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RcsB, a response regulator of the FixJ/NarL family, is at the center of a complex network of regulatory inputs and outputs. Cell surface stress is sensed by an outer membrane lipoprotein, RcsF, which regulates interactions of the inner membrane protein IgaA, lifting negative regulation of a phosphorelay. In vivo evidence supports a pathway in which histidine kinase RcsC transfers phosphate to phosphotransfer protein RcsD, resulting in phosphorylation of RcsB. RcsB acts either alone or in combination with RcsA to positively regulate capsule synthesis and synthesis of small RNA (sRNA) RprA as well as other genes, and to negatively regulate motility. RcsB in combination with other FixJ/NarL auxiliary proteins regulates yet other functions, independent of RcsB phosphorylation. Proper expression of Rcs and its targets is critical for success of Escherichia coli commensal strains, for proper development of biofilm, and for virulence in some pathogens. New understanding of how the Rcs phosphorelay works provides insight into the flexibility of the two-component system paradigm.
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Supplemental Figure 1. Genomic context for rcs genes
Information was gathered from EcoCyc, the online database collating information about the E. coli genome (4) as well as from other sources. Repressor proteins are shown in red boxes around promoters and transcriptional activators are shown in green boxes. Promoter sites are marked with verified sigma factor requirements (bold) or presumed sigma factor usage (regular text). rcsD (previously yojN) and rcsB are in an operon convergent with the rcsC operon, separated by repetitive sequences. Mapped promoters for rcsB include two in the 3′ end of rcsD, and the promoter that allows expression of both rcsD and rcsB, shown to be repressed by H-NS via direct protein binding (5). The rcsC promoter has not been mapped, but as the nearest gene (atoS) is divergent, it is presumed to be monocistronic. igaA (yrfF) is shown with two presumed σ70 promoters and genes that are co-cistronic in Salmonella (2). Genes yrfG, HslR, and HslO have mapped σ32 (σH) promoters (7). rcsA is monocistronic, with a mapped promoter activated by RcsAB (1) and GadE (3) and repressed by H-NS at an unknown binding site (6). rcsF is shown in an operon with trmO, also known as tsaA, encoding a tRNA modifying enzyme.
References:
1. Ebel W, Trempy JE. 1999. Escherichia coli RcsA, a positive activator of colanic acid capsular polysaccharide synthesis, functions to activate its own expression. J. Bacteriol. 181:577-84
2. Garcĺa-Calderón CB, Casadesús J, Francisco RM. 2009. Regulation of igaA and the rcs system by the mviaresponse regulator in salmonella enterica. Journal of Bacteriology 191:2743-52
3. Hommais F, Krin E, Coppee JY, Lacroix C, Yeramian E, et al. 2004. GadE (YhiE): a novel activator involved in the response to acid environment in Escherichia coli. Microbiology 150:61-72
4. Keseler IM, Mackie A, Santos-Zavaleta A, Billington R, Bonavides-Martinez C, et al. 2017. The EcoCyc database: reflecting new knowledge about Escherichia coli K-12. Nucleic Acids Research 45:D543-D50
5. Krin E, Danchin A, Soutourina O. 2010. Decrypting the H-NS-dependent regulatory cascade of acid stress resistance in Escherichia coli. BMC Mcirobiology 10:273
6. Sledjeski D, Gottesman S. 1995. A small RNA acts as an antisilencer of the H-NS-silenced rcs Agene of Escherichia coli. Proc. Natl. Acad. Sci. USA 92:2003-7
7. Wade JT, Roa DC, Grainger DC, Hurd D, Busby SJW, et al. 2006. Extensive functional overlap between σ factors in Escherichia coli. Nat Struct Mol Biol 13:806-14
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