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固氮蓝藻鱼腥藻PCC 7120菌株中的蔗糖合成受双组分响应调节因子OrrA的控制。

Sucrose synthesis in the nitrogen-fixing Cyanobacterium Anabaena sp. strain PCC 7120 is controlled by the two-component response regulator OrrA.

作者信息

Ehira Shigeki, Kimura Satoshi, Miyazaki Shogo, Ohmori Masayuki

机构信息

Department of Biological Sciences, Graduate School of Science and Engineering, Tokyo Metropolitan University, Hachioji, Tokyo, Japan Department of Biological Science, Faculty of Science and Engineering, Chuo University, Bunkyo-ku, Tokyo, Japan Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama, Japan

Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University, Saitama, Japan.

出版信息

Appl Environ Microbiol. 2014 Sep;80(18):5672-9. doi: 10.1128/AEM.01501-14. Epub 2014 Jul 7.

Abstract

The filamentous, nitrogen-fixing cyanobacterium Anabaena sp. strain PCC 7120 accumulates sucrose as a compatible solute against salt stress. Sucrose-phosphate synthase activity, which is responsible for the sucrose synthesis, is increased by salt stress, but the mechanism underlying the regulation of sucrose synthesis remains unknown. In the present study, a response regulator, OrrA, was shown to control sucrose synthesis. Expression of spsA, which encodes a sucrose-phosphate synthase, and susA and susB, which encode sucrose synthases, was induced by salt stress. In the orrA disruptant, salt induction of these genes was completely abolished. The cellular sucrose level of the orrA disruptant was reduced to 40% of that in the wild type under salt stress conditions. Moreover, overexpression of orrA resulted in enhanced expression of spsA, susA, and susB, followed by accumulation of sucrose, without the addition of NaCl. We also found that SigB2, a group 2 sigma factor of RNA polymerase, regulated the early response to salt stress under the control of OrrA. It is concluded that OrrA controls sucrose synthesis in collaboration with SigB2.

摘要

丝状固氮蓝藻鱼腥藻Anabaena sp.菌株PCC 7120积累蔗糖作为抵御盐胁迫的相容性溶质。负责蔗糖合成的蔗糖磷酸合酶活性会因盐胁迫而增加,但蔗糖合成调控的潜在机制仍不清楚。在本研究中,一种应答调节因子OrrA被证明可控制蔗糖合成。编码蔗糖磷酸合酶的spsA以及编码蔗糖合酶的susA和susB的表达受盐胁迫诱导。在orrA缺失突变体中,这些基因的盐诱导作用完全消失。在盐胁迫条件下,orrA缺失突变体的细胞蔗糖水平降至野生型的40%。此外,orrA的过表达导致spsA、susA和susB的表达增强,随后蔗糖积累,且无需添加氯化钠。我们还发现,RNA聚合酶的2组sigma因子SigB2在OrrA的控制下调节对盐胁迫的早期应答。得出的结论是,OrrA与SigB2协同控制蔗糖合成。

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