Post-segregational killing by restriction modification gene complexes: Observations of individual cell deaths

Handa, Nobuhiko; Kobayashi, Ichizo

doi:10.1016/s0300-9084(99)00201-1

Cited by 44 publications

(47 citation statements)

References 19 publications

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“…2) is similar to that observed with other type II RM gene complexes (19,20,36,48). The drastic loss of viability observed earlier with the mutant EcoRII RM gene complex by the same protocol (7,65) is likely to have been caused by the thermosensitivity conferred by the mutant modification enzyme.…”

Section: Discussionsupporting

confidence: 78%

“…A few of the r ϩ cells appeared anucleated. These features are common to postsegregational host killing after loss of other type II RM gene complexes (e.g., EcoRI and PaeR7I) (19,20,36,48). These results suggested that the EcoRII RM gene complex mediates postsegregational killing similarly to the previously examined type II RM gene complexes.…”

Section: Resultssupporting

confidence: 55%

“…When we first characterized the EcoRII RM gene complex (65), it showed a drastic level of cell killing compared with the other RM systems examined (19,20,36,48). The cell killing was observed by forcing plasmid loss by shifting to a nonpermissive temperature for the replicon with the RM gene complex.…”

Section: Resultsmentioning

confidence: 99%

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Maintenance Forced by a Restriction-Modification System Can Be Modulated by a Region in Its Modification Enzyme Not Essential for Methyltransferase Activity

et al. 2008

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Several type II restriction-modification gene complexes can force their maintenance on their host bacteria by killing cells that have lost them in a process called postsegregational killing or genetic addiction. It is likely to proceed by dilution of the modification enzyme molecule during rounds of cell division following the gene loss, which exposes unmethylated recognition sites on the newly replicated chromosomes to lethal attack by the remaining restriction enzyme molecules. This process is in apparent contrast to the process of the classical types of postsegregational killing systems, in which built-in metabolic instability of the antitoxin allows release of the toxin for lethal action after the gene loss. In the present study, we characterize a mutant form of the EcoRII gene complex that shows stronger capacity in such maintenance. This phenotype is conferred by an L80P amino acid substitution (T239C nucleotide substitution) mutation in the modification enzyme. This mutant enzyme showed decreased DNA methyltransferase activity at a higher temperature in vivo and in vitro than the nonmutated enzyme, although a deletion mutant lacking the N-terminal 83 amino acids did not lose activity at either of the temperatures tested. Under a condition of inhibited protein synthesis, the activity of the L80P mutant was completely lost at a high temperature. In parallel, the L80P mutant protein disappeared more rapidly than the wild-type protein. These results demonstrate that the capability of a restrictionmodification system in forcing maintenance on its host can be modulated by a region of its antitoxin, the modification enzyme, as in the classical postsegregational killing systems.

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Section: Discussionsupporting

confidence: 78%

Section: Resultssupporting

confidence: 55%

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Maintenance Forced by a Restriction-Modification System Can Be Modulated by a Region in Its Modification Enzyme Not Essential for Methyltransferase Activity

et al. 2008

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“…Despite their function in cellular defense, these gene complexes tend to propagate as selfish elements to promote their own survival and increase their relative frequency (28,41,88). For example, the failure to segregate R-M-encoding plasmids equally during cell division results in cell death for the progeny lacking these plasmids (28,89). Intact copies of the gene complex survive in other cells of the clone.…”

Section: Additional Functions Of R-m Systems Selfish Genesmentioning

confidence: 99%

Diverse Functions of Restriction-Modification Systems in Addition to Cellular Defense

Vasu

Nagaraja

2013

Microbiol Mol Biol Rev

509

462

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SUMMARY Restriction-modification (R-M) systems are ubiquitous and are often considered primitive immune systems in bacteria. Their diversity and prevalence across the prokaryotic kingdom are an indication of their success as a defense mechanism against invading genomes. However, their cellular defense function does not adequately explain the basis for their immaculate specificity in sequence recognition and nonuniform distribution, ranging from none to too many, in diverse species. The present review deals with new developments which provide insights into the roles of these enzymes in other aspects of cellular function. In this review, emphasis is placed on novel hypotheses and various findings that have not yet been dealt with in a critical review. Emerging studies indicate their role in various cellular processes other than host defense, virulence, and even controlling the rate of evolution of the organism. We also discuss how R-M systems could have successfully evolved and be involved in additional cellular portfolios, thereby increasing the relative fitness of their hosts in the population.

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“…In bacteria, methylation is best studied as part of restriction-modification (R-M) systems that have long been considered as contributing to bacterial immune response against incoming DNA including phages 4 . However, recent research has suggested that R-M systems may be 'selfish' elements that protect themselves against removal, through post-segregational killing of newly born progeny by pre-existing and stable restriction enzyme molecules [5][6][7][8][9][10][11] .…”

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confidence: 99%

Genomics of DNA cytosine methylation in Escherichia coli reveals its role in stationary phase transcription

et al. 2012

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DnA cytosine methylation regulates gene expression in mammals. In bacteria, its role in gene expression and genome architecture is less understood. Here we perform high-throughput sequencing of bisulfite-treated genomic DnA from Escherichia coli K12 to describe, for the first time, the extent of cytosine methylation of bacterial DnA at single-base resolution. Whereas most target sites (C m CWGG) are fully methylated in stationary phase cells, many sites with an extended CC m CWGG motif are only partially methylated in exponentially growing cells. We speculate that these partially methylated sites may be selected, as these are slightly correlated with the risk of spontaneous, non-synonymous conversion of methylated cytosines to thymines. microarray analysis in a cytosine methylation-deficient mutant of E. coli shows increased expression of the stress response sigma factor Rpos and many of its targets in stationary phase. Thus, DnA cytosine methylation is a regulator of stationary phase gene expression in E. coli.

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Post-segregational killing by restriction modification gene complexes: Observations of individual cell deaths

Cited by 44 publications

References 19 publications

Maintenance Forced by a Restriction-Modification System Can Be Modulated by a Region in Its Modification Enzyme Not Essential for Methyltransferase Activity

Maintenance Forced by a Restriction-Modification System Can Be Modulated by a Region in Its Modification Enzyme Not Essential for Methyltransferase Activity

Diverse Functions of Restriction-Modification Systems in Addition to Cellular Defense

Genomics of DNA cytosine methylation in Escherichia coli reveals its role in stationary phase transcription

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