Suppr超能文献

鲍曼不动杆菌对锌饥饿的反应

The Response of Acinetobacter baumannii to Zinc Starvation.

作者信息

Nairn Brittany L, Lonergan Zachery R, Wang Jiefei, Braymer Joseph J, Zhang Yaofang, Calcutt M Wade, Lisher John P, Gilston Benjamin A, Chazin Walter J, de Crécy-Lagard Valerie, Giedroc David P, Skaar Eric P

机构信息

Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Department of Chemistry, Indiana University, Bloomington, IN 47405, USA.

出版信息

Cell Host Microbe. 2016 Jun 8;19(6):826-36. doi: 10.1016/j.chom.2016.05.007.

Abstract

Zinc (Zn) is an essential metal that vertebrates sequester from pathogens to protect against infection. Investigating the opportunistic pathogen Acinetobacter baumannii's response to Zn starvation, we identified a putative Zn metallochaperone, ZigA, which binds Zn and is required for bacterial growth under Zn-limiting conditions and for disseminated infection in mice. ZigA is encoded adjacent to the histidine (His) utilization (Hut) system. The His ammonia-lyase HutH binds Zn very tightly only in the presence of high His and makes Zn bioavailable through His catabolism. The released Zn enables A. baumannii to combat host-imposed Zn starvation. These results demonstrate that A. baumannii employs several mechanisms to ensure bioavailability of Zn during infection, with ZigA functioning predominately during Zn starvation, but HutH operating in both Zn-deplete and -replete conditions to mobilize a labile His-Zn pool.

摘要

锌(Zn)是一种必需金属,脊椎动物会从病原体中摄取锌以预防感染。在研究机会致病菌鲍曼不动杆菌对锌饥饿的反应时,我们鉴定出一种假定的锌金属伴侣蛋白ZigA,它能结合锌,并且在锌限制条件下对细菌生长以及在小鼠体内的播散性感染都是必需的。ZigA与组氨酸(His)利用(Hut)系统相邻编码。组氨酸氨裂解酶HutH仅在高浓度组氨酸存在时才能非常紧密地结合锌,并通过组氨酸分解代谢使锌具有生物可利用性。释放出的锌使鲍曼不动杆菌能够对抗宿主造成的锌饥饿。这些结果表明,鲍曼不动杆菌采用多种机制来确保感染期间锌的生物可利用性,其中ZigA主要在锌饥饿期间发挥作用,而HutH在锌缺乏和充足的条件下均起作用,以调动不稳定的组氨酸-锌池。

相似文献

1
The Response of Acinetobacter baumannii to Zinc Starvation.
Cell Host Microbe. 2016 Jun 8;19(6):826-36. doi: 10.1016/j.chom.2016.05.007.
2
The Acinetobacter baumannii Znu System Overcomes Host-Imposed Nutrient Zinc Limitation.
Infect Immun. 2019 Nov 18;87(12). doi: 10.1128/IAI.00746-19. Print 2019 Dec.
4
Multi-metal Restriction by Calprotectin Impacts De Novo Flavin Biosynthesis in Acinetobacter baumannii.
Cell Chem Biol. 2019 May 16;26(5):745-755.e7. doi: 10.1016/j.chembiol.2019.02.011. Epub 2019 Mar 21.
5
Acinetobacter baumannii response to host-mediated zinc limitation requires the transcriptional regulator Zur.
J Bacteriol. 2014 Jul;196(14):2616-26. doi: 10.1128/JB.01650-14. Epub 2014 May 9.
6
Histidine Utilization Is a Critical Determinant of Pathogenesis.
Infect Immun. 2020 Jun 22;88(7). doi: 10.1128/IAI.00118-20.
9
Coupling of zinc and GTP binding drives G-domain folding in Acinetobacter baumannii ZigA.
Biophys J. 2024 Apr 16;123(8):979-991. doi: 10.1016/j.bpj.2024.03.010. Epub 2024 Mar 8.
10
The Role of Zinc Efflux during Infection.
ACS Infect Dis. 2020 Jan 10;6(1):150-158. doi: 10.1021/acsinfecdis.9b00351. Epub 2019 Nov 8.

引用本文的文献

1
Amino acid competition shapes Acinetobacter baumannii gut carriage.
Cell Host Microbe. 2025 Aug 13;33(8):1396-1411.e9. doi: 10.1016/j.chom.2025.07.003. Epub 2025 Aug 4.
2
Zinc Alleviates Gut Barrier Dysfunction by Promoting the Methylation of AKT.
Adv Sci (Weinh). 2025 Sep;12(33):e08280. doi: 10.1002/advs.202508280. Epub 2025 Jul 11.
3
Bacteria Under Metal Stress-Molecular Mechanisms of Metal Tolerance.
Int J Mol Sci. 2025 Jun 14;26(12):5716. doi: 10.3390/ijms26125716.
4
The zinc metalloprotein MigC impacts cell wall biogenesis through interactions with an essential Mur ligase in Acinetobacter baumannii.
PLoS Pathog. 2025 Jun 16;21(6):e1013209. doi: 10.1371/journal.ppat.1013209. eCollection 2025 Jun.
5
Signaling in : Quorum sensing and nucleotide second messengers.
Comput Struct Biotechnol J. 2025 May 22;27:2168-2175. doi: 10.1016/j.csbj.2025.05.032. eCollection 2025.
6
Chalkophore-mediated respiratory oxidase flexibility controls virulence.
Elife. 2025 Jun 5;14:RP105794. doi: 10.7554/eLife.105794.
7
10
Type I-E* CRISPR-Cas of upregulates bacterial virulence by targeting endogenous histidine utilization system.
mSphere. 2025 Jun 25;10(6):e0021525. doi: 10.1128/msphere.00215-25. Epub 2025 May 19.

本文引用的文献

2
Bacillithiol is a major buffer of the labile zinc pool in Bacillus subtilis.
Mol Microbiol. 2014 Nov;94(4):756-70. doi: 10.1111/mmi.12794. Epub 2014 Oct 7.
3
Acinetobacter baumannii response to host-mediated zinc limitation requires the transcriptional regulator Zur.
J Bacteriol. 2014 Jul;196(14):2616-26. doi: 10.1128/JB.01650-14. Epub 2014 May 9.
6
Allosteric inhibition of a zinc-sensing transcriptional repressor: insights into the arsenic repressor (ArsR) family.
J Mol Biol. 2013 Apr 12;425(7):1143-57. doi: 10.1016/j.jmb.2013.01.018. Epub 2013 Jan 23.
8
Regulation of the histidine utilization (hut) system in bacteria.
Microbiol Mol Biol Rev. 2012 Sep;76(3):565-84. doi: 10.1128/MMBR.00014-12.
9
Nutritional immunity: transition metals at the pathogen-host interface.
Nat Rev Microbiol. 2012 Jul 16;10(8):525-37. doi: 10.1038/nrmicro2836.
10
YeiR: a metal-binding GTPase from Escherichia coli involved in metal homeostasis.
Metallomics. 2012 May;4(5):488-97. doi: 10.1039/c2mt20012k. Epub 2012 Apr 17.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验