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

Nucleic Acids Research
Alessandro NegriIwona Mruk

Abstract

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 in...Continue Reading

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Datasets Mentioned

BETA
GSE126248
AY787793

Methods Mentioned

BETA
gene knock-outs
RNA-seq
PCR

Software Mentioned

HMMER
phmmer

Related Concepts

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