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应答调节因子Slr1588对集胞藻PCC 6803的盐适应性具有调节作用,但并非至关重要。

The Response Regulator Slr1588 Regulates But Is Not Crucial for Salt Acclimation of sp. PCC 6803.

作者信息

Song Kuo, Hagemann Martin, Tan Xiaoming, Lu Xuefeng

机构信息

Key Laboratory of Biofuels, Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of SciencesQingdao, China.

Department of Plant Physiology, Institute of Biological Sciences, University of RostockRostock, Germany.

出版信息

Front Microbiol. 2017 Jun 26;8:1176. doi: 10.3389/fmicb.2017.01176. eCollection 2017.

Abstract

Cyanobacterial sucrose biosynthesis is stimulated under salt stress, which could be used for biotechnological sugar production. It has been shown that the response regulator Slr1588 negatively regulates the gene encoding sucrose-phosphate synthase and mutation of the gene also affected the salt tolerance of (Chen et al., 2014). The latter finding is contrary to earlier observations (Hagemann et al., 1997b). Here, we observed that ectopic expression of did not restore the salt tolerance of the mutant, making the essential function of this response regulator for salt tolerance questionable. Subsequent experiments showed that deletion of the entire coding sequence of compromised the expression of the downstream situated gene, which encodes glucosylglycerol-phosphate phosphatase for synthesis of the primary osmolyte glucosylglycerol. Mutation of by deleting the N-terminal part of this protein (Δ-F976) did not affect expression, glucosylglycerol accumulation as well as salt tolerance, while the mutation of resulted in the previously reported salt-sensitive phenotype. In the Δ-F976 mutant was up-regulated but sucrose content was lowered due to increased invertase activity. Our results reveal that Slr1588 is acting as a repressor for as previously suggested but it is not crucial for the overall salt acclimation of .

摘要

盐胁迫下蓝藻蔗糖生物合成受到刺激,这可用于生物技术制糖。研究表明,应答调节因子Slr1588对编码蔗糖磷酸合酶的基因起负调控作用,该基因的突变也影响了集胞藻的耐盐性(Chen等人,2014年)。后一发现与早期观察结果相反(Hagemann等人,1997b)。在此,我们观察到Slr1588的异位表达并未恢复集胞藻突变体的耐盐性,这使得该应答调节因子对耐盐性的基本功能存疑。后续实验表明,删除Slr1588的整个编码序列会损害位于下游的ggp基因的表达,该基因编码用于合成主要渗透溶质葡糖基甘油的葡糖基甘油磷酸磷酸酶。通过删除该蛋白的N端部分(Δ-F976)对Slr1588进行突变并不影响ggp基因表达、葡糖基甘油积累以及耐盐性,而Slr1588的突变则导致先前报道的盐敏感表型。在Δ-F976突变体中,ggp基因上调,但由于转化酶活性增加,蔗糖含量降低。我们的结果表明,如先前所述,Slr1588作为ggp基因的阻遏物起作用,但它对集胞藻的整体盐适应并不关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f29/5483463/c58c04dee10c/fmicb-08-01176-g001.jpg

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