Induction of clpP expression by cell-wall targeting antibiotics in Streptococcus mutans.
Induction of clpP expression by cell-wall targeting antibiotics in Streptococcus mutans.
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变形链球菌细胞壁靶向抗生素诱导 clpP 表达。
DOI：
10.1099/mic.0.000920
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Biswas,Indranil
中科院分区：
文献类型：
--
作者：
Khara,Pratick;Biswas,Saswati;Biswas,Indranil
变形链球菌是人类口腔中与龋齿相关的主要细菌之一。这种细菌的致病性归因于其快速反应和适应口腔不断变化的条件的能力。这种适应性反应的主要参与者是ClpP，一种在应激反应期间参与降解错误折叠蛋白质的细胞内蛋白酶。突变体编码的erse lpP基因的上游区域唯一地含有多个串联重复序列（RS）。在这里，我们探讨了clpP的表达与各种压力，并报告了一些新的发现。首先，我们发现在亚抑制浓度下，某些细胞壁损伤抗生素能够诱导lpP表达。具体来说，第三代和第四代头孢菌素的目标青霉素结合蛋白3（PBP 3）强烈增强的lpP表达。然而，当使用对PBP 3具有较低亲和力的第一代头孢菌素时，clpP的诱导较弱。令人惊讶的是，主要靶向PBP 2的碳青霉烯类诱导clpP的表达最少。其次，我们发现单个RS元件能够像野生型的7个RS元件一样有效地诱导clpP表达。第三，我们发现RS元件介导的clpP表达的调节是菌株依赖性的，这表明特定的宿主因子可能参与了clpP的转录。最后，我们观察到ClpP调节其自身的表达，因为在aclpP缺陷的突变体中clpP-gusA的表达更高。这表明ClpP参与参与其自身转录的激活剂的降解。
Streptococcus mutansis one of the major bacteria of the human oral cavity that is associated with dental caries. The pathogenicity of this bacterium is attributed to its ability to rapidly respond and adapt to the ever-changing conditions of the oral cavity. The major player in this adaptive response is ClpP, an intracellular protease involved in degradation of misfolded proteins during stress responses.S. mutansencodes a singleclpPgene with an upstream region uniquely containing multiple tandem repeat sequences (RSs). Here, we explored expression ofclpPwith respect to various stresses and report some new findings. First, we found that at sub-inhibitory concentration, certain cell-wall damaging antibiotics were able to induceclpPexpression. Specifically, third- and fourth-generation cephalosporins that target penicillin-binding protein 3 (PBP3) strongly enhanced theclpPexpression. However, induction ofclpPwas weak when the first-generation cephalosporins with lower affinity to PBP3 were used. Surprisingly, carbapenems, which primarily target PBP2, induced expression ofclpPthe least. Second, we found that a single RS element was capable of inducingclpPexpression as efficiently as with the wild-type seven RS elements. Third, we found that the RS-element-mediated modulation ofclpPexpression was strain dependent, suggesting that specific host factors might be involved in the transcription. And finally, we observed that ClpP regulates its own expression, as the expression ofclpP-gusAwas higher in aclpP-deficient mutant. This suggests that ClpP is involved in the degradation of activator(s) involved in its own transcription.
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DOI：
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发表时间：
1988
期刊：
Reviews of infectious diseases
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DOI：
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1986
期刊：
The Journal of infectious diseases
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DOI：
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发表时间：
1986
期刊：
Journal of General Microbiology
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K. Knox;L. Hardy;A. J. Wicken
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