Expression data from Escherichia coli after treatment with nalidixic acid (NA)
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ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE56251 | GEO | 2014/03/27
SECONDARY ACCESSION(S): PRJNA242745
REPOSITORIES: GEO
Similar Datasets
Project description:Having found that LexA degradation was significantly higher under apoptotic like death (ALD) than under SOS conditions, we hypothesized that additional genes tightly regulated by LexA would be transcribed under ALD conditions. We used microarray analysis to test the transcription pattern of up-regulated genes in ALD. We added no NA (n.t.), 100 M-BM-5g/ml NA, or 10 M-BM-5g/ml NA to cultures of the WT MC4100relA+, or its M-NM-^TmazEF or M-NM-^TmazEFlexA3 derivatives.
2014-03-27 | E-GEOD-56251 | biostudies-arrayexpress
Project description:Shimoni2009 - Escherichia Coli SOS
Simple model, involving only the basic components of the circuit, sufficient to explain the peaks in the promoter activities of recA and lexA.
This model is described in the article:
Stochastic analysis of the SOS response in Escherichia coli.
Shimoni Y, Altuvia S, Margalit H, Biham O
PloS one. 2009; 4(5):e5363
Abstract:
BACKGROUND: DNA damage in Escherichia coli evokes a response mechanism called the SOS response. The genetic circuit of this mechanism includes the genes recA and lexA, which regulate each other via a mixed feedback loop involving transcriptional regulation and protein-protein interaction. Under normal conditions, recA is transcriptionally repressed by LexA, which also functions as an auto-repressor. In presence of DNA damage, RecA proteins recognize stalled replication forks and participate in the DNA repair process. Under these conditions, RecA marks LexA for fast degradation. Generally, such mixed feedback loops are known to exhibit either bi-stability or a single steady state. However, when the dynamics of the SOS system following DNA damage was recently studied in single cells, ordered peaks were observed in the promoter activity of both genes (Friedman et al., 2005, PLoS Biol. 3(7):e238). This surprising phenomenon was masked in previous studies of cell populations. Previous attempts to explain these results harnessed additional genes to the system and deployed complex deterministic mathematical models that were only partially successful in explaining the results.
PRINCIPAL FINDINGS: Here we apply stochastic methods, which are better suited for dynamic simulations of single cells. We show that a simple model, involving only the basic components of the circuit, is sufficient to explain the peaks in the promoter activities of recA and lexA. Notably, deterministic simulations of the same model do not produce peaks in the promoter activities.
SIGNIFICANCE: We conclude that the double negative mixed feedback loop with auto-repression accounts for the experimentally observed peaks in the promoter activities. In addition to explaining the experimental results, this result shows that including additional regulations in a mixed feedback loop may dramatically change the dynamic functionality of this regulatory module. Furthermore, our results suggests that stochastic fluctuations strongly affect the qualitative behavior of important regulatory modules even under biologically relevant conditions, thus emphasizing the importance of stochastic analysis of regulatory circuits.
This model is hosted on BioModels Database and identified by: MODEL2937159804.
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2005-01-01 | MODEL2937159804 | BioModels
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:Suppression of the SOS response in combination with drugs has been proposed as a potential target to tackle antimicrobial resistance. The SOS response is the pathway used to repair bacterial DNA damage induced by antimicrobials such as quinolones. The extent of lexA-regulated protein expression and other associated systems under pressure of agents that damage bacterial DNA in clinical isolates remains unclear. The aim of this study was to assess the impact of this strategy on the proteome profile of Escherichia coli clinical strains.
2024-04-04 | PXD050358 | Pride
Project description:We examined the DNA damage response of bacterium E. coli using the replication inhibitor azidothyimdine (AZT), and RNA-Seq analysis. We confirm the induction of classic SOS loci by AZT and identify several genes, including many of the pyrimidine pathway, that are induced dependent on LexA cleavage, but have not been previously demonstrated to be DNA damage-inducible. Despite a strong dependence on LexA, these genes lack LexA boxes and their regulation by LexA is likely to be indirect via unknown factors. We show that stringent starvation protein, SspA, is as important as LexA in the regulation of AZT-induced genes. Our experiments identify a new set of LexA-independent DNA damage inducible genes, including 22 small RNA genes, some of which appear to activated by SspA. Motility and chemotaxis genes are strongly down-regulated by AZT, possibly as a result of one of more of the small RNAs or other transcription factors such as AppY and GadE, whose expression is elevated by AZT. Genes controlling the iron siderophore, enterobactin, and iron homeostasis are also strongly induced, independent of LexA. We confirm that IraD anti-adaptor protein and its upstream genes are induced, independent of LexA and that a second anti-adaptor, IraM is also strongly AZT-inducible, independent of LexA, suggesting that RpoS stabilization via these anti-adaptor proteins is an integral part of DNA damage tolerance.
2024-06-26 | GSE263906 | 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: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
Project description:UV Irradiation of the wild-type and lexA MG1655 Escherichia coli. Cells were irradiated at ~2x10^8 cells/ml in the Davis medium by 15-W germicidal lamp (254 nm, 0.66J/m^2/sec). Set also includes respective controls for unirradiated cells collected at 20 and 60 min time points. Comparison between lexA mutant and the isogenic wild-type prior the UV treatment is also included as part of the set. The SOS response in UV-irradiated Escherichia coli includes the upregulation of several dozen genes that are negatively regulated by the LexA repressor. Using DNA microarrays containing amplified DNA fragments from 95.5% of all open reading frames identified on the E. coli chromosome, we have examined the changes in gene expression following UV exposure in both wild-type cells and lexA1 mutants, which are unable to induce genes under LexA control. We report here the time courses of expression of the genes surrounding the 26 documented lexA-regulated regions on the E. coli chromosome. We observed 17 additional sites that responded in a lexA-dependent manner and a large number of genes that were upregulated in a lexA-independent manner although upregulation in this manner was generally not more than twofold. In addition, several transcripts were either downregulated or degraded following UV irradiation. These newly identified UV-responsive genes are discussed with respect to their possible roles in cellular recovery following exposure to UV irradiation. Data from the set are presented and analysed in the manuscript "Comparative gene expression profiles following UV exposure in wild type and SOS deficient Escherichia coli." Courcelle J; Khodursky A; Peter B; Brown PO; Hanawalt PC, Genetics 158: 41-64 May 2001 Keywords: other
2001-07-30 | GSE9 | GEO
Project description:YbjN, an enterobacteria-specific protein, is a multicopy suppressor of ts9 temperature sensitivity in Escherichia coli. Microarray study revealed that the expression level of ybjN was inversely correlated with the expression of flagellar, fimbrial and acid resistance genes. Over-expression of ybjN significantly down-regulated genes involved in the citric acid cycle, glycolysis, the glyoxylate shunt, oxidative phosphorylation, and amino acid and nucleotide metabolism. On the other hand, over-expression of ybjN up-regulated toxin-antitoxin modules, the SOS responsive pathway, cold shock proteins and starvation-induced transporter genes. Our results collectively suggest that YbjN may play important roles in regulating bacterial multicellular behaviors, metabolism and survival under various stress conditions in Es. coli.
2011-10-15 | GSE28630 | GEO
Project description:Ribonucleotides are frequently incorporated into DNA and can be used as a marker of DNA replication enzymology. To investigate on a genome-wide scale, how E. coli pol V accesses undamaged chromosomal DNA during the SOS response, we mapped the location of ribonucleotides incorporated by steric gate variants of pol V across the entire E. coli genome. To do so, we used strains that are deficient in ribonucleotide excision repair (DrnhB), constitutively express all SOS-regulated genes [lexA(Def)] and constitutively “activated” RecA* (recA730). The strains also harbor two steric gate variants of E. coli pol V (Y11A or F10L), or a homolog of pol V, (pol VR391-Y13A). Ribonucleotides are frequently incorporated by the pol V-Y11A and pol VR391-Y13A variants, with a preference to the lagging strand. In contrast, the pol V-F10L variant incorporates less ribonucleotides and no strand preference was observed. Sharp transitions in strand specificity are observed at replication origin (oriC), while a gradient is observed at the termination region. To activate RecA* in a recA+ strain, we treated the strains with ciprofloxacin and genome-wide mapped the location of the incorporated ribonucleotides. Again, the polV-Y11A steric gate variant, exhibited a lagging strand preference. Our data is consistent with a specific role for pol V in lagging strand DNA synthesis across the entire E. coli genome during the SOS response.
2021-03-22 | GSE158570 | GEO