Epigenetics Mediated by Restriction Modification Systems

Mruk, Iwona; Kobayashi, Ichizo

doi:10.1002/9781119004813.ch38

Cited by 2 publications

(1 citation statement)

References 111 publications

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“…First, the cell genome acquires the new epigenetic status related to the specificity of the introduced MTase. As a result, all genomic target sites are methylated, forming a new, unique set of epigenetic markers, which generates a cell-specific methylome dependent on the repertoire of active MTases (15–17). The methyl group may change expression of a single gene if it is located within the promoter/operator region, by blocking either RNA polymerase recruitment or binding by transcription factors.…”

Section: Introductionmentioning

confidence: 99%

Transcriptome analyses of cells carrying the Type II Csp231I restriction–modification system reveal cross-talk between two unrelated transcription factors: C protein and the Rac prophage repressor

Negri

Jąkalski

Szczuka

et al. 2019

Nucleic Acids Research

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Restriction-modification (R–M) systems represent an effective mechanism of defence against invading bacteriophages, and are widely spread among bacteria and archaea. In acquiring a Type II R–M system via horizontal gene transfer, the new hosts become more resistant to phage infection, through the action of a restriction endonuclease (REase), which recognizes and cleaves specific target DNAs. To protect the host cell's DNA, there is also a methyltransferase (MTase), which prevents DNA cleavage by the cognate REase. In some R–M systems, the host also accepts a cis-acting transcription factor (C protein), which regulates the counteracting activities of REase and MTase to avoid host self-restriction. Our study characterized the unexpected phenotype of Escherichia coli cells, which manifested as extensive cell filamentation triggered by acquiring the Csp231I R–M system from Citrobacter sp. Surprisingly, we found that the cell morphology defect was solely dependent on the C regulator. Our transcriptome analysis supported by in vivo and in vitro assays showed that C protein directly silenced the expression of the RacR repressor to affect the Rac prophage-related genes. The rac locus ydaST genes, when derepressed, exerted a toxicity indicated by cell filamentation through an unknown mechanism. These results provide an apparent example of transcription factor cross-talk, which can have significant consequences for the host, and may represent a constraint on lateral gene transfer.

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Section: Introductionmentioning

confidence: 99%

Transcriptome analyses of cells carrying the Type II Csp231I restriction–modification system reveal cross-talk between two unrelated transcription factors: C protein and the Rac prophage repressor

Negri

Jąkalski

Szczuka

et al. 2019

Nucleic Acids Research

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A mobile restriction–modification system provides phage defence and resolves an epigenetic conflict with an antagonistic endonuclease

Birkholz

Jackson

Fagerlund

et al. 2022

Nucleic Acids Research

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Epigenetic DNA methylation plays an important role in bacteria by influencing gene expression and allowing discrimination between self-DNA and intruders such as phages and plasmids. Restriction–modification (RM) systems use a methyltransferase (MTase) to modify a specific sequence motif, thus protecting host DNA from cleavage by a cognate restriction endonuclease (REase) while leaving invading DNA vulnerable. Other REases occur solitarily and cleave methylated DNA. REases and RM systems are frequently mobile, influencing horizontal gene transfer by altering the compatibility of the host for foreign DNA uptake. However, whether mobile defence systems affect pre-existing host defences remains obscure. Here, we reveal an epigenetic conflict between an RM system (PcaRCI) and a methylation-dependent REase (PcaRCII) in the plant pathogen Pectobacterium carotovorum RC5297. The PcaRCI RM system provides potent protection against unmethylated plasmids and phages, but its methylation motif is targeted by the methylation-dependent PcaRCII. This potentially lethal co-existence is enabled through epigenetic silencing of the PcaRCII-encoding gene via promoter methylation by the PcaRCI MTase. Comparative genome analyses suggest that the PcaRCII-encoding gene was already present and was silenced upon establishment of the PcaRCI system. These findings provide a striking example for selfishness of RM systems and intracellular competition between different defences.

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Epigenetics Mediated by Restriction Modification Systems

Cited by 2 publications

References 111 publications

Transcriptome analyses of cells carrying the Type II Csp231I restriction–modification system reveal cross-talk between two unrelated transcription factors: C protein and the Rac prophage repressor

Transcriptome analyses of cells carrying the Type II Csp231I restriction–modification system reveal cross-talk between two unrelated transcription factors: C protein and the Rac prophage repressor

A mobile restriction–modification system provides phage defence and resolves an epigenetic conflict with an antagonistic endonuclease

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