Interaction of the RcsB Response Regulator with Auxiliary Transcription Regulators in Escherichia coli

Abstract

The Rcs phosphorelay is a two-component signal transduction system that is induced by cell envelope stress. RcsB, the response regulator of this signaling system, is a pleiotropic transcription regulator, which is involved in the control of various stress responses, cell division, motility, and biofilm formation. RcsB regulates transcription either as a homodimer or together with auxiliary regulators, such as RcsA, BglJ, and GadE in Escherichia coli. In this study, we show that RcsB in addition forms heterodimers with MatA (also known as EcpR) and with DctR. Our data suggest that the MatA-dependent transcription regulation is mediated by the MatA-RcsB heterodimer and is independent of RcsB phosphorylation. Furthermore, we analyzed the relevance of amino acid residues of the active quintet of conserved residues, and of surface-exposed residues for activity of RcsB. The data suggest that the activity of the phosphorylation-dependent dimers, such as RcsA-RcsB and RcsB-RcsB, is affected by mutation of residues in the vicinity of the phosphorylation site, suggesting that a phosphorylation-induced structural change modulates their activity. In contrast, the phosphorylation-independent heterodimers BglJ-RcsB and MatA-RcsB are affected by only very few mutations. Heterodimerization of RcsB with various auxiliary regulators and their differential dependence on phosphorylation add an additional level of control to the Rcs system that is operating at the output level.

Interplay of PhoP and DevR response regulators defines expression of the dormancy regulon in virulent Mycobacterium tuberculosis

“…Heterodimers between RR proteins have now been discovered in multiple instances (52)(53)(54)(55), suggesting that heterodimer formation may be a fundamental mechanism contributing to the concerted regulation of overlapping regulons in M. tuberculosis. We recently elucidated heterodimeric interactions between M. tuberculosis DevR and NarL RRs for co-regulation of gene expression during aerobic nitrate metabolism (22).…”

Rcs Phosphorelay Activation in Cardiolipin-Deficient Escherichia coli Reduces Biofilm Formation

“…The initiation of the Rcs signaling system leads to the phosphorylation of RcsB, enabling it to dimerize and function as a transcriptional regulator (28). Phosphorylated RcsB can also form a heterodimer with the auxiliary protein RcsA (29); the RcsB-RcsB and RcsA-RcsB complexes control the expression of a number of genes involved in acid resistance, as well as the colanic acid and curli synthesis operons, osmotically inducible peroxidase gene osmC, and the small regulatory RNA rprA (30)(31)(32). We found that activation of the Rcs pathway has little or no effect on Δcls cells growing planktonically.…”

Involvement of Two-Component Signaling on Bacterial Motility and Biofilm Development

“…Regulation of flhD requires heterodimer formation of RcsB with the auxiliary protein RcsA, followed by binding to the conserved RcsAB box on the flhD promoter (40). Heterodimer formation can occur with a range of transcriptional regulators (41)(42)(43), often in a way that is unaffected by the phosphorylation state of RcsB (43,44) and instead favored at high concentrations of the protein (45). Altogether, the RcsCDB system has a myriad of functions in E. coli and other members of the family Enterobacteriaceae (9,(46)(47)(48)(49).…”