Presence of 5-methylcytosine in CC(A/T)GG sequences (Dcm methylation) in DNAs from different bacteria

Gómez-Eichelmann, M C; Levy-Mustri, A; Ramı́rez-Santos, Jesús

doi:10.1128/jb.173.23.7692-7694.1991

Cited by 30 publications

(26 citation statements)

References 24 publications

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“…A dcm homologue in Klebsiella pneumoniae was truncated and excluded from analysis. Its distribution is in accord with the distribution of Dcm-type methylation at 5Ј-CCWGG sequences (12). Each of these Dcm homologues was followed by a sequence very similar to that of the E. coli vsr gene.…”

Section: Resultssupporting

confidence: 58%

A DNA Methyltransferase Can Protect the Genome from Postdisturbance Attack by a Restriction-Modification Gene Complex

et al. 2002

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In prokaryotic genomes, some DNA methyltransferases form a restriction-modification gene complex, but some others are present by themselves. Dcm gene product, one of these orphan methyltransferases found in Escherichia coli and related bacteria, methylates DNA to generate 5-C m CWGG just as some of its eukaryotic homologues do. Vsr mismatch repair function of an adjacent gene prevents C-to-T mutagenesis enhanced by this methylation but promotes other types of mutation and likely has affected genome evolution. The reason for the existence of the dcm-vsr gene pair has been unclear. Earlier we found that several restriction-modification gene complexes behave selfishly in that their loss from a cell leads to cell killing through restriction attack on the genome. There is also increasing evidence for their potential mobility. EcoRII restriction-modification gene complex recognizes the same sequence as Dcm, and its methyltransferase is phylogenetically related to Dcm. In the present work, we found that stabilization of maintenance of a plasmid by linkage of EcoRII gene complex, likely through postsegregational cell killing, is diminished by dcm function. Disturbance of EcoRII restriction-modification gene complex led to extensive chromosome degradation and severe loss of cell viability. This cell killing was partially suppressed by chromosomal dcm and completely abolished by dcm expressed from a plasmid. Dcm, therefore, can play the role of a "molecular vaccine" by defending the genome against parasitism by a restriction-modification gene complex.Epigenetic methylation of DNA is a prominent phenomenon in many organisms. It occurs after passage of the replication fork and involves enzymatic transfer of a methyl group to specific bases on the DNA. The specific methylation of certain cytosine residues to 5-methylcytosine (5-m C) has been shown to affect gene expression in several organisms. In several eukaryotes, C-5 methylation is known to inactivate transposons and may have been maintained as a mechanism to defend the genome from genomic parasites (51). In the prokaryotes, many DNA methyltransferases are found as a component of a restriction-modification (RM) gene complex. Some methyltransferases are found paired with a restriction enzyme gene inactivated by a mutation (20,25,30), while others are not paired with a restriction enzyme homologue. Dcm in Escherichia coli and related bacteria is one of these "orphan" methyltransferases (39).In the E. coli chromosome, approximately 1% of the cytosine residues are methylated by Dcm to generate the sequence 5Ј-C m CWGG (W ϭ A or T) (39). 5-m C can deaminate to form thymine, which can lead to the production of C-to-T mutations. This mutation is prevented by the product of a contiguous gene, vsr, through the very-short-patch mismatch repair reaction (28,46). However, Vsr can increase other types of mutation under some other conditions, and the actions of Dcm and Vsr most likely have affected genome evolution (6,11,13,29,31). The reason for the existence of the dcm-vsr gene pair...

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Section: Resultssupporting

confidence: 58%

A DNA Methyltransferase Can Protect the Genome from Postdisturbance Attack by a Restriction-Modification Gene Complex

et al. 2002

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“…PVP-SE1 gp9 is homologous to an enterobacterial phage TLS protein defined as a DNA cytosine methyltransferase. gp9 may thus methylate cytosine residues at endonuclease sites, allowing the phage to escape restriction mediated by enzymes encoded in its hosts (20).…”

Section: Resultsmentioning

confidence: 99%

Genomic and Proteomic Characterization of the Broad-Host-Range Salmonella Phage PVP-SE1: Creation of a New Phage Genus

Santos

Kropinski

Ceyssens

et al. 2011

J Virol

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(Bacterio)phage PVP-SE1, isolated from a German wastewater plant, presents a high potential value as a biocontrol agent and as a diagnostic tool, even compared to the well-studied typing phage Felix 01, due to its broad lytic spectrum against different Salmonella strains. Sequence analysis of its genome (145,964 bp) shows it to be terminally redundant and circularly permuted. Its G؉C content, 45.6 mol%, is lower than that of its hosts (50 to 54 mol%). We found a total of 244 open reading frames (ORFs), representing 91.6% of the coding capacity of the genome. Approximately 46% of encoded proteins are unique to this phage, and 22.1% of the proteins could be functionally assigned. This myovirus encodes a large number of tRNAs (n ‫؍‬ 24), reflecting its lytic capacity and evolution through different hosts. Tandem mass spectrometric analysis using electron spray ionization revealed 25 structural proteins as part of the mature phage particle. The genome sequence was found to share homology with 140 proteins of the Escherichia coli bacteriophage rV5. Both phages are unrelated to any other known virus, which suggests that an "rV5-like virus" genus should be created within the Myoviridae to contain these two phages.

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“…At the other extreme, Pasteurella haemolytica has been reported to be naturally deficient in excision repair (29). The methyl-directed mismatch repair system (33) and the very short patch repair system (26,28) of E. coli may also be different, since neither adenine nor cytosine methylation is universal (21,44). Thus, it is already clear that there are considerable variations on the E. coli DNA repair model.…”

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confidence: 99%

DNA repair mutants of Rhodobacter sphaeroides

et al. 1995

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The genome of the photosynthetic eubacterium Rhodobacter sphaeroides 2.4.1 comprises two chromosomes and five endogenous plasmids and has a 65% G؉C base composition. Because of these characteristics of genome architecture, as well as the physiological advantages that allow this organism to live in sunlight when in an anaerobic environment, the sensitivity of R. sphaeroides to UV radiation was compared with that of the more extensively studied bacterium Escherichia coli. R. sphaeroides was found to be more resistant, being killed at about 60% of the rate of E. coli. To begin to analyze the basis for this increased resistance, a derivative of R. sphaeroides, strain 2.4.1⌬S, which lacks the 42-kb plasmid, was mutagenized with a derivative of Tn5, and the transposon insertion mutants were screened for increased UV sensitivity (UV s ). Eight UV s strains were isolated, and the insertion sites were determined by contour-clamped homogeneous electric field pulsed-field gel electrophoresis. These mapped to at least five different locations in chromosome I. Preliminary analysis suggested that these mutants were deficient in the repair of DNA damage. This was confirmed for three loci by DNA sequence analysis, which showed the insertions to be within genes homologous to uvrA, uvrB, and uvrC, the subunits of the nuclease responsible for excising UV damage.The photosynthetic bacterium Rhodobacter sphaeroides was the first prokaryote shown to have multiple chromosomes (48). Wild-type strain 2.4.1 comprises a genome of two circular chromosomes, as well as five additional plasmids with unknown functions. This genome architecture raises significant questions pertaining to DNA metabolism, an area about which virtually nothing is known in this multichromosomal prokaryote. Furthermore, the nature of DNA replication, repair, and recombination in R. sphaeroides is of interest because of other aspects of the lifestyle of this organism. Being photosynthetic, it is subjected to potentially lethal UV irradiation, making its mode of DNA repair of special interest. The high GϩC content (65%) of the R. sphaeroides genome makes this of further interest because of the expected higher content of Z DNA, the greater need for uracil repair following cytosine deamination, and the role of the latter process in UV mutagenesis when it occurs in pyrimidine dimers (49). In addition, R. sphaeroides can use a range of compounds as terminal electron acceptors, including toxic metal oxides and organic compounds with a potential for free radical formation (34). Thus, it is not only likely but probable that there are specific mechanisms that protect the genome against damage from these compounds.The current paradigm for prokaryotic DNA replication, repair, and recombination is based on DNA metabolism in Escherichia coli. Since this is an enteric organism with exposure to a limited environment and has a single chromosome with a base composition of about 50% GϩC, there is reason to expect that the E. coli model is incomplete or not entirely appropriate for free...

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Presence of 5-methylcytosine in CC(A/T)GG sequences (Dcm methylation) in DNAs from different bacteria

Cited by 30 publications

References 24 publications

A DNA Methyltransferase Can Protect the Genome from Postdisturbance Attack by a Restriction-Modification Gene Complex

A DNA Methyltransferase Can Protect the Genome from Postdisturbance Attack by a Restriction-Modification Gene Complex

Genomic and Proteomic Characterization of the Broad-Host-Range Salmonella Phage PVP-SE1: Creation of a New Phage Genus

DNA repair mutants of Rhodobacter sphaeroides

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