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. 2022 Sep 26;11(19):2995. doi: 10.3390/cells11192995

Figure 1.

Figure 1

Summarised colistin resistance mechanism associated with MgrB inactivation in Klebsiella pneumoniae. PhoQ is stimulated by low extracellular cationic magnesium or cationic antimicrobial peptides (CAMPs) under low pH conditions, leading to increased PhoP phosphorylation. This, in turn, drives the transcription of mgrB. The accumulation of MgrB results in a negative feedback loop to inhibit the kinase activity of PhoQ, which subsequently suppresses PhoP phosphorylation. Mutations (denoted by red-coloured thunder symbols) in mgrB or MgrB inactivation disrupting the PhoP/PhoQ pathway eliminates this partial adaptation. The disruption of mgrB can mediate the activation of the arnBCADTEF operon for the addition of L-Ara4N to lipid A. Phosphorylated PhoP can also directly activate the arnBCADTEF operon without other PmrA/PmrB-activated proteins in K. pneumoniae. OM, outer membrane; CM, cytoplasmic membrane, LPS, lipopolysaccharide, L-Ara4N, 4-amino-4-deoxy-L-arabinose. (Created with BioRender.com, accessed on 16 August 2022).