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UhpA氨基末端磷酸化模块参与大肠杆菌中uhpT转录的激活。

Involvement of the amino-terminal phosphorylation module of UhpA in activation of uhpT transcription in Escherichia coli.

作者信息

Webber C A, Kadner R J

机构信息

Department of Microbiology, University of Virginia School of Medicine, Charlottesville 22908, USA.

出版信息

Mol Microbiol. 1997 Jun;24(5):1039-48. doi: 10.1046/j.1365-2958.1997.4021765.x.

Abstract

The UhpA protein is required for expression of the sugar phosphate transporter UhpT in Escherichia coli and is regulated by phosphate transfer from the transmembrane UhpBC sensor kinase complex. UhpA action requires the sensor kinase complex and the site of phosphorylation, Asp-54, under normal conditions, but not when UhpA is overexpressed. Directed mutagenesis of the uhpA gene allowed examination of the role of several residues of UhpA in response to phosphorylation and in transcription activation. Residues Asp-9, Asp-54, and Lys-101 are highly conserved and required for function in other response regulators. Changes at any of these residues in UhpA resulted in complete loss of phosphorylation-dependent activity, but did not affect the high-level, constitutive, UhpBC-independent expression when the UhpA variants were overexpressed. Thus, these residues are important for the response to the phosphorylation pathway but not for transcription activation. Eight independent uhpA mutants selected for activity in the absence of UhpBC function carried the F17-->V or H170-->Y substitutions. Other substitutions for Phe-17 conferred various phenotypes, ranging from inducible to high-level constitutive behaviour. Residues in helix-1 flanking Phe-17 were converted to Ala or other residues. Alanine substitutions at Val-13, Arg-14, and Leu-20 resulted in complete loss of phosphorylation-dependent activation. Change of Gly-16 to Ala had no effect, but changes to other residues resulted in loss of function. Alanine substitutions at Phe-17 and at Gln-19 resulted in high-level constitutive expression, and changes at Ala-18 and Leu-21 had only modest effects. Most interesting was the L20-->A substitution, which conferred low uhpT expression when overexpressed and interfered with action of the wild-type chromosomal allele. The combination of the L20-->A change with changes at Phe-17, Asp-54 and His-170 indicated that the trans-dominant action of L20-->A occurred at several steps. The observations that UhpA can activate uhpT transcription in its unphosphorylated state are consistent with its occupancy of low-affinity binding sites necessary for promoter function. We propose that the effect of phosphorylation of UhpA is to enhance its oligomerization on the DNA surface to extend to the low-affinity sites, and that helix-1 participates in the process of oligomer formation.

摘要

磷酸转运蛋白UhpT在大肠杆菌中的表达需要UhpA蛋白,且UhpA蛋白受跨膜UhpBC传感激酶复合物的磷酸转移调控。在正常条件下,UhpA发挥作用需要传感激酶复合物和磷酸化位点Asp-54,但UhpA过表达时则不需要。对uhpA基因进行定向诱变,可研究UhpA的几个残基在磷酸化响应和转录激活中的作用。Asp-9、Asp-54和Lys-101残基高度保守,是其他响应调节因子发挥功能所必需的。UhpA中这些残基的任何一个发生变化都会导致磷酸化依赖性活性完全丧失,但当UhpA变体过表达时,并不影响其高水平、组成型、不依赖UhpBC的表达。因此,这些残基对于磷酸化途径的响应很重要,但对于转录激活并不重要。在缺乏UhpBC功能的情况下,为获得活性而选择的8个独立的uhpA突变体携带F17→V或H170→Y替换。Phe-17的其他替换产生了各种表型,从可诱导型到高水平组成型行为。Phe-17两侧螺旋-1中的残基被替换为Ala或其他残基。Val-13、Arg-14和Leu-20处的丙氨酸替换导致磷酸化依赖性激活完全丧失。Gly-16替换为Ala没有影响,但替换为其他残基则导致功能丧失。Phe-17和Gln-19处的丙氨酸替换导致高水平组成型表达,Ala-18和Leu-21处的变化只有适度影响。最有趣的是L20→A替换,过表达时导致uhpT低水平表达,并干扰野生型染色体等位基因的作用。L20→A变化与Phe-17、Asp-54和His-170处变化的组合表明,L20→A的反式显性作用发生在几个步骤。UhpA在其未磷酸化状态下可激活uhpT转录的观察结果与其占据启动子功能所需的低亲和力结合位点一致。我们提出UhpA磷酸化的作用是增强其在DNA表面的寡聚化,从而扩展到低亲和力位点,并且螺旋-1参与寡聚体形成过程。

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