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      Characterization of the GATC regulatory network in E. coli

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          Abstract

          Background

          The tetranucleotide GATC is methylated in Escherichia. coli by the DNA methyltransferase (Dam) and is known to be implicated in numerous cellular processes. Mutants lacking Dam are characterized by a pleiotropic phenotype. The existence of a GATC regulated network, thought to be involved in cold and oxygen shift, had been proposed and its existence has recently been confirmed. The aim of this article is to describe the components of the GATC regulated network of E. coli in detail and propose a role of this network in the light of an evolutionary advantage for the organism.

          Results

          We have classified the genes of the GATC network according to the EcoCyc functional classes. Comparisons with all of E. coli's genes and the genes involved in the SOS and stress response show that the GATC network forms a group apart. The functional classes that characterize the network are the Energy metabolism (in particular respiration), Fatty acid/ Phospholipid metabolism and Nucleotide metabolism.

          Conclusions

          The network is thought to come into play when the cell undergoes coldshock and is likely to enter stationary phase.

          The respiration is almost completely under GATC control and according to our hypothesis it will be blocked at the moment of coldshock; this might give the cell a selective advantage as it increases its chances for survival when entering stationary phase under coldshock. We predict the accumulation of formate and possibly succinate, which might increase the cell's resistance, in this case to antimicrobial agents, when entering stationary phase.

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          Most cited references31

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          A 12-cistron Escherichia coli operon (hyf) encoding a putative proton-translocating formate hydrogenlyase system.

          The nucleotide sequence has been determined for a twelve-gene operon of Escherichia coli designated the hyf operon (hyfABCDEFGHIR-focB). The hyf operon is located at 55.8-56.0 min and encodes a putative nine-subunit hydrogenase complex (hydrogenase four or Hyf), a potential formate- and sigma 54-dependent transcriptional activator, HyfR (related to FhlA), and a possible formate transporter, FocB (related to FocA). Five of the nine Hyf-complex subunits are related to subunits of both the E. coli hydrogenase-3 complex (Hyc) and the proton-translocating NADH:quinone oxidoreductases (complex I and Nuo), whereas two Hyf subunits are related solely to NADH:quinone oxidoreductase subunits. The Hyf components include a predicted 523 residue [Ni-Fe] hydrogenase (large subunit) with an N-terminus (residues 1-170) homologous to the 30 kDa or NuoC subunit of complex I. It is proposed that Hyf, in conjunction with formate dehydrogenase H (Fdh-H), forms a hitherto unrecognized respiration-linked proton-translocating formate hydrogenlyase (FHL-2). It is likely that HyfR acts as a formate-dependent regulator of the hyf operon and that FocB provides the Hyf complex with external formate as substrate.
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            Over 1000 genes are involved in the DNA damage response of Escherichia coli.

            Changes in gene expression after treatment of Escherichia 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 one or 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 100 are novel. From those genes involved in DNA metabolism that have not previously been shown to be induced by DNA damage, 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 downregulated in response to DNA damage are numerous protein biosynthesis genes. Analysis of the gene expression data highlighted the essential involvement of sigma(s)-regulated genes and the general stress response network in the response to DNA damage.
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              Oxidative stress defense and deterioration of growth-arrested Escherichia coli cells.

              Analysis of protein carbonylation demonstrates that the stasis-induced catalases and cytoplasmic superoxide dismutases (SOD) have a role in preventing accelerated protein oxidation during growth arrest of Escherichia coli cells. A larger number of proteins are carbonylated in cells lacking cytoplasmic SOD compared with cells lacking catalases, OxyR, or RpoS which, in turn, exhibit a larger number of oxidized proteins than the wild-type parent. Proteins exclusively oxidized during stasis in mutants lacking cytoplasmic SOD include GroEL, EF-G, and the acidic isoform of H-NS indicating that these mutants experience problems in peptide elongation and maintaining protein and DNA architecture. These mutants also survive stasis poorly. Likewise, but to a much lesser extent, mutations in oxyR, an oxidative stress regulator, shorten the life-span of stationary phase cells. The low plating efficiency of cells lacking OxyR is the result of their inability to grow on standard culture plates unless plating is performed anaerobically or with high concentration of catalase. In contrast, cells lacking cytoplasmic SOD appear to die prior to plating. Our data points to the importance of oxidative stress defense in stasis survival, and we also demonstrate that the life-span of growth-arrested wild-type E. coli cells can be significantly extended by omitting oxygen.
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                Author and article information

                Journal
                BMC Genomics
                BMC Genomics
                BioMed Central (London )
                1471-2164
                2004
                20 July 2004
                : 5
                : 48
                Affiliations
                [1 ]Laboratoire Génome et Informatique, UMR 8116, CNRS – Université d'Evry Val d'Essonne, Tour Evry 2, 523 Place des Terrasses, 91034 Evry cedex, France
                [2 ]METabolic EXplorer S.A., Biop ô le Clermont-Limagne, 63 360 Saint-Beauzire, France
                [3 ]Previous address: Hong Kong University- Pasteur Research Centre Ltd, Dexter HC Man Building, 8 Sassoon Road, Pokfulam, Hong Kong
                Article
                1471-2164-5-48
                10.1186/1471-2164-5-48
                493266
                15265237
                0f8374fc-2067-47e7-9a27-43455da9475f
                Copyright © 2004 Riva et al; licensee BioMed Central Ltd.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 30 March 2004
                : 20 July 2004
                Categories
                Research Article

                Genetics
                Genetics

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