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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Bacteriocins are proteinaceous antimicrobials produced by bacteria, which are active against other strains of the same species. R-type pyocins are phage tail-like bacteriocins produced by Pseudomonas aeruginosa, a Gram-negative opportunistic pathogen known to be problematic in chronic infections. Due to their anti-pseudomonal activity, R-pyocins have potential as therapeutics in infection. However little is understood regarding the effects of cell lysis in infection, nor the specific timing of R-pyocin induction and release. Similar to prophages, R-pyocins are located on the chromosome and are induced by the SOS response via DNA-damaging agents. Following SOS activation, R-pyocins are produced and then released into the environment by lysis of the producing cells. While several DNA-damaging agents are known to induce R-pyocin activity – including mitomycin C, ciprofloxacin, and hydrogen peroxide – it is unknown if all agents induce R-pyocin production to the same magnitude or along the same temporal regime. The induction of R-pyocins by the SOS response in P. aeruginosa also suggests that there may be regulatory ties between pyocins and chromosomal prophages - also induced under the same response. However, the regulation of R-pyocins and prophage have yet to be disentangled. There are two more lytic systems in P. aeruginosa that may also play a role in R-pyocin release: the Alp and the Cid systems, which have previously been ignored in much of the R-pyocin work thus far.
Using chromosomal transcriptional reporters, we have generated a number of strains to (i) quantify the regulatory activity of various R-pyocin genes, (ii) assess gene expression by disparate induction agents, (iii) establish a timeline of R-pyocin regulation, from induction to lysis, and (vi) disentangle the involvement of prophage and other lytic systems in the regulation of pyocins in P. aeruginosa. Overall, our work provides a more cohesive picture of R-pyocin regulation in P. aeruginosa.
