Resistance to oxidative stress by inner membrane protein ElaB is regulated by OxyR and RpoS

Resistance to oxidative stress by inner membrane protein ElaB is regulated by OxyR and RpoS
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内膜蛋白 ElaB 对氧化应激的抵抗力受 OxyR 和 RpoS 调节

DOI:
10.1111/1751-7915.13369
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发表时间:
2019-03-01
影响因子:
5.7
通讯作者:
Wang, Xiaoxue
Wang, Xiaoxue
中科院分区:
工程技术2区
文献类型:
--
作者:
Guo, Yunxue;Li, Yangmei;Wang, Xiaoxue

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C-尾锚定内膜蛋白是含有C-末端跨膜结构域但缺乏用于膜靶向的N-末端信号序列的蛋白质家族。它们广泛存在于真核生物和原核生物中,在真核生物的膜运输、细胞凋亡和蛋白质转运中起着重要作用。最近,我们在大肠杆菌中鉴定并表征了一种新的C-尾锚定内膜ElaB,其受固定相σ因子RpoS调控。ElaB对抗氧化应激很重要,但确切的机制尚不清楚。在这里,我们表明,ElaB的功能作为自适应氧化应激反应的一部分,通过保持膜的完整性。ElaB的产生在转录水平上由氧化应激诱导。此外,elaB的表达也通过关键调节因子OxyR通过elaB启动子中的OxyR结合位点进行调节。OxyR在指数生长期诱导elaB的表达,而过量的OxyR在稳定期以Rpos依赖的方式降低elaB的表达。此外,在长时间孵育后,与野生型细胞相比,elaB的缺失降低了适应性。因此,我们确定了ElaB在氧化应激下是如何调节的:RpoS和OxyR协调控制内膜蛋白ElaB的表达。
C-tail anchored inner membrane proteins are a family of proteins that contain a C-terminal transmembrane domain but lack an N-terminal signal sequence for membrane targeting. They are widespread in eukaryotes and prokaryotes and play critical roles in membrane traffic, apoptosis and protein translocation in eukaryotes. Recently, we identified and characterized in Escherichia coli a new C-tail anchored inner membrane, ElaB, which is regulated by the stationary phase sigma factor RpoS. ElaB is important for resistance to oxidative stress but the exact mechanism is unclear. Here, we show that ElaB functions as part of the adaptive oxidative stress response by maintaining membrane integrity. Production of ElaB is induced by oxidative stress at the transcriptional level. Moreover, elaB expression is also regulated by the key regulator OxyR via an OxyR binding site in the promoter of elaB. OxyR induces the expression of elaB in the exponential growth phase, while excess OxyR reduces elaB expression in an RpoS-dependent way in the stationary phase. In addition, deletion of elaB reduced fitness compared to wild-type cells after prolonged incubation. Therefore, we determined how ElaB is regulated under oxidative stress: RpoS and OxyR coordinately control the expression of inner membrane protein ElaB.