Ethanolamine Activates a Sensor Histidine Kinase Regulating Its Utilization in Enterococcus faecalis
Ethanolamine Activates a Sensor Histidine Kinase Regulating Its Utilization in Enterococcus faecalis
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DOI：
10.1128/jb.00952-08
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发表时间：
2008-11-01
影响因子：
3.2
通讯作者：
Perego, Marta
中科院分区：
文献类型：
--
作者：
Del Papa, Maria Florencia;Perego, Marta
粪肠球菌是一种人体肠道的革兰氏阳性共生细菌。它的机会致病性因获得多种抗生素耐药性而增强，使肠球菌感染的治疗成为一个日益困难的问题。这种生物在各种各样的生态位中定居和生存的非凡能力至少部分归因于双组分系统（TCS）介导的信号转导途径。在这里，粪肠杆菌利用乙醇胺作为唯一碳源的能力取决于RR-HK17 (EF1633-EF1632) TCS。乙醇胺是人类肠道中丰富的化合物，因此，细菌利用乙醇胺作为碳和氮来源的能力可能为生存和定植提供了优势。反应调节因子RR17突变菌株在含有乙醇胺的合成培养基中停止了粪肠球菌的生长。乙醇胺的存在诱导了应答调节基因的转录。乙醇胺在体外诱导HK17传感器组氨酸激酶的自磷酸化速率增加15倍，表明这是该激酶传感器结构域识别的配体。这些结果表明，RR-HK17 TCS作为肠球菌对细菌入侵部位（动物宿主肠道）存在的特定营养条件的反应的协调者。
Enterococcus faecalis is a gram-positive commensal bacterium of the human intestinal tract. Its opportunistic pathogenicity has been enhanced by the acquisition of multiple antibiotic resistances, making the treatment of enterococcal infections an increasingly difficult problem. The extraordinary capacity of this organism to colonize and survive in a wide variety of ecological niches is attributable, at least in part, to signal transduction pathways mediated by two-component systems (TCS). Here, the ability of E. faecalis to utilize ethanolamine as the sole carbon source is shown to be dependent upon the RR-HK17 (EF1633-EF1632) TCS. Ethanolamine is an abundant compound in the human intestine, and thus, the ability of bacteria to utilize it as a source of carbon and nitrogen may provide an advantage for survival and colonization. Growth of E. faecalis in a synthetic medium with ethanolamine was abolished in the response regulator RR17 mutant strain. Transcription of the response regulator gene was induced by the presence of ethanolamine. Ethanolamine induced a 15-fold increase in the rate of autophosphorylation in vitro of the HK17 sensor histidine kinase, indicating that this is the ligand recognized by the sensor domain of the kinase. These results assign a role to the RR-HK17 TCS as coordinator of the enterococcal response to specific nutritional conditions existing at the site of bacterial invasion, the intestinal tract of an animal host.