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The role of stress in colicin regulation

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Abstract

Bacteriocins produced by Enterobacteriaceae are high molecular weight toxic proteins that kill target cells through a variety of mechanisms, including pore formation and nucleic acid degradation. What is remarkable about these toxins is that their expression results in death to the producing cells and therefore bacteriocin induction have to be tightly regulated, often confined to times of stress. Information on the regulation of bacteriocins produced by enteric bacteria is sketchy as their expression has only been elucidated in a handful of bacteria. Here, we review the known regulatory mechanisms of enteric bacteriocins and explore the expression of 12 of them in response to various triggers: DNA-damaging agents, stringent response, catabolite repression, oxidative stress, growth phase, osmolarity, cold shock, nutrient deprivation, anaerobiosis and pH stress. Our results indicate that the expression of bacteriocins is mostly confined to mutagenic triggers, while all other triggers tested are limited inducers.

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Acknowledgments

This work was supported by US National Institutes of Health Grant R01A1064588-01A2 and the Israeli Ministry for Science and Technology: Slovenia-Israel Research Cooperation.

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Correspondence to Osnat Gillor.

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Communicated by Erko Stackebrandt.

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203_2014_1017_MOESM1_ESM.pdf

Expression of BW25113 (WT) and JW5702-4 (CRP mutant) strains, each harboring reporter vectors controlled by colicin E1, E2 or D promoters. Light emission was measured 8 h after induction by various concentrations of glucose (a) and glycerol (b). Colicin expression is reported as the response ratio: the ratio between reporter cell light emissions at changing glucose/glycerol concentrations and at optimal glucose level (11.1 mM glucose). Each point is the mean of at least two replicates (PDF 120 kb)

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Ghazaryan, L., Tonoyan, L., Ashhab, A.A. et al. The role of stress in colicin regulation. Arch Microbiol 196, 753–764 (2014). https://doi.org/10.1007/s00203-014-1017-8

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  • DOI: https://doi.org/10.1007/s00203-014-1017-8

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