Copper efflux regulator CsoR is involved in the regulation of ycnJ expression, leading to a new model for copper homeostasis in B. subtilis. CsoR from Bacillus subtilis, which is encoded upstream of the copZA operon, is 37% homologous to M. tuberculosis CsoR, and elevated copper levels in B. subtilis are sensed by CsoR, which leads to derepression of the copZA copper efflux operon. Under low intracellular Cu⁺ conditions, CsoR binds to promoter regions of copper efflux genes and represses their transcription. When Cu⁺ levels rise, Cu⁺ binds directly to CsoR, causing it to release from DNA, thereby derepressing genes involved in copper efflux and sequestration. The copper ion (Cu⁺) effector pathway is a bacterial homeostasis and detoxification system that protects cells from the toxic effects of excess monovalent copper (Cu⁺) while ensuring its availability for essential enzymatic functions. This pathway is regulated by CsoR (Copper-sensitive operon Repressor), a Cu⁺-responsive transcriptional regulator. Key components of the CsoR regulog include: csoR – Encodes the CsoR transcriptional repressor itself, forming part of a feedback loop that maintains copper homeostasis by sensing and responding to intracellular Cu⁺ concentrations. copA – Encodes a P-type ATPase copper efflux pump, which actively exports excess Cu⁺ from the cytoplasm to prevent toxicity. copZ – Encodes a copper chaperone protein that binds and safely delivers Cu⁺ to target proteins or to CopA for efflux, preventing uncontrolled copper-mediated redox reactions and oxidative damage.

Copper ion, (Cu+) - CsoR References