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本文引用的文献

1
Decline in ribosomal fidelity contributes to the accumulation and stabilization of the master stress response regulator sigmaS upon carbon starvation.核糖体保真度的下降有助于在碳饥饿时主应激反应调节因子σS的积累和稳定。
Genes Dev. 2007 Apr 1;21(7):862-74. doi: 10.1101/gad.409407.
2
Acyl carrier protein/SpoT interaction, the switch linking SpoT-dependent stress response to fatty acid metabolism.酰基载体蛋白/SpoT相互作用,将依赖SpoT的应激反应与脂肪酸代谢联系起来的开关。
Mol Microbiol. 2006 Nov;62(4):1048-63. doi: 10.1111/j.1365-2958.2006.05442.x.
3
Induction of expression of hfq by DksA is essential for Shigella flexneri virulence.DksA诱导hfq表达对福氏志贺氏菌的毒力至关重要。
Mol Microbiol. 2006 Oct;62(2):469-79. doi: 10.1111/j.1365-2958.2006.05376.x.
4
The nucleotide-binding site of bacterial translation initiation factor 2 (IF2) as a metabolic sensor.细菌翻译起始因子2(IF2)的核苷酸结合位点作为一种代谢传感器。
Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):13962-7. doi: 10.1073/pnas.0606384103. Epub 2006 Sep 12.
5
The PhoP/PhoQ two-component system stabilizes the alternative sigma factor RpoS in Salmonella enterica.PhoP/PhoQ双组分系统可稳定肠炎沙门氏菌中的替代σ因子RpoS。
Proc Natl Acad Sci U S A. 2006 Sep 5;103(36):13503-8. doi: 10.1073/pnas.0606026103. Epub 2006 Aug 28.
6
ppGpp with DksA controls gene expression in the locus of enterocyte effacement (LEE) pathogenicity island of enterohaemorrhagic Escherichia coli through activation of two virulence regulatory genes.携带DksA的鸟苷四磷酸(ppGpp)通过激活两个毒力调节基因,控制肠出血性大肠杆菌肠细胞脱落位点(LEE)致病岛中的基因表达。
Mol Microbiol. 2006 Jul;61(1):194-205. doi: 10.1111/j.1365-2958.2006.05217.x.
7
Modulating RssB activity: IraP, a novel regulator of sigma(S) stability in Escherichia coli.调节RssB活性:IraP,大肠杆菌中σ(S)稳定性的新型调节因子。
Genes Dev. 2006 Apr 1;20(7):884-97. doi: 10.1101/gad.1400306.
8
DksA potentiates direct activation of amino acid promoters by ppGpp.DksA增强了ppGpp对氨基酸启动子的直接激活作用。
Proc Natl Acad Sci U S A. 2005 May 31;102(22):7823-8. doi: 10.1073/pnas.0501170102. Epub 2005 May 17.
9
Iron limitation induces SpoT-dependent accumulation of ppGpp in Escherichia coli.铁限制诱导大肠杆菌中由SpoT介导的鸟苷四磷酸(ppGpp)积累。
Mol Microbiol. 2005 May;56(4):958-70. doi: 10.1111/j.1365-2958.2005.04601.x.
10
RpoS proteolysis is regulated by a mechanism that does not require the SprE (RssB) response regulator phosphorylation site.RpoS蛋白水解由一种不需要SprE(RssB)应答调节因子磷酸化位点的机制调控。
J Bacteriol. 2004 Nov;186(21):7403-10. doi: 10.1128/JB.186.21.7403-7410.2004.

通过抗适配蛋白IraP实现的ppGpp对RpoS降解的调控

ppGpp regulation of RpoS degradation via anti-adaptor protein IraP.

作者信息

Bougdour Alexandre, Gottesman Susan

机构信息

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Proc Natl Acad Sci U S A. 2007 Jul 31;104(31):12896-901. doi: 10.1073/pnas.0705561104. Epub 2007 Jul 19.

DOI:10.1073/pnas.0705561104
PMID:17640895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1937563/
Abstract

IraP is a small protein that interferes with the delivery of sigma(S) (RpoS) to the ClpXP protease by blocking the action of RssB, an adaptor protein for sigma(S) degradation. IraP was previously shown to mediate stabilization of sigma(S) during phosphate starvation. Here, we show that iraP is transcribed in response to phosphate starvation; this response is mediated by ppGpp. The iraP promoter is positively regulated by ppGpp, dependent on the discriminator region of the iraP promoter. Sensing of phosphate starvation requires SpoT but not RelA. The results demonstrate a target for positive regulation by ppGpp and suggest that the cell use of ppGpp to mediate a variety of starvation responses operates in part by modulating sigma(S) levels.

摘要

IraP是一种小蛋白,它通过阻断RssB(一种用于σ(S)降解的接头蛋白)的作用,干扰σ(S)(RpoS)向ClpXP蛋白酶的传递。IraP先前已被证明在磷酸盐饥饿期间介导σ(S)的稳定。在这里,我们表明iraP是响应磷酸盐饥饿而转录的;这种反应由ppGpp介导。iraP启动子受到ppGpp的正调控,依赖于iraP启动子的鉴别区域。对磷酸盐饥饿的感知需要SpoT而不是RelA。结果证明了ppGpp正调控的一个靶点,并表明细胞利用ppGpp介导多种饥饿反应部分是通过调节σ(S)水平来实现的。