摘要
钾离子(K^+)是维持生命体存活的必需元素。原核生物进化出一系列K^+转运系统,如Kdp系统﹑Ktr系统和Trk系统等,来维持胞内相对恒定的K^+浓度。环二腺苷酸单磷酸(cyclic diadenosine monophosphate,c-di-AMP)是新发现的第二信使分子,可以与K^+转运系统中的KdpD、KtrA和TrkA结合。当胞内c-di-AMP浓度高时,c-di-AMP会与K^+转运蛋白结合,降低其转运活性。c-di-AMP的靶标除蛋白质外,还有RNA元件,即c-di-AMP的核糖开关。高浓度的c-di-AMP与其核糖开关结合后,可抑制下游K^+转运蛋白编码基因,如kdp、ktr和trk操纵子以及kup基因的转录,从而调控K^+的转运。总之,胞内高浓度的c-di-AMP抑制细菌对K^+的吸收。c-di-AMP调控K^+转运机制的研究,不仅丰富了K^+转运的调控方式,而且也扩大了c-di-AMP的调控范围,为细菌的利用与防治提供了新思路。
Potassium ion （K^＋） is a ubiquitous monovalent cation necessary for all living cells. To maintain homeostatic intracellular K^＋ concentration, most prokaryotes possess several unique K^＋ uptake systems to transport K^＋. A newly found second messenger--cyclic diadenosine monophosphate （c-di-AMP）, plays an important role in regulating K^＋ transport by binding to several K^＋ transport-related proteins, such as KdpD, KtrA and TrkA. When the intracellular c-di-AMP concentration is high, c-di-AMP can bind its receptor or effector proteins to inhibit transporter activity. In addition, riboswitch could also be targeted by c-di-AMP to control the transcription of downstream K^＋ transporter genes, including ktr, trk and kdp operon and kup gene. High intracellular c-di-AMP concentration depresses bacterial K^＋ uptake. Therefore, understanding the mechanism of K^＋ transport inhibition by c-di-AMP not only enriches the regulation mode of the K^＋ transport, but also sparkle new ideas for the control and applications of bacteria.
作者
蔡霞
何进
Xia Cai Jin He(State Key Laboratory of Agricultural Microbiology, College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, Hubei Province, Chin)
出处
《微生物学报》
CAS
CSCD
北大核心
2017年第10期1434-1442,共9页
Acta Microbiologica Sinica
基金
国家自然科学基金(31270105)
中央高校基本科研专科基金(2662015PY175)~~
