Journal
EMBO REPORTS
Volume 8, Issue 5, Pages 458-464Publisher
WILEY
DOI: 10.1038/sj.embor.7400957
Keywords
plasmid R1; stability system; parD; toxin-antitoxin pair; RNA decay
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Funding
- Medical Research Council [MC_U105365008] Funding Source: researchfish
- Medical Research Council [MC_U105365008] Funding Source: Medline
- MRC [MC_U105365008] Funding Source: UKRI
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Plasmids are units of extrachromosomal genetic inheritance found in all kingdoms of life. They replicate autonomously and undergo stable propagation in their hosts. Despite their small size, plasmid replication and gene expression constitute a metabolic burden that compromises their stable maintenance in host cells. This pressure has driven the evolution of strategies to increase plasmid stability-a process accelerated by the ability of plasmids to transfer horizontally between cells and to exchange genetic material with their host and other resident episomal DNAs. These abilities drive the adaptability and diversity of plasmids and their host cells. Indeed, survival functions found in plasmids have chromosomal homologues that have an essential role in cellular responses to stress. An analysis of these functions in the prokaryotic plasmid R1, and of their intricate interrelationships, reveals remarkable overall similarities with other gene- and cell-survival strategies found within and beyond the prokaryotic world.
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