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The RpoS-dependent general stress response & biofilm formation of E. coli
Depending on the nutrient supply, bacteria can occur in very different physiological states: they either grow and divide or they enter into stationary phase, where remaining resources are used for maintenance and developing a pronounced multiple stress resistance. Stationary phase physiology of E. coli and other gamma-proteobacteria is mainly determined by RpoS (σs), an alternative sigma subunit of RNA polymerase (RNAP). RpoS, which controls >500 genes in E. coli, is itself regulated at the levels of transcription, translation and proteolysis, with this complex regulatory network acting as a signal integration machinery for a plethora of diverse stress signals. The temporal succession of growth and entry into stationary phase in a liquid planktonic culture translates into a spatial pattern in a macrocolony biofilm – growing flagellated cells are found in the bottom layer and outer colony edges, i.e. close to the nutrient-providing agar, whereas starving, matrix-encased and multiple stress resistant cells populate the upper layer. RpoS is in fact essential for matrix production, since it activates the expression of the transcription factor MlrA, which – together with RpoS-RNAP and a c-di-GMP signaling module (PdeR, DgcM) – activates the expression of CsgD, a biofilm regulator that directly activates the curli genes and indirectly controls cellulose biosynthesis. Moreover, about half of the GGDEF/EAL genes involved in c-di-GMP signaling are under RpoS control.
After clarifying the fundamental principles of RpoS function and its own hugely complex predominantly post-transcriptional regulation, recent work in our group has been addressing the following questions:
- How does RpoS-RNAP – in cooperation with MlrA and YdaM and other DNA-binding factors – activate the csgD promoter?
- How does spatial regulation of RpoS accumulation and activity in a macrocolony biofilm work? Which signals are relevant for RpoS induction and how do the different levels of control of RpoS contribute?
Hengge, R. (2020) Linking bacterial growth, survival and multicellularity - small signaling molecules as triggers and drivers. Curr. Opin. Microbiol. 55: 57-66. doi: 10.1016/J.mib.2020.02.007.
Klauck, G., D.O. Serra, A. Possling, and R. Hengge (2018) Spatial organisation of different sigma factor activities and c-di-GMP signalling within the 3D landscape of a bacterial biofilm. Open Biol. 8: 180066. doi: 10.1098/rsob.180066.
Serra, D.O., and R. Hengge (2014) Stress responses go three-dimensional - the spatial order of physiological differentiation in bacterial macrocolony biofilms. Environ. Microbiol. 16, 1455-1471.
Pesavento, C., and R. Hengge (2012) The global repressor FliZ antagonizes gene expression by sigma-S–containing RNA polymerase due to overlapping DNA binding specificity. Nucl. Acids Res. 40, 4783-4793.
Hengge, R. (2011) The general stress response in Gram-negative bacteria. In: Bacterial Stress Responses (eds. G. Storz and R. Hengge), ASM Press, Washington, D.C., pp. 251-289.
Hengge, R. (2009) Proteolysis of sigma-S (RpoS) and the general stress response in Escherichia coli. Res. Microbiol. 160, 667-676.
Pesavento, C., G. Becker, N. Sommerfeldt, A. Possling, N. Tschowri, A. Mehlis, and R. Hengge (2008) Inverse regulatory coordination of motility and curli-mediated adhesion of E.coli. Genes Dev. 22, 2434-2446.
