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大肠杆菌中含锰超氧化物歧化酶生物合成的Fur依赖性调控的铁特异性

Iron specificity of the Fur-dependent regulation of the biosynthesis of the manganese-containing superoxide dismutase in Escherichia coli.

作者信息

Privalle C T, Fridovich I

机构信息

Department of Biochemistry, Duke University Medical Center, Durham, North Carolina 27710.

出版信息

J Biol Chem. 1993 Mar 5;268(7):5178-81.

PMID:8444893
Abstract

The Fur protein, which regulates iron uptake in Escherichia coli, also represses the biosynthesis of the manganese-containing superoxide dismutase (MnSOD). A strain of E. coli bearing a lacZ fusion to the aerobactin operon was used to compare the metal specificities of the regulation of MnSOD and of aerobactin by Fur. Iron, but not manganese, acted as a corepressor of the Fur-dependent inhibition of MnSOD biosynthesis. The iron-mediated inhibition of MnSOD biosynthesis was dependent upon an intact fur locus, indicating that the effect of iron is mediated by the fur gene product. The suppression of the accumulation of MnSOD by iron, but not by manganese, was not due to destabilization of the MnSOD polypeptide by iron. Thus this effect of iron was also seen in a sodA::lacZ operon fusion in which the production of beta-galactosidase was regulated by the sodA promoter. In contrast, both iron and manganese served as corepressors of aerobactin biosynthesis. It thus appears that the effectiveness of specific metal cations to act as corepressors with Fur varies with the gene being regulated by the Fur-metal complex.

摘要

在大肠杆菌中调节铁摄取的Fur蛋白,也会抑制含锰超氧化物歧化酶(MnSOD)的生物合成。利用一株携带与气杆菌素操纵子融合的lacZ的大肠杆菌菌株,来比较Fur对MnSOD和气杆菌素调节的金属特异性。铁而非锰,作为Fur依赖性抑制MnSOD生物合成的辅阻遏物。铁介导的对MnSOD生物合成的抑制依赖于完整的fur基因座,表明铁的作用是由fur基因产物介导的。铁而非锰对MnSOD积累的抑制,并非由于铁使MnSOD多肽不稳定。因此,在sodA::lacZ操纵子融合中也观察到了铁的这种作用,其中β-半乳糖苷酶的产生由sodA启动子调控。相比之下,铁和锰均作为气杆菌素生物合成的辅阻遏物。因此,特定金属阳离子作为Fur辅阻遏物的有效性,会因Fur-金属复合物所调控的基因而异。

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