中文摘要：研究分析了基因组删减肺炎支原体的c-di-AMP信号通路。结果表明，所分析的肺炎支原体能够产生c-di-AMP，并能检测到二腺苷酸环化酶CdaM（MPN244），这种酶是二腺苷酸环化酶的新家族成员。在两种可降解磷酸二酯酶中，只有PdeM (MPN549)在c-di-AMP的分解过程中发挥作用。已有报道提出NrnA (MPN140)能够分解短链寡核糖核苷酸。研究进一步从肺炎支原体中分离得到c-di-AMP绑定蛋白KtrC。KtrC是低亲和力钾转运蛋白KtrCD的胞质调节亚单元。结果表明，c-di-AMP的绑定过程抑制了KtrCD的活性，最终限制了钾的吸收。本研究表明，控制钾稳态是肺炎支原体c-di-AMP的重要功能。
 
外文摘要：Bacteria often use cyclic dinucleotides as second messengers for signal transduction. While the classical molecule c-di-GMP is involved in lifestyle selection, the functions of the more recently discovered signaling nucleotide cyclic di-AMP are less defined. For many Gram-positive bacteria, c-di-AMP is essential for growth suggesting its involvement in a key cellular function. We have analyzed c-di-AMP signaling in the genome-reduced pathogenic bacterium Mycoplasma pneumoniae. Our results demonstrate that these bacteria produce c-di-AMP, and we could identify the diadenylate cyclase CdaM (MPN244). This enzyme is the founding member of a novel family of diadenylate cyclases. Of two potential c-di-AMP degrading phosphodiesterases, only PdeM (MPN549) is active in c-di-AMP degradation, whereas NrnA (MPN140) was reported to degrade short oligoribonucleotides. As observed in other bacteria, both the c-di-AMP synthesizing and the degrading enzymes are essential for M. pneumoniae suggesting control of a major homeostatic process. To obtain more insights into the nature of this process, we have identified a c-di-AMP-binding protein from M. pneumoniae, KtrC. KtrC is the cytoplasmic regulatory subunit of the low affinity potassium transporter KtrCD. It is established that binding of c-di-AMP inhibits the KtrCD activity resulting in a limitation of potassium uptake. Our results suggest that the control of potassium homeostasis is the essential function of c-di-AMP in M. pneumoniae.
外文关键词：second messenger； diadenylate cyclase； phosphodiesterase； c-di-AMP； potassium uptake； Mollicutes
作者：Blotz, C; Treffon, K; Kaever, V; Schwede, F; Hammer, E; Stulke, J
作者单位：德国哥廷根大学
期刊名称：FRONTIERS IN MICROBIOLOGY
期刊影响因子：4.076
出版年份：2017
出版刊次：7
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