The Adc regulon mediates zinc homeostasis in Streptococcus mutans,Molecular Oral Microbiology

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The Adc regulon mediates zinc homeostasis in Streptococcus mutans
Molecular Oral Microbiology ( IF 2.8 ) Pub Date : 2021-08-05 , DOI: 10.1111/omi.12350
Yangyang Pan _{1,

2} , Yang Chen _{1,

3} , Jiamin Chen ₁ , Qizhao Ma _{1,

3} , Tao Gong ₁ , Shuxing Yu _{1,

3} , Qiong Zhang _{1,

3} , Jing Zou _{1,

3} , Yuqing Li ₁

Affiliation

Zinc (Zn²⁺) is an essential divalent trace metal for living cells. Intracellular zinc homeostasis is critical to the survival and virulence of bacteria. Thus, the frequent fluctuations of salivary zinc, caused by the low physiological level and the frequent exogenous zinc introduction, present a serious challenge for bacteria colonizing the oral cavity. However, the regulation strategies to keep intracellular Zn²⁺ homeostasis in Streptococcus mutans, an important causative pathogen of dental caries, are unknown. Because zinc uptake is primarily mediated by an ATP-binding ABC transporter AdcABC in Streptococcus strains, we examined the function of AdcABC and transcription factor AdcR in S. mutans in this study. The results demonstrated that deletion of either adcA or adcCB gene impaired the growth but enhanced the extracellular polymeric matrix production in S. mutans, both of which could be relieved after excessive Zn²⁺ supplementation. Using RNA sequencing analysis, quantitative reverse transcription polymerase chain reaction examination, LacZ-reporter studies, and electrophoretic mobility shift assay, we showed that a MarR (multiple antibiotic resistance regulator) family transcription factor, AdcR, negatively regulates the expression of the genes adcR, adcC, adcB, and adcA by acting on the adcRCB and adcA promoters in response to Zn²⁺ concentration in their environmental niches. The deletion of adcR increases the sensitivity of S. mutans to excessive Zn²⁺ supply. Taken together, our findings suggest that Adc regulon, which consists of a Zn²⁺ uptake transporter AdcCBA and a Zn²⁺-responsive repressor AdcR, plays a prominent role in the maintenance of intracellular zinc homeostasis of S. mutans.

中文翻译：

Adc 调节子介导变形链球菌中的锌稳态

锌 (Zn ²⁺ ) 是活细胞必不可少的二价微量金属。细胞内锌稳态对细菌的存活和毒力至关重要。因此，由于生理水平低和外源性锌的频繁引入导致唾液锌的频繁波动，对口腔定植的细菌提出了严峻的挑战。然而，在变异链球菌（一种重要的龋齿病原体）中保持细胞内 Zn ²⁺稳态的调节策略尚不清楚。因为锌吸收主要由链球菌菌株中的 ATP 结合 ABC 转运蛋白 AdcABC 介导，我们检查了 AdcABC 和转录因子 AdcR 在变形链球菌中的功能在这个研究中。结果表明，adcA或adcCB基因的缺失会损害S. mutans的生长，但会增加细胞外聚合物基质的产生，这两种情况都可以在过量补充Zn ²⁺后得到缓解。使用 RNA 测序分析、定量逆转录聚合酶链反应检测、LacZ 报告基因研究和电泳迁移率变化测定，我们发现 MarR（多重抗生素抗性调节剂）家族转录因子 AdcR 负向调节基因adcR的表达，adcC、adcB和adcA通过作用于adcRCB和adcA启动子响应其环境生态位中的Zn ²⁺浓度。adcR的缺失增加了变形链球菌对过量 Zn ²⁺供应的敏感性。综上所述，我们的研究结果表明，由 Zn ²⁺摄取转运蛋白 AdcCBA 和 Zn ²⁺响应性阻遏物 AdcR组成的 Adc 调节子在维持变形链球菌的细胞内锌稳态中起重要作用。

更新日期：2021-09-14

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