Streptococcus mutans copper chaperone, CopZ, is critical for biofilm formation and competitiveness.

Streptococcus mutans copper chaperone, CopZ, is critical for biofilm formation and competitiveness.
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DOI:
10.1111/omi.12150
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发表时间:
2016-12
影响因子:
3.7
通讯作者:
Wu H
Wu H
中科院分区:
医学3区
文献类型:
--
作者:
Garcia SS;Du Q;Wu H

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口腔是一个动态的环境,其特征是数百种细菌,唾液以及营养物质和金属离子(如铜)的流入。虽然唾液中存在生理水平的铜,但口腔经常受到铜离子流入的挑战。在高浓度下,铜是有毒的,因此必须受到病原体的严格管制,以便持续存在并引起疾病。致龋病原体变形链球菌使用编码负DNA结合阻遏物(CopY)的copYAZ操纵子、P1-ATP酶铜输出蛋白(CopA)和铜分子伴侣(CopZ)来管理过量的铜。copYAZ操纵子在调控和铜转运到受体中的这些假设作用使我们研究了它们对S.变形杆菌的毒性。突变缺陷的铜伴侣CopZ,但不是CopY或CopA,受损的生物膜形成和竞争力对链球菌。CopZ突变体生物膜的表征揭示了葡萄糖基转移酶的分泌减少和突变蛋白基因的表达减少。这些数据表明,CopZ对生物膜和竞争力的功能是独立的铜抗性和CopZ是生物膜和其他毒力因子的全局调节剂。CopZ的进一步表征可能导致新的生物膜途径的鉴定。
The oral cavity is a dynamic environment characterized by hundreds of bacterial species, saliva, and an influx of nutrients and metal ions such as copper. While there is a physiologic level of copper in the saliva, the oral cavity is often challenged with an influx of copper ions. At high concentrations copper is toxic and must therefore be strictly regulated by pathogens in order to persist and cause disease. The cariogenic pathogen Streptococcus mutans manages excess copper using the copYAZ operon that encodes a negative DNA-binding repressor (CopY), the P1-ATPase copper exporter (CopA), and the copper chaperone (CopZ). These hypothetical roles of the copYAZ operon in regulation and copper transport to receptors led us to investigate their contribution to S. mutans virulent properties. Mutants defective in the copper chaperone CopZ, but not CopY or CopA, were impaired in biofilm formation and competitiveness against commensal streptococci. Characterization of the CopZ mutant biofilm revealed a decreased secretion of glucosyltransferases and reduced expression of mutacin genes. These data suggest that the function of copZ on biofilm and competitiveness is independent of copper resistance and CopZ is a global regulator for biofilm and other virulence factors. Further characterization of CopZ may lead to the identification of new biofilm pathways.
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