Cargando…

Colicin E2 expression in Escherichia coli biofilms: Induction and regulation revisited

Colicins, bacteriocins produced by the gram-negative bacterium Escherichia coli, are tightly regulated by the DNA damage response regulatory system (SOS), and are thus triggered at times of stress. Colicins' regulation and expression profiles were primarily studied in suspended (planktonic) cul...

Descripción completa

Detalles Bibliográficos
Autores principales: Bayramoglu-Güven, Bihter, Ghazaryan, Lusine, Toubiana, David, Gillor, Osnat
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9742991/
https://www.ncbi.nlm.nih.gov/pubmed/36518173
http://dx.doi.org/10.1016/j.crmicr.2022.100171
Descripción
Sumario:Colicins, bacteriocins produced by the gram-negative bacterium Escherichia coli, are tightly regulated by the DNA damage response regulatory system (SOS), and are thus triggered at times of stress. Colicins' regulation and expression profiles were primarily studied in suspended (planktonic) cultures yet, in their natural environments E. coli cells are sessile, assembled in biofilms. We hypothesized that colicin expression would differ between planktonic and biofilm E. coli cultures, even when induced by the same triggers. To test our hypothesis, we compared colicin E2 expression and SOS regulated genes in planktonic and biofilm cultures of E. coli, in response to DNA damaging agents and oxygen depletion. The results indicate that uninduced biofilms express more transcripts of the colicin operon than uninduced planktonic cells. Whole genome expression profiles confirmed that in uninduced biofilms, SOS genes are upregulated compared to planktonic cultures. However, DNA damaging agents and oxygen depletion augmented colicin expression in planktonic cells, while only marginal increase was recorded in biofilms. Our results suggest that the regulation of colicin E2 expression in E. coli biofilms considerably differ from planktonic cells, thus the induction of colicins in their host natural environment, i.e., the gastrointestinal tract, needs to be re-evaluated.