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Replication–transcription conflicts in bacteria

Key Points

  • DNA replication and transcription share the same DNA template. Encounters between the replication and transcription machineries can lead to conflicts that result in disruption of replication, genome instability and reduced fitness.

  • Replication–transcription conflicts can occur both at DNA lesions or independently of DNA lesions under stress conditions.

  • Replication–transcription conflicts can occur when replication and transcription are co-directional (when genes are encoded on the leading strand), but are more severe when transcription is oriented head-on to replication (when genes are encoded on the lagging strand).

  • Bacteria use various mechanisms to prevent replication–transcription conflicts from occurring and to resolve conflicts that have occurred by repairing and restarting stalled replication forks.

  • Factors involved in avoiding and resolving replication–transcription conflicts include evolutionary pressures on genome organization that favour genes on the leading strand, accessory helicases, and modulators of transcription and translation.

Abstract

DNA replication and transcription use the same template and occur concurrently in bacteria. The lack of temporal and spatial separation of these two processes leads to their conflict, and failure to deal with this conflict can result in genome alterations and reduced fitness. In recent years major advances have been made in understanding how cells avoid conflicts between replication and transcription and how such conflicts are resolved when they do occur. In this Review, we summarize these findings, which shed light on the significance of the problem and on how bacterial cells deal with unwanted encounters between the replication and transcription machineries.

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Figure 1: Bacterial replication and replication–transcription conflicts.
Figure 2: Representative mechanisms of avoiding and resolving replication–transcription conflicts.
Figure 3: Possible fates of a replication fork that has stalled owing to conflicts with transcription.

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Acknowledgements

The authors thank S. S. Thirupathy for comments on the manuscript. Work on replication–transcription conflicts in the J.D.W. laboratory was supported, in part, by grant GM084003, and work in the A.D.G. laboratory was supported, in part, by grant GM41934, both from the US National Institutes of Health (NIH). H.M. was supported, in part, by postdoctoral fellowship GM093408 from the NIH and by funds from the University of Washington, Seattle, USA, and its Department of Microbiology. Y.Z. was supported, in part, by grant RP101499 from the Cancer Prevention Research Institute of Texas (CPRIT) Training Program.

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Merrikh, H., Zhang, Y., Grossman, A. et al. Replication–transcription conflicts in bacteria. Nat Rev Microbiol 10, 449–458 (2012). https://doi.org/10.1038/nrmicro2800

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