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鱼腥藻PCC 7120菌株中hepA基因5'端元件及hepK对hepA的调控

Regulation of hepA of Anabaena sp. strain PCC 7120 by elements 5' from the gene and by hepK.

作者信息

Zhu J, Kong R, Wolk C P

机构信息

MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824, USA.

出版信息

J Bacteriol. 1998 Aug;180(16):4233-42. doi: 10.1128/JB.180.16.4233-4242.1998.

Abstract

In Anabaena spp., synthesis of the heterocyst envelope polysaccharide, required if the cell is to fix dinitrogen under aerobic conditions, is dependent on the gene hepA. A transcriptional start site of hepA was localized 104 bp 5' from its translational initiation codon. A 765-bp open reading frame, denoted hepC, was found farther upstream. Inactivation of hepC led to constitutive expression of hepA and prevented the synthesis of heterocyst envelope polysaccharide. However, the glycolipid layer of the heterocyst envelope was synthesized. A hepK mutation blocked both the synthesis of the heterocyst envelope polysaccharide and induction of hepA. The predicted product of hepK resembles a sensory protein-histidine kinase of a two-component regulatory system. Analysis of the region between hepC and hepA indicated that DNA sequences required for the induction of hepA upon nitrogen deprivation are present between bp -574 and -440 and between bp -340 and -169 relative to the transcriptional start site of hepA. Gel mobility shift assays provided evidence that one or more proteins bind specifically to the latter sequence. The Fox box sequence downstream from hepA appeared inessential for the induction of hepA.

摘要

在鱼腥藻属中,若细胞要在有氧条件下固定二氮,则需要合成异形胞包膜多糖,这依赖于hepA基因。hepA的转录起始位点位于其翻译起始密码子上游104 bp处。在更上游发现了一个765 bp的开放阅读框,命名为hepC。hepC的失活导致hepA的组成型表达,并阻止了异形胞包膜多糖的合成。然而,异形胞包膜的糖脂层被合成。hepK突变同时阻断了异形胞包膜多糖的合成和hepA的诱导。hepK的预测产物类似于双组分调节系统的传感蛋白-组氨酸激酶。对hepC和hepA之间区域的分析表明,相对于hepA的转录起始位点,在bp -574和-440之间以及bp -340和-169之间存在氮剥夺时诱导hepA所需的DNA序列。凝胶迁移率变动分析提供了证据,表明一种或多种蛋白质与后一个序列特异性结合。hepA下游的Fox框序列似乎对hepA的诱导无关紧要。

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