Department of Clinical Pathology, Cheng Hsin General Hospital, Taipei 11220; Taiwan.
Department of Restaurant, Hotel and Institutional Management, 24205, Fu-Jen Catholic University, New Taipei City 24205, Taiwan.
Int J Mol Sci. 2019 Apr 10;20(7):1770. doi: 10.3390/ijms20071770.
Manganese-dependent superoxide dismutase (MnSOD, SodA) and iron-dependent SOD (FeSOD, SodB) are critical cytosolic enzymes for alleviating superoxide stress. Distinct from the singular gene in most bacteria, harbors two genes, and . The roles of SodA1, SodA2, and SodB of in alleviating superoxide stress were investigated. The expression of genes was determined by promoter- transcriptional fusion assay and qRT-PCR. and expressions were proportional to the bacterial logarithmic growth, but unaffected by menadione (MD), iron, or manganese challenges. SodA1 was intrinsically unexpressed and inducibly expressed by MD. Complementary expression of was observed when was inactivated. The individual or combined deletion mutants were constructed using the gene replacement strategy. The functions of SODs were assessed by evaluating cell viabilities of different mutants in MD, low iron-stressed, and/or low manganese-stressed conditions. Inactivation of SodA1 or SodA2 alone did not affect bacterial viability; however, simultaneously inactivating and significantly compromised bacterial viability in both aerobic growth and stressed conditions. SodA1 can either rescue or support SodA2 when SodA2 is defective or insufficiently potent. The presence of two MnSODs gives an advantage against superoxide stress.
锰依赖型超氧化物歧化酶（MnSOD，SodA）和铁依赖型 SOD（FeSOD，SodB）是缓解超氧自由基应激的重要细胞溶质酶。与大多数细菌中单一的基因不同， 拥有两个基因 和 。研究了 中 SodA1、SodA2 和 SodB 在缓解超氧自由基应激中的作用。通过启动子转录融合测定和 qRT-PCR 确定了基因的表达。基因的表达与细菌对数生长期成正比，但不受 menadione（MD）、铁或锰的挑战影响。SodA1 是固有不表达的，可被 MD 诱导表达。当 失活时，观察到 的互补表达。使用基因替换策略构建了单个或组合的缺失突变体。通过评估不同 突变体在 MD、缺铁和/或缺锰胁迫条件下的细胞存活率来评估 SOD 的功能。单独失活 SodA1 或 SodA2 不会影响细菌活力；然而，同时失活 和 显著降低了有氧生长和应激条件下细菌的活力。当 SodA2 有缺陷或不够有效时，SodA1 可以拯救或支持 SodA2。两种 MnSOD 的存在使 具有对抗超氧自由基应激的优势。
