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Transcriptome analysis of cells carrying Type II Csp231I restriction-modification (RM) system reveal the crosstalk between two unrelated transcription factors - C protein and Rac prophage repressor

ABSTRACT: Our transcriptome analysis supported by other in vivo and in vitro assays showed that C protein can directly silence the RacR repressor and thus affect the Rac prophage-related genes.

ORGANISM(S): Escherichia coli

PROVIDER: GSE126248 | GEO | 2019/07/30

REPOSITORIES: GEO

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Transcriptome analysis of cells carrying Type II Csp231I restriction-modification (RM) system reveal the crosstalk between two unrelated transcription factors - C protein and Rac prophage repressor

Project description:Transcriptome analysis of cells carrying Type II Csp231I restriction-modification (RM) system reveal the crosstalk between two unrelated transcription factors - C protein and Rac prophage repressor

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2025-05-07 | PXD059580 | Pride

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.

Project description: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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Molecular basis for lethal cross-talk between two unrelated bacterial transcription factors - the regulatory protein of a restriction-modification system and the repressor of a defective prophage.

Project description:Bacterial gene expression depends on the efficient functioning of global transcriptional networks, however their interconnectivity and orchestration rely mainly on the action of individual DNA binding proteins called transcription factors (TFs). TFs interact not only with their specific target sites, but also with secondary (off-target) sites, and vary in their promiscuity. It is not clear yet what mechanisms govern the interactions with secondary sites, and how such rewiring affects the overall regulatory network, but this could clearly constrain horizontal gene transfer. Here, we show the molecular mechanism of one such off-target interaction between two unrelated TFs in Escherichia coli: the C regulatory protein of a Type II restriction-modification system, and the RacR repressor of a defective prophage. We reveal that the C protein interferes with RacR repressor expression, resulting in derepression of the toxic YdaT protein. These results also provide novel insights into regulation of the racR-ydaST operon. We mapped the C regulator interaction to a specific off-target site, and also visualized C protein dynamics, revealing intriguing differences in single molecule dynamics in different genetic contexts. Our results demonstrate an apparent example of horizontal gene transfer leading to adventitious TF cross-talk with negative effects on the recipient's viability. More broadly, this study represents an experimentally-accessible model of a regulatory constraint on horizontal gene transfer.

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