Psr is involved in regulation of glucan production, and double deficiency of BrpA and Psr is lethal in Streptococcus mutans
Psr is involved in regulation of glucan production, and double deficiency of BrpA and Psr is lethal in Streptococcus mutans
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DOI：
10.1099/mic.0.063032-0
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发表时间：
2013-03-01
期刊：
影响因子：
2.8
通讯作者：
Wen, Zezhang T.
中科院分区：
文献类型：
--
作者：
Bitoun, Jacob P.;Liao, Sumei;Wen, Zezhang T.
变形链球菌是龋齿的主要致病菌，含有分别由 brpA 和 psr 编码的 LytR-CpsA-Psr 家族蛋白的两个旁系同源物。先前的研究表明，BrpA 在细胞被膜生物发生/稳态中发挥重要作用，并影响链球菌的应激反应和生物膜形成。变形菌，这种细菌的致龋性至关重要的特征。在本研究中，构建了 Psr 缺陷突变体 TW251。 TW251 的表征表明，Psr 的缺乏对生长速率没有任何重大影响。然而，当在pH 2.8下进行酸灭活时，TW251的存活率与亲本菌株UA159相比急剧下降。此外，TW251 在生物膜形成方面也表现出重大缺陷，尤其是在蔗糖生长过程中。与UA159相比，TW251的生物膜主要是平面的并且缺乏细胞外葡聚糖。实时 PCR 和蛋白质印迹分析表明，Psr 缺陷显着降低了葡萄糖基转移酶 C 的表达，葡萄糖基转移酶 C 是一种已知在链球菌生物膜形成中起主要作用的蛋白质。突变体。透射电子显微镜分析表明，BrpA 的缺陷导致细胞包膜和细胞分裂的改变，并且在 Psr 缺陷和 BrpA 下调突变体 TW314 中观察到最显着的缺陷。在类似条件下，Psr 突变体 TW251 没有观察到这种效应。这些结果表明，虽然 BrpA 和 Psr 之间在功能上存在相似之处，但这两个旁系同源物之间也存在明显的差异。与枯草芽孢杆菌一样，但与金黄色葡萄球菌不同，链球菌的生存需要功能性 BrpA 或 Psr。突变体。
Streptococcus mutans, the primary causative agent of dental caries, contains two paralogues of the LytR-CpsA-Psr family proteins encoded by brpA and psr, respectively. Previous studies have shown that BrpA plays an important role in cell envelope biogenesis/homeostasis and affects stress responses and biofilm formation by Strep. mutans, traits critical to cariogenicity of this bacterium. In this study, a Psr-deficient mutant, TW251, was constructed. Characterization of TW251 showed that deficiency of Psr did not have any major impact on growth rate. However, when subjected to acid killing at pH 2.8, the survival rate of TW251 was decreased dramatically compared with the parent strain UA159. In addition, TW251 also displayed major defects in biofilm formation, especially during growth with sucrose. When compared to UA159, the biofilms of TW251 were mainly planar and devoid of extracellular glucans. Real-time-PCR and Western blot analyses revealed that deficiency of Psr significantly decreased the expression of glucosyltransferase C, a protein known to play a major role in biofilm formation by Strep. mutans. Transmission electron microscopy analysis showed that deficiency of BrpA caused alterations in cell envelope and cell division, and the most significant defects were observed in TW314, a Psr-deficient and BrpA-down mutant. No such effects were observed with Psr mutant TW251 under similar conditions. These results suggest that while there are similarities in functions between BrpA and Psr, distinctive differences also exist between these two paralogues. Like Bacillus subtilis but different from Staphylococcus aureus, a functional BrpA or Psr is required for viability in Strep. mutans.