A Type III protein-RNA toxin-antitoxin system from Bacillus thuringiensis promotes plasmid retention during spore development
Taylor & Francis
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Short, F., Monson, R., & Salmond, G. (2015). A Type III protein-RNA toxin-antitoxin system from Bacillus thuringiensis promotes plasmid retention during spore development. RNA Biology, 12 933-937. https://doi.org/10.1080/15476286.2015.1073438
Members of the Bacillus cereus sensu lato group of bacteria often contain multiple large plasmids, including those encoding virulence factors in B. anthracis. Bacillus species can develop into spores in response to stress. During sporulation the genomic content of the cell is heavily compressed, which could result in counterselection of extrachromosomal genomic elements, unless they have robust stabilisation and segregation systems. Toxin-antitoxin (TA) systems are near-ubiquitous in prokaryotes and have multiple biological roles, including plasmid stabilisation during vegetative growth. Here, we have shown that a Type III TA system, based on an RNA antitoxin and endoribonuclease toxin, from plasmid pAW63 in Bacillus thuringiensis serovar kurstaki HD-73 can dramatically promote plasmid retention in populations undergoing sporulation and germination, and we provide evidence that this occurs through the post-segregational killing of plasmid-free forespores. Our findings show how an extremely common genetic module can be used to ensure plasmid maintenance during stress-induced developmental transitions, with implications for plasmid dynamics in B. cereus s.l. bacteria.
Type III Toxin-Antitoxin, Endoribonuclease, RNA antitoxin, Sporulation, Post-segregation killing, Bacillus cereus group
This work was supported by a Commonwealth Scholarship from the Commonwealth Scholarships Commission (UK) and Sir Henry Wellcome Postdoctoral fellowship to FLS, and the Biotechnology and Biological Sciences Research Council (UK). .
External DOI: https://doi.org/10.1080/15476286.2015.1073438
This record's URL: https://www.repository.cam.ac.uk/handle/1810/248971
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Licence URL: http://creativecommons.org/licenses/by/4.0/