The Streptococcus mutans Serine/Threonine Kinase, PknB, Regulates Competence Development, Bacteriocin Production, and Cell Wall Metabolism

The Streptococcus mutans Serine/Threonine Kinase, PknB, Regulates Competence Development, Bacteriocin Production, and Cell Wall Metabolism
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DOI:
10.1128/iai.01167-09
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发表时间:
2010-05-01
影响因子:
3.1
通讯作者:
van der Ploeg, Jan R.
van der Ploeg, Jan R.
中科院分区:
医学2区
文献类型:
--
作者:
Banu, Liliana Danusia;Conrads, Georg;van der Ploeg, Jan R.

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细菌可以通过使用双组分系统(TCS)和丝氨酸苏氨酸激酶和磷酸酶来检测、传递和反应来自外部世界的信号。变形链球菌含有一个丝氨酸苏氨酸激酶,由pKnB编码。编码丝氨酸-苏氨酸磷酸酶PPPL的基因位于pKnB的上游。本研究对pKnB和PPPL单突变体以及一株pKnB PPPL双突变体的表型进行了研究。所有突变体都表现出遗传转化能力和生物膜形成的降低,细胞形状异常,在几种复杂的介质中生长慢于野生型菌株,并表现出耐酸性降低。突变体降低了致龋性,但在大鼠龋齿模型中没有明显的定植缺陷。全基因组转录组分析显示,pounB突变体与细菌素生产和遗传能力相关的基因表达降低。在突变体中差异调控的基因中,有几个可能参与了细胞壁的新陈代谢。其中一个这样的基因SMU 2146c和两个编码细菌素的基因在一个Vick突变体中也被下调,该突变体编码一种参与氧化应激反应的传感器激酶。综上所述,这些结果使我们推测PKnB可能调节双组分信号转导系统VicKR和ComDE的活性。实时逆转录聚合酶链式反应(RT-PCR)结果显示,突变体中下调的基因在PPPL突变体中表达上调,表明PPPL起到了抑制PuncB的作用。
Bacteria can detect, transmit, and react to signals from the outside world by using two-component systems (TCS) and serine-threonine kinases and phosphatases. Streptococcus mutans contains one serine-threonine kinase, encoded by pknB. A gene encoding a serine-threonine phosphatase, pppL, is located upstream of pknB. In this study, the phenotypes of pknB and pppL single mutants and a pknB pppL double mutant were characterized. All mutants exhibited a reduction in genetic transformability and biofilm formation, showed abnormal cell shapes, grew slower than the wild-type strain in several complex media, and exhibited reduced acid tolerance. The mutants had reduced cariogenic capacity but no significant defects in colonization in a rat caries model. Whole-genome transcriptome analysis revealed that a pknB mutant showed reduced expression of genes involved in bacteriocin production and genetic competence. Among the genes that were differentially regulated in the pknB mutant, several were likely to be involved in cell wall metabolism. One such gene, SMU.2146c, and two genes encoding bacteriocins were shown to also be downregulated in a vicK mutant, which encodes a sensor kinase involved in the response to oxidative stress. Collectively, the results lead us to speculate that PknB may modulate the activity of the two-component signal transduction systems VicKR and ComDE. Real-time reverse transcriptase PCR (RT-PCR) showed that genes downregulated in the pknB mutant were upregulated in the pppL mutant, indicating that PppL serves to counteract PknB.