Unbalanced restriction impairs SOS-induced DNA repair effects

Katna, Anna; Boratynski, Robert; Furmanek-Blaszk, Beata; Zolcinska, Natalia; Sektas, Marian

doi:10.4014/jmb.0907.07005

Cited by 7 publications

(7 citation statements)

References 42 publications

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“…Moreover, the experiments described with yet another R–M system substantiate the idea that REases can cause cell death ( Supplementary Figure S2 ). Induction of SOS response has been examined in the case of MboII R–M system ( 48 ) which exhibits star activity. It is likely that the MboII also induces PCD.…”

Section: Discussionmentioning

confidence: 99%

Restriction endonuclease triggered bacterial apoptosis as a mechanism for long time survival

Nagamalleswari

Rao

Vasu

et al. 2017

Nucleic Acids Research

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Programmed cell death (PCD) under certain conditions is one of the features of bacterial altruism. Given the bacterial diversity and varied life style, different PCD mechanisms must be operational that remain largely unexplored. We describe restriction endonuclease (REase) mediated cell death by an apoptotic pathway, beneficial for isogenic bacterial communities. Cell death is pronounced in stationary phase and when the enzyme exhibits promiscuous DNA cleavage activity. We have elucidated the molecular mechanism of REase mediated cell killing and demonstrate that released nutrients from dying cells support the growth of the remaining cells in the population. These findings illustrate a new intracellular moonlighting role for REases which are otherwise established host defence arsenals. REase induced PCD appears to be a cellular design to replenish nutrients for cells undergoing starvation stress and the phenomenon could be wide spread in bacteria, given the abundance of restriction–modification (R–M) systems in the microbial population.

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Section: Discussionmentioning

confidence: 99%

Restriction endonuclease triggered bacterial apoptosis as a mechanism for long time survival

Nagamalleswari

Rao

Vasu

et al. 2017

Nucleic Acids Research

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“…This result clearly indicates the C protein improves its host cell fitness, and is vital for R-M system propagation. Loss of fitness for C-deleted R-M system cells might occur due to autorestriction of its host genome when the R-M system activities are not finely balanced leading eventually to cell death and a heavily perturbed the mixed cell population ratio ( 8 , 9 , 80 , 81 ). We also tested whether the C.Csp231I may be essential when R-M system needs to enter the unprotected new cell.…”

Section: Discussionmentioning

confidence: 99%

“…Type II R-M system activity may be harmful to its host, when expression of the REase and MTase is not finely balanced. Toxic REase action may cause double-strand breaks in a genome, and it can be lethal for the host if unrepaired ( 8 , 9 ). It resembles the functioning of many toxin-antitoxin units and other genetic addiction elements, which demand a counterbalance to toxicity to avoid the post-segregational killing of the host ( 10 – 12 ).…”

Section: Introductionmentioning

confidence: 99%

Natural C-independent expression of restriction endonuclease in a C protein-associated restriction-modification system

2015

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Restriction–modification (R-M) systems are highly prevalent among bacteria and archaea, and appear to play crucial roles in modulating horizontal gene transfer and protection against phage. There is much to learn about these diverse enzymes systems, especially their regulation. Type II R-M systems specify two independent enzymes: a restriction endonuclease (REase) and protective DNA methyltransferase (MTase). Their activities need to be finely balanced in vivo. Some R-M systems rely on specialized transcription factors called C (controller) proteins. These proteins play a vital role in the temporal regulation of R-M gene expression, and function to indirectly modulate the horizontal transfer of their genes across the species. We report novel regulation of a C-responsive R-M system that involves a C protein of a poorly-studied structural class - C.Csp231I. Here, the C and REase genes share a bicistronic transcript, and some of the transcriptional auto-control features seen in other C-regulated R-M systems are conserved. However, separate tandem promoters drive most transcription of the REase gene, a distinctive property not seen in other tested C-linked R-M systems. Further, C protein only partially controls REase expression, yet plays a role in system stability and propagation. Consequently, high REase activity was observed after deletion of the entire C gene, and cells bearing the ΔC R-M system were outcompeted in mixed culture assays by those with the WT R-M system. Overall, our data reveal unexpected regulatory variation among R-M systems.

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“…Second, the new REase might serve as an efficient anti-phage defence as long as its activity is precisely controlled to minimize genome damage (14). Nevertheless, global response to DNA damage (SOS response) is often triggered when the R–M system is not balanced (26) or not transmitted properly to progeny cells, resulting in post-segregational cell killing (27). In the latter case, the remaining REase may cleave the genome no longer fully protected by MTase, and the cell may die unless DNA repair occurs (28,29).…”

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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Unbalanced restriction impairs SOS-induced DNA repair effects

Cited by 7 publications

References 42 publications

Restriction endonuclease triggered bacterial apoptosis as a mechanism for long time survival

Restriction endonuclease triggered bacterial apoptosis as a mechanism for long time survival

Natural C-independent expression of restriction endonuclease in a C protein-associated restriction-modification system

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

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