this large number of genes into a dozen to two dozen small clusters of genes with similar expression profiles. This assignment allowed us to describe systematically the changes in the level of gene expression in response to DNA damage. Among the damage-induced genes more than a hundred are novel. From those genes involved in DNA metabolism that have not been previously shown to be induced by DNA damage, for example, the mutS gene involved in mismatch repair is especially noteworthy. In addition to the SOS response, we observed the induction of other stress response pathways such as those of oxidative stress and osmotic protection. Among the genes that are down-regulated in response to DNA damage are numerous protein biosynthesis genes. Analysis of the gene expression data highlighted the essential involvement of sigmaS regulated genes and the general stress response network in the response to DNA damage. Keywords = DNA damage, recA, SOS
2010-06-05 | E-GEOD-33 | biostudies-arrayexpress
Project description:Zebularine is a non-methylable cytidine analog that is used in epigenetic and cancer research. Its application has been shown to activate several transcriptionally silenced genetic elements; however, extent of this activation and other effects on the transcriptome are unknown. Here, we show that zebularine treatment induces preferentially genes associated with DNA damage repair response and this activation is strongly ATR-dependent. The set of up- and down-regulated genes after 24 h zebularine treatment is almost fully contained in the set of genes with changed transcription in response to 24 h MMC treatment. We identified only few genes that were up-regulated in common by longer (5 days) zebularine treatment and loss of epigenetic control in ddm1 mutant. Our results suggest that zebularine does not induce global activation of targets of transcriptional gene silencing and indicate previously unanticipated DNA damaging effects associated with zebularine-treatment.
2014-11-18 | GSE63355 | GEO
Project description:LexA is a transcriptional repressor for genes requiring expression primarily during SOS response in response to stress such as that caused by DNA alkylating agent Mitomycin C (MMC). LexA undergoes self-cleavage under stress conditions thereby lifting the repression on genes whose expression is required for stress response. In our experiment LexA binding sites in the genome were determined in untreated and MMC treated (overnight, 14h) cultures using a LexA-3xFLAG strain and anti-FLAG monoclonal antibodies. Wild type Streptomyces venezuelae (unFLAGged LexA) cultures, with and without MMC treatment were used as negative controls.
2022-07-06 | E-MTAB-11603 | biostudies-arrayexpress