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S. aureusUSA300 isolates utilize thecopBLandcopAZgene products to prevent Cu intoxication. We created and examined a ΔcopAZΔcopBLmutant strain (cop‐). Thecop‐ strain was sensitive to Cu and accumulated intracellular Cu. We screened a transposon (Tn) mutant library in thecop‐ background and isolated strains with Tn insertions in themntABCoperon that permitted growth in the presence of Cu. The mutations were inmntAand they were recessive. Under the growth conditions utilized, MntABC functioned in manganese (Mn) import. When cultured with Cu, strains containing amntA::Tnaccumulated less Cu than the parent strain. Mn(II) supplementation improved growth whencop‐ was cultured with Cu and this phenotype was dependent upon the presence of MntR, which is a repressor ofmntABCtranscription. A ΔmntRstrain had an increased Cu load and decreased growth in the presence of Cu, which was abrogated by the introduction ofmntA::Tn. Over‐expression ofmntABCincreased cellular Cu load and sensitivity to Cu. The presence of amntA::Tnmutation protected iron‐sulfur (FeS) enzymes from inactivation by Cu. The data presented are consistent with a model wherein defective MntABC results in decreased cellular Cu accumulation and protection to FeS enzymes from Cu poisoning.