S. aureus USA300 isolates utilize the copBL and copAZ gene products to prevent Cu intoxication. We created and examined a ΔcopAZ ΔcopBL mutant strain (cop‐). The cop‐ strain was sensitive to Cu and accumulated intracellular Cu. We screened a transposon (Tn) mutant library in the cop‐ background and isolated strains with Tn insertions in the mntABC operon that permitted growth in the presence of Cu. The mutations were in mntA and they were recessive. Under the growth conditions utilized, MntABC functioned in manganese (Mn) import. When cultured with Cu, strains containing a mntA::Tn accumulated less Cu than the parent strain. Mn(II) supplementation improved growth when cop‐ was cultured with Cu and this phenotype was dependent upon the presence of MntR, which is a repressor of mntABC transcription. A ΔmntR strain had an increased Cu load and decreased growth in the presence of Cu, which was abrogated by the introduction of mntA::Tn. Over‐expression of mntABC increased cellular Cu load and sensitivity to Cu. The presence of a mntA::Tn mutation 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.

中文翻译：

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缺乏功能性MntABC锰输入系统的金黄色葡萄球菌对铜的抗性增加

S. aureus USA300 分离株利用copBL和copAZ基因产物来防止铜中毒。我们创建并检查了一个 Δ copAZ Δ copBL突变菌株 ( cop ‐)。cop-菌株对铜敏感，并在细胞内积累铜。我们在cop - 背景中筛选了一个转座子 (Tn) 突变体库，并分离了在mntABC操纵子中插入 Tn 的菌株，这些菌株允许在 Cu 存在下生长。突变在mntA中并且是隐性的。在所利用的生长条件下，MntABC 在锰 (Mn) 输入中起作用。当用 Cu 培养时，菌株含有mntA::Tn积累的铜比母株少。当cop-与 Cu 一起培养时， Mn(II) 的补充改善了生长，这种表型取决于 MntR 的存在，MntR 是mntABC转录的阻遏物。在存在 Cu 的情况下， Δ mntR菌株具有增加的 Cu 负载和减少的生长，这被引入mntA::Tn所消除。mntABC的过表达增加了细胞的铜负荷和对铜的敏感性。mntA::Tn的存在突变保护铁硫 (FeS) 酶免于被 Cu 失活。提供的数据与模型一致，其中有缺陷的 MntABC 导致细胞 Cu 积累减少和对 FeS 酶免受铜中毒的保护。