Therefore, microorganisms have evolved efficient mechanisms to maintain metal ion homeostasis. The uptake of metal ions is controlled by the ferric uptake regulator or the Diphtheria toxin repressor family of proteins. The Fur superfamily comprises different proteins with distinct regulatory roles. Manganese is a trace element that is essential for many cellular functions in all organisms. For example, Mn2+ is required as a cofactor for super-oxide dismutase, which is critical for preventing cellular oxidative stress. However, high manganese levels inhibit calcium influx and promote the exchange of accumulated Ca2+, and inhibit RNA and protein synthesis. Thus, maintaining metal ion homeostasis is necessary for all organisms. D. radiodurans is well known for its extreme resistance to radiation and oxidants and its high intracellular Mn/Fe ratio is an important factor that contributes to this resistance. In this study, we identified a unique Mur homolog that is encoded by dr0865, and data showed that it is Mn2+-specific regulator. The RNA-seq data identified 562 genes that showed at least a twofold change in expression between the Mt-0865 mutant and the wild-type R1 strain, which indicates that these genes were regulated by dr0865 either through direct or indirect mechanisms. Using the Kyoto Encyclopedia of Genes and Genomes database, we found that genes involved in metabolic pathways, the biosynthesis of secondary metabolites, oxidative phosphorylation and nitrogen metabolism were significantly repressed in the mutant strain. This indicates that the Mt-0865 mutant is likely to suffer more cellular damage under Mn2+ stress than the wild-type strain. This phenomenon may be caused by higher Mn2+ levels in the mutant, which would increase ROS levels and lead to DNA damage. Copper is an essential metal but is toxic at high doses. Elevated copper contamination levels resulting from human activities have been widely documented. Currently, the field of toxicology is moving away from the measurement of single endpoints and toward measurements of how organisms respond to toxic exposures at the cellular level. Similarly, copper toxicology is moving from studying conditions of acute toxicity and toward investigating how organisms respond to copper toxicity. Copper toxicity results from the accumulation of oxidative damage generated by reactive oxygen species via Fenton-like reaction processes. Therefore, the induction of antioxidant enzymes is an important protective mechanism that minimizes organisms’ oxidative damage from copper. The central LY2109761 TGF-beta inhibitor objective of treating cancer is to kill cancerous tissue while leaving healthy tissue intact. Effective cancer drugs must therefore distinguish between cancer cells and healthy cells. Additionally, optimal cancer treatment should also be robust to biological variability such as tumor and healthy cell heterogeneity.