A conserved CusR-dependent regulatory pathway couples copper homeostasis with oxidative stress resistance in Klebsiella pneumoniae.

CusR is a pivotal regulator in Klebsiella pneumoniae that coordinates copper homeostasis and oxidative stress defense, with its D56 residue essential for copper efflux control.

• Why it matters: Host copper toxicity also generates oxidative stress, but how bacteria couple copper detoxification to reactive oxygen protection is incompletely understood.
• What they did: CusR loss causes profound copper tolerance defects, intracellular copper accumulation, and hydrogen peroxide hypersensitivity with elevated reactive oxygen species; CusR directly activates cusCFBA via promoter binding, while copA regulation is CusR-independent.
• The result: Substituting CusR D56 on plasmids or chromosomes abolishes copper efflux regulation, disrupts copper homeostasis, and exacerbates oxidative stress susceptibility, supporting a conserved Asp-dependent CusR–CusCFBA axis.

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