An osmolality/salinity-responsive enhancer 1 (OSRE1) in intron 1 promotes salinity induction of tilapia glutamine synthetase
An osmolality/salinity-responsive enhancer 1 (OSRE1) in intron 1 promotes salinity induction of tilapia glutamine synthetase
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DOI：
10.1038/s41598-020-69090-z
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发表时间：
2020-07-21
影响因子：
4.6
通讯作者：
Kultz, Dietmar
中科院分区：
文献类型：
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作者：
Kim, Chanhee;Kultz, Dietmar
广盐罗非鱼（Oreochromis mossambicus）是耐受从淡水到> 3倍海水的宽盐度范围的鱼类。尽管维持淡水和海水鱼中血浆稳态的血糖调节的生理效应机制是众所周知的，但控制高血糖调节（淡水）和低血糖调节（海水）之间切换的相应分子机制仍然大多是难以捉摸的。在这项研究中，我们表明，谷氨酰胺合成酶的高渗诱导代表了这一开关的突出部分。蛋白质组学分析O. mossambicus OMB细胞系的研究表明，谷氨酰胺合成酶受高渗透压的转录调控。因此，O.研究了莫桑比克谷氨酰胺合成酶。使用增强子捕获分析，我们发现了一种新的内含子1正介导谷氨酰胺合成酶转录的对DNA敏感的机制。内含子1包括一个单一的功能性拷贝的渗透压/盐度响应元件，渗透压/盐度响应增强子1（OSRE 1）。与常规增强子不同，内含子1对谷氨酰胺合成酶的高渗诱导是位置依赖性的。但无论内含子1的位置，OSRE 1从内含子1删除废除高渗增强活性。这些发现表明，正确的内含子1定位和内含子1中的OSRE 1的存在是精确增强高渗谷氨酰胺合成酶表达所必需的。
Euryhaline tilapia (Oreochromis mossambicus) are fish that tolerate a wide salinity range from fresh water to > 3x seawater. Even though the physiological effector mechanisms of osmoregulation that maintain plasma homeostasis in fresh water and seawater fish are well known, the corresponding molecular mechanisms that control switching between hyper- (fresh water) and hypo-osmoregulation (seawater) remain mostly elusive. In this study we show that hyperosmotic induction of glutamine synthetase represents a prominent part of this switch. Proteomics analysis of the O. mossambicus OmB cell line revealed that glutamine synthetase is transcriptionally regulated by hyperosmolality. Therefore, the 5 ' regulatory sequence of O. mossambicus glutamine synthetase was investigated. Using an enhancer trapping assay, we discovered a novel osmosensitive mechanism by which intron 1 positively mediates glutamine synthetase transcription. Intron 1 includes a single, functional copy of an osmoresponsive element, osmolality/salinity-responsive enhancer 1 (OSRE1). Unlike for conventional enhancers, the hyperosmotic induction of glutamine synthetase by intron 1 is position dependent. But irrespective of intron 1 position, OSRE1 deletion from intron 1 abolishes hyperosmotic enhancer activity. These findings indicate that proper intron 1 positioning and the presence of an OSRE1 in intron 1 are required for precise enhancement of hyperosmotic glutamine synthetase expression.