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Fis、IHF和H-NS对大肠杆菌nir启动子处FNR依赖性转录激活的抑制:一种复杂核蛋白组装体对转录起始的调控

Suppression of FNR-dependent transcription activation at the Escherichia coli nir promoter by Fis, IHF and H-NS: modulation of transcription initiation by a complex nucleo-protein assembly.

作者信息

Browning D F, Cole J A, Busby S J

机构信息

School of Biosciences, The University of Birmingham, Birmingham B15 2TT, UK.

出版信息

Mol Microbiol. 2000 Sep;37(5):1258-69. doi: 10.1046/j.1365-2958.2000.02087.x.

Abstract

Expression from the Escherichia coli nir promoter is co-dependent on both the FNR protein (an anaerobically triggered transcription activator) and the NarL or NarP proteins (transcription activators triggered by nitrite and nitrate). Under anaerobic conditions, FNR binds to a site centred between positions -41 and -42, activating transcription of the nir operon. In previous work, we showed that this activation is suppressed by the binding of Fis protein, and at least one other protein, to sequence elements located upstream of the nir promoter. We proposed that the binding of NarL or NarP to a site centred between positions -69 and -70 counteracts this suppression, resulting in increased transcription in response to nitrite or nitrate. Here we have further investigated the different proteins that downregulate the nir promoter. We show that the nir promoter is repressed by three DNA binding proteins, Fis, IHF and H-NS. We demonstrate that, in addition to binding to its previously characterized upstream site located at position -142, Fis also binds to a second downstream site located at position +23. A second suppressing factor is IHF, that binds to a site located at position -88. Finally, the nucleoid associated protein, H-NS, preferentially binds to upstream sequences at the nir promoter and represses promoter activity. The association of Fis, IHF and H-NS suggests that nir promoter DNA is sequestrated into a highly ordered nucleo-protein structure that represses FNR-dependent transcription activation. NarL and NarP can relieve both IHF- and Fis-mediated repression, but are unable to counteract H-NS-mediated repression.

摘要

大肠杆菌nir启动子的表达同时依赖于FNR蛋白(一种厌氧触发的转录激活因子)和NarL或NarP蛋白(由亚硝酸盐和硝酸盐触发的转录激活因子)。在厌氧条件下,FNR结合到位于-41和-42位之间的中心位点,激活nir操纵子的转录。在之前的工作中,我们表明这种激活被Fis蛋白以及至少一种其他蛋白与nir启动子上游序列元件的结合所抑制。我们提出NarL或NarP与位于-69和-70位之间的中心位点的结合可抵消这种抑制作用,从而导致响应亚硝酸盐或硝酸盐时转录增加。在此,我们进一步研究了下调nir启动子的不同蛋白。我们发现nir启动子被三种DNA结合蛋白Fis、IHF和H-NS所抑制。我们证明,除了结合其先前鉴定的位于-142位的上游位点外,Fis还结合位于+23位的第二个下游位点。第二个抑制因子是IHF,它结合位于-88位的位点。最后,类核相关蛋白H-NS优先结合nir启动子的上游序列并抑制启动子活性。Fis、IHF和H-NS的结合表明nir启动子DNA被隔离到一种高度有序的核蛋白结构中,该结构抑制FNR依赖的转录激活。NarL和NarP可以解除IHF和Fis介导的抑制,但无法抵消H-NS介导的抑制。

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