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首页> 外文期刊>Pfluegers Archiv: European Journal of Physiology >Tissue-specific expression and in vivo regulation of zebrafish orthologues of mammalian genes related to symptomatic hypomagnesemia
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Tissue-specific expression and in vivo regulation of zebrafish orthologues of mammalian genes related to symptomatic hypomagnesemia

机译：与症状性低镁血症有关的哺乳动物基因的斑马鱼直向同源物的组织特异性表达和体内调控

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Introduction of zebrafish as a model for human diseases with symptomatic hypomagnesemia urges to identify the regulatory transport genes involved in zebrafish Mg2+ physiology. In humans, mutations related to hypomagnesemia are located in the genes TRPM6 and CNNM2, encoding for a Mg 2+ channel and transporter, respectively; EGF (epidermal growth factor); SLC12A3, which encodes for the Na+-Cl- co-transporter NCC; KCNA1 and KCNJ10, encoding for the K+ channels Kv1.1 and Kir4.1, respectively; and FXYD2, which encodes for the γ-subunit of the Na+,K+-ATPase. Orthologues of these genes were found in the zebrafish genome. For cnnm2, kcna1 and kcnj10, two conserved paralogues were retrieved. Except for fxyd2, kcna1b and kcnj10 duplicates, transcripts of orthologues were detected in ionoregulatory organs such as the gills, kidney and gut. Gene expression analyses in zebrafish acclimated to a Mg2+-deficient (0 mM Mg2+) or a Mg2+-enriched (2 mM Mg2+) water showed that branchial trpm6, gut cnnm2b and renal slc12a3 responded to ambient Mg2+. When changing the Mg2+ composition of the diet (the main source for Mg2+ in fish) to a Mg2+-deficient (0.01 % (w/w) Mg) or a Mg2+-enriched diet (0.7 % (w/w) Mg), mRNA expression of branchial trpm6, gut trpm6 and cnnm2 duplicates, and renal trpm6, egf, cnnm2a and slc12a3 was the highest in fish fed the Mg2+-deficient diet. The gene regulation patterns were in line with compensatory mechanisms to cope with Mg2+-deficiency or surplus. Our findings suggest that trpm6, egf, cnnm2 paralogues and slc12a3 are involved in the in vivo regulation of Mg2+ transport in ionoregulatory organs of the zebrafish model.
机译：斑马鱼作为有症状的低镁血症人类疾病的模型的引入促使人们确定与斑马鱼Mg2 +生理相关的调节转运基因。在人类中，与低镁血症有关的突变位于基因TRPM6和CNNM2中，分别编码Mg 2+通道和转运蛋白。 EGF（表皮生长因子）; SLC12A3，其编码Na + -Cl-共转运蛋白NCC; KCNA1和KCNJ10，分别为K +通道Kv1.1和Kir4.1编码; FXYD2，它编码Na +，K + -ATPase的γ亚基。在斑马鱼基因组中发现了这些基因的直向同源物。对于cnnm2，kcna1和kcnj10，检索了两个保守的旁系同源物。除了fxyd2，kcna1b和kcnj10复制品外，直向同源物的转录本在ion，肾和肠道等离子调节器官中也被检测到。斑马鱼适应不足Mg2 +（0 mM Mg2 +）或富含Mg2 +（2 mM Mg2 +）的水的基因表达分析表明，小枝trpm6，肠cnnm2b和肾slc12a3对周围Mg2 +响应。当饮食中的Mg2 +组成（鱼类中Mg2 +的主要来源）变为缺乏Mg2 +的饮食（0.01％（w / w）Mg）或富含Mg2 +的饮食（0.7％（w / w）Mg）时，mRNA在缺乏Mg2 +饮食的鱼中，小肠trpm6，肠trpm6和cnnm2的表达重复，而肾trpm6，例如egf，cnnm2a和slc12a3最高。基因调控模式与应对Mg2 +缺乏或过剩的补偿机制相一致。我们的发现表明，trpm6，egf，cnnm2旁系同源物和slc12a3参与了斑马鱼模型电离器官中Mg2 +转运的体内调节。

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