Role of the Rcs Phosphorelay in Intrinsic Resistance to Penicillin, Phosphomycin, and Cefsulodin in Escherichia coli K12

The Regulator of Capsule Synthesis (Rcs) of Escherichia coli detects cell wall stress and elicits a stress response. The Rcs phosphorelay system consists of the outer membrane kinase sensor RcsF, the inner membrane kinases RcsC and RcsD, and then response regulator RcsB. RcsB regulates the transcription of rprA, a non-coding RNA which affects the translation and stability of multiple mRNAs. Prior studies reported that RcsB is critical for resistance against cell wall antibiotics. Conversely, other studies found that a ΔrcsB strain did not alter resistance to the tested cell wall antibiotics. In this study, we attempted to replicate the experiments that demonstrate RcsB as a critical factor for resistance against cell wall antibiotics such as penicillin, phosphomycin, and cefsulodin. Additionally, we utilized the more sensitive plating efficiency assay to discern any differences in strain sensitivity. We show that deletion of RcsB does not lead to decreased antibiotic resistance. Our findings suggest that RcsB is not essential for resistance to antibiotics targeting the cell wall. We further propose that the loss of Rcs function to
cell wall stress may be compensated by other pathways such as the Cpx pathway, which also regulates rprA.