第二信使分子c-di-AMP调控细菌中钾离子转运的机制

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.