Respiratory chain components are required for peptidoglycan recognition protein-induced thiol depletion and killing in Bacillus subtilis and Escherichia coli.

Respiratory chain components are required for peptidoglycan recognition protein-induced thiol depletion and killing in Bacillus subtilis and Escherichia coli.
复制标题

DOI:
10.1038/s41598-020-79811-z
复制
发表时间:
2021-01-08
期刊:
影响因子:
4.6
通讯作者:
Dziarski R
Dziarski R
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Yang CK;Kashyap DR;Kowalczyk DA;Rudner DZ;Wang X;Gupta D;Dziarski R

文献摘要

参考文献

相似文献

哺乳动物肽聚糖识别蛋白(PGRP或PGLYRP)通过诱导协同氧化、硫醇和金属应激来杀死细菌。对枯草芽孢杆菌转座子插入文库的Tn-seq筛选显示,分支酸合成的莽草酸途径中的突变体在PGLYRP 4处理后具有高存活率。这些基因的缺失突变体减少了甲基萘醌(MK)的量,增加了对杀伤的抗性,并减弱了PGLYRP 4处理后巯基的消耗。这些作用可被MK逆转或通过抑制MK合成而再现。细胞色素aa 3 -600或NADH脱氢酶(NDH)基因的缺失也增加了B。枯草芽孢杆菌对PGLYRP 4诱导的杀伤的抗性和减弱的硫醇消耗。PGLYRP 4处理还抑制了B。枯草呼吸类似地,在大肠杆菌中,泛醌(UQ)合成,甲酸脱氢酶(FDH),NDH-1,或细胞色素bd-I基因的缺失减弱PGLYRP 4诱导的巯基耗尽。在B中,PGLYRP 4诱导低水平的细胞质膜去极化。枯草芽孢杆菌和E.大肠杆菌可能不是巯基耗尽的原因。因此,我们的研究结果表明,呼吸电子传递链组分,细胞色素aa 3 -600,MK,和NDH在B。subtilis,细胞色素bd-I、UQ、FDH-O和NDH-1。大肠杆菌中,是PGLYRP 4诱导的杀伤和巯基耗尽所必需的,并表明在革兰氏阳性和革兰氏阴性细菌中PGLYRP 4诱导的巯基耗尽和杀伤机制的保守性。
Mammalian peptidoglycan recognition proteins (PGRPs or PGLYRPs) kill bacteria through induction of synergistic oxidative, thiol, and metal stress. Tn-seq screening of Bacillus subtilis transposon insertion library revealed that mutants in the shikimate pathway of chorismate synthesis had high survival following PGLYRP4 treatment. Deletion mutants for these genes had decreased amounts of menaquinone (MK), increased resistance to killing, and attenuated depletion of thiols following PGLYRP4 treatment. These effects were reversed by MK or reproduced by inhibiting MK synthesis. Deletion of cytochrome aa3-600 or NADH dehydrogenase (NDH) genes also increased B. subtilis resistance to PGLYRP4-induced killing and attenuated thiol depletion. PGLYRP4 treatment also inhibited B. subtilis respiration. Similarly in Escherichia coli, deletion of ubiquinone (UQ) synthesis, formate dehydrogenases (FDH), NDH-1, or cytochrome bd-I genes attenuated PGLYRP4-induced thiol depletion. PGLYRP4-induced low level of cytoplasmic membrane depolarization in B. subtilis and E. coli was likely not responsible for thiol depletion. Thus, our results show that the respiratory electron transport chain components, cytochrome aa3-600, MK, and NDH in B. subtilis, and cytochrome bd-I, UQ, FDH-O, and NDH-1 in E. coli, are required for both PGLYRP4-induced killing and thiol depletion and indicate conservation of the PGLYRP4-induced thiol depletion and killing mechanisms in Gram-positive and Gram-negative bacteria.
DOI: 10.1128/jb.01156-09
发表时间: 2010-02-01
影响因子: 3.2
作者:
Bekker, Martijn;Alexeeva, Svetlana;Hellingwerf, Klaas
通讯作者: Hellingwerf, Klaas
DOI: 10.1099/mic.0.2007/006098-0
发表时间: 2007-06-01
期刊: MICROBIOLOGY-SGM
影响因子: 2.8
作者:
Bekker, M.;Kramer, G.;de Mattos, M. J. Teixeira
通讯作者: de Mattos, M. J. Teixeira
DOI: 10.1073/pnas.0707723105
发表时间: 2008-06-17
影响因子: 11.1
作者:
Leichert, Lars I.;Gehrke, Florian;Jakob, Ursula
通讯作者: Jakob, Ursula
DOI: 10.1038/nm.2357
发表时间: 2011-06-01
期刊: NATURE MEDICINE
影响因子: 82.9
作者:
Kashyap, Des Raj;Wang, Minhui;Dziarski, Roman
通讯作者: Dziarski, Roman
大肠杆菌K-12的构造框架,单基因敲除突变体:Keio Collection。
DOI: 10.1038/msb4100050
发表时间: 2006
影响因子: 9.9
作者:
通讯作者: --