Streptomyces coelicolor is a soil-dwelling bacterium that is medically important due to its ability to produce several antibiotics, and nickel accumulation within this organism has been shown to prevent the production of the antibiotic undecylprodigiosin. The transcriptional repressor important in regulation of nickel uptake is the homodimeric Nur. Under nickel-sufficient conditions, Nur binds Ni²⁺ ions, undergoes a conformational change, and binds to DNA to repress transcription of nickel uptake genes. When intracellular Ni²⁺ is limited, Nur repression is lifted, allowing expression of nickel transporters to restore optimal levels. The nickel ion (Ni²⁺) effector pathway is essential for regulating nickel homeostasis in bacteria, ensuring the proper uptake of this important but potentially toxic trace metal. This pathway is regulated by Nur (Nickel uptake regulator), a Ni²⁺-responsive transcriptional repressor that controls the expression of genes involved in nickel transport and homeostasis. Key genes in the Nur regulog include: nikA – Encodes the periplasmic nickel-binding protein of the high-affinity NikABCDE ABC transporter system, which captures nickel ions and delivers them to the transporter. nikB, nikC, nikD, nikE – These genes encode the membrane-spanning and ATPase components of the NikABCDE transporter complex. Together, they form a high-affinity nickel uptake system that imports Ni²⁺ across the membrane into the cytoplasm.

Nickel ion, (Ni2+) (Limited Info Operon) References