Organization and sequence of the HpaII restriction-modification system and adjacent genes

Kulakauskas, Saulius; Barsomian, Janet M.; Lubys, Arvydas; Roberts, Richard J.; Wilson, Geoffrey G.

doi:10.1016/0378-1119(94)90348-4

Cited by 22 publications

(12 citation statements)

References 40 publications

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“…The orthologous systems EcoHK31I from E. coli and EaeI from Enterobacter agglomerans are also adjacent to P4 Int-like ORFs, but there is no Psu ortholog present (36). This phenomenon of a common location for disparate RM systems is similar to one seen in Haemophilus, not known to involve defective prophages, where unrelated systems are found inserted next to the gene for valyl-tRNA synthetase (34).…”

Section: Discussionmentioning

confidence: 76%

Mobility of a Restriction-Modification System Revealed by Its Genetic Contexts in Three Hosts

et al. 2002

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The flow of genes among prokaryotes plays a fundamental role in shaping bacterial evolution, and restriction-modification systems can modulate this flow. However, relatively little is known about the distribution and movement of restriction-modification systems themselves. We have isolated and characterized the genes for restriction-modification systems from two species of Salmonella, S. enterica serovar Paratyphi A and S. enterica serovar Bareilly. Both systems are closely related to the PvuII restriction-modification system and share its target specificity. In the case of S. enterica serovar Paratyphi A, the restriction endonuclease is inactive, apparently due to a mutation in the subunit interface region. Unlike the chromosomally located Salmonella systems, the PvuII system is plasmid borne. We have completed the sequence characterization of the PvuII plasmid pPvu1, originally from Proteus vulgaris, making this the first completely sequenced plasmid from the genus Proteus. Despite the pronounced similarity of the three restriction-modification systems, the flanking sequences in Proteus and Salmonella are completely different. The SptAI and SbaI genes lie between an equivalent pair of bacteriophage P4-related open reading frames, one of which is a putative integrase gene, while the PvuII genes are adjacent to a mob operon and a XerCD recombination (cer) site.Restriction-modification (RM) systems are nearly ubiquitous among bacteria (both eubacteria and archaea). To date, the only complete bacterial genome sequences lacking candidate RM systems are from the obligate intracellular parasites Chlamydia and Rickettsia. Chlamydia trachomatis is the only known cellular organism that lacks an S-adenosyl-L-methionine (AdoMet) synthetase (63), and a type II RM system with separately active endonuclease and AdoMet-dependent methyltransferase proteins could be dangerous in this context. The other bacterial genomes have between 1 and 22 predicted RM systems (74,75). Even bacteria with the smallest genomes, Mycoplasma and Ureaplasma, have made room for these systems. RM systems provide a defense against DNA bacteriophages, as revealed both by direct experiment and indirectly by the fact that many bacteriophages take specific countermeasures against RM systems (9). In addition to initiating the destruction of some foreign DNAs, RM systems may also promote recombination (6, 51) and improve the spread of some genes by separating them from linked deleterious alleles (4, 42), thus playing both positive and negative roles in modulating the flow of genes among prokaryotes. In the case of type II RM systems, selfish behavior also contributes to their ubiquity (24,45,46). RM system ubiquity is consistent with the selectable phenotypes just summarized, but these phenotypes only help to explain why the systems are maintained once they have entered a given bacterium. It is less clear how these systems move throughout the microbial biosphere. To this end, it would be useful to track the movement of a given RM system by finding very clos...

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Section: Discussionmentioning

confidence: 76%

Mobility of a Restriction-Modification System Revealed by Its Genetic Contexts in Three Hosts

et al. 2002

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“…The endonuclease introduces double-strand breaks which, if not repaired, cause destruction of the chromosome and eventual death of the cell. The ability of an intracellular restriction endonuclease to digest DNA and cause cell death was shown in a temperature-sensitive mutant of the EcoRI endonuclease (12) and by heat inactivation of the temperature-sensitive methylase in a cloned HpaII R-M system (16).…”

Section: Resultsmentioning

confidence: 99%

DNA restriction-modification systems mediate plasmid maintenance

1995

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Two plasmid-carried restriction-modification (R-M) systems, EcoRI (from pMB1 of Escherichia coli) and Bsp6I (from pXH13 of Bacillus sp. strain RFL6), enhance plasmid segregational stability in E. coli and Bacillus subtilis, respectively. Inactivation of the endonuclease or the presence of the methylase in trans abolish the stabilizing activity of the R-M systems. We propose that R-M systems mediate plasmid segregational stability by postsegregational killing of plasmid-free cells. Plasmid-encoded methyltransferase modifies host DNA and thus prevents its digestion by the restriction endonuclease. Plasmid loss entails degradation and/or dilution of the methylase during cell growth and appearance of unmethylated sites in the chromosome. Double-strand breaks, introduced at these sites by the endonuclease, eventually cause the death of the plasmid-free cells. Contribution to plasmid stability is a previously unrecognized biological role of the R-M systems.The stable inheritance of plasmids in a bacterial population is ensured by different types of maintenance systems, the components of which are encoded either by the plasmid itself or by the chromosome of the host (33). Well-studied examples include the site-specific recombination systems, which resolve plasmid multimers, such as lox-cre of prophage P1 and cer-xer of plasmid ColE1, and active partition systems, such as par of prophage P1 and sop of plasmid F (33).A different class of systems is based on the mechanism termed postsegregational killing (8, 17), and accounts for killing or reducing the growth of plasmid-free cells. These systems comprise two components: a relatively stable toxin and an unstable ''antidote''. In the case of plasmid loss, rapid decay of the antidote allows the action of the toxin. A well-characterized example is that of the hok-sok system of plasmid R1. Synthesis of Hok protein leads to damage of the cell membrane and, eventually, cell death. Translation of long-lived hok mRNA is prevented by the unstable antisense sok RNA. As a result, the hok gene product is expressed only in the cells which have lost R1 during cell division (8,30). Plasmid F also encodes a system of a different type, the toxic protein CcdB, which efficiently traps gyrase. The antidote, CcdA protein, not only prevents the gyrase poisoning activity of CcdB but also reverts its effect on gyrase (1). Similarly, the poison-antipoison components of the pem system of R100 are also proteins (31). Postsegregational killing by such systems efficiently ensures the retention of plasmids in the population. For example, the hok/ sok system, when introduced into unstable pBR322 or p15 derivatives, decreases the appearance of plasmid-free cells by a factor of 10 3 to 10 5 (7). Two components of these systems, one causing cell death and the other protecting from the killing, recall another large family of proteins, the restriction-modification (R-M) systems. R-M systems, which occur primarily in bacteria, are classified into three main groups, according to their components and cofactor ...

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“…Diverse mechanisms for the mutagenicity of 5mC have been proposed previously (24,26), but in Escherichia coli, two appear to be the most relevant: (i) an increased rate of spontaneous hydrolytic deamination, promoted by the methyl group on C-5 of the pyrimidine ring (5,18,25,28), and (ii) relatively inefficient correction of the resulting G ⅐ T base pair in DNA (18). The mutational load caused by even low levels of 5mC in a prokaryotic genome apparently decreases evolutionary fitness, as argued by the following observations: (i) the gene responsible for forming 5mC at CC(A/T)GG in E. coli (dcm) is part of an operon encoding a corresponding sequence-specific G ⅐ T repair enzyme (vsr) (11), (ii) other DNA methyl transferases that form 5mC in bacteria are linked to genes resembling vsr (16), and (iii) vsr does not suppress all the mutagenesis caused by dcm expression (4,18).…”

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confidence: 99%

Cytosine Methylation by the Sua I Restriction-Modification System: Implications for Genetic Fidelity in a Hyperthermophilic Archaeon

Grogan

2003

J Bacteriol

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5-Methylcytosine in chromosomal DNA represents a potential source of frequent spontaneous mutation for hyperthermophiles. To determine the relevance of this threat for the archaeon Sulfolobus acidocaldarius, the mode of GGCC methylation by its restriction-modification system, SuaI, was investigated. Distinct isoschizomers of the SuaI endonuclease were used to probe the methylation state of GGCC in native S. acidocaldarius DNA. In addition, the methylation sensitivity of the SuaI endonuclease was determined with synthetic oligonucleotide substrates and modified natural DNAs. The results show that the SuaI system uses N 4 methylation to block cleavage of its recognition site, thereby avoiding the creation of G ⅐ T mismatches by spontaneous deamination at extremely high temperature.

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Organization and sequence of the HpaII restriction-modification system and adjacent genes

Cited by 22 publications

References 40 publications

Mobility of a Restriction-Modification System Revealed by Its Genetic Contexts in Three Hosts

Mobility of a Restriction-Modification System Revealed by Its Genetic Contexts in Three Hosts

DNA restriction-modification systems mediate plasmid maintenance

Cytosine Methylation by the Sua I Restriction-Modification System: Implications for Genetic Fidelity in a Hyperthermophilic Archaeon

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