第二信使分子c-di-AMP调控细菌中钾离子转运的机制

Second messenger c-di-AMP regulates potassium ion transport in bacteria

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 diadenosinemonophosphate，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。

Abstract:

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.