国家自然科学基金(31270105);中央高校基本科研专科基金(2662015PY175)
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。
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.
蔡霞,何进. 第二信使分子c-di-AMP调控细菌中钾离子转运的机制[J]. 微生物学报, 2017, 57(10): 1434-1442
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