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大西洋鲑的硫酸盐稳态与鳃和肾脏中鲑鱼特异性的同源基因的差异调控有关。

Sulfate homeostasis in Atlantic salmon is associated with differential regulation of salmonid-specific paralogs in gill and kidney.

机构信息

NORCE, Norwegian Research Center, NORCE Environment, Bergen, Norway.

Department of Biological Science, University of Bergen, Bergen, Norway.

出版信息

Physiol Rep. 2021 Oct;9(19):e15059. doi: 10.14814/phy2.15059.

DOI:10.14814/phy2.15059
PMID:34617680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8495805/
Abstract

Sulfate ( ) regulation is challenging for euryhaline species as they deal with large fluctuations of during migratory transitions between freshwater (FW) and seawater (SW), while maintaining a stable plasma concentration. Here, we investigated the regulation and potential role of sulfate transporters in Atlantic salmon during the preparative switch from uptake to secretion. A preparatory increase in kidney and gill sodium/potassium ATPase (Nka) enzyme activity during smolt development indicate preparative osmoregulatory changes. In contrast to gill Nka activity a transient decrease in kidney Nka after direct SW exposure was observed and may be a result of reduced glomerular filtration rates and tubular flow through the kidney. In silico analyses revealed that Atlantic salmon genome comprises a single slc13a1 gene and additional salmonid-specific duplications of slc26a1 and slc26a6a, leading to new paralogs, namely the slc26a1a and -b, and slc26a6a1 and -a2. A kidney-specific increase in slc26a6a1 and slc26a1a during smoltification and SW transfer, suggests an important role of these sulfate transporters in the regulatory shift from absorption to secretion in the kidney. Plasma in FW smolts was 0.70 mM, followed by a transient increase to 1.14 ± 0.33 mM 2 days post-SW transfer, further decreasing to 0.69 ± 0.041 mM after 1 month in SW. Our findings support the vital role of the kidney in excretion through the upregulated slc26a6a1, the most likely secretory transport candidate in fish, which together with the slc26a1a transporter likely removes excess , and ultimately enable the regulation of normal plasma levels in SW.

摘要

硫酸盐(Sulfate)调节对广盐性物种具有挑战性,因为它们在淡水(FW)和海水(SW)之间的洄游过渡期间会经历硫酸盐浓度的大幅波动,同时维持稳定的血浆硫酸盐浓度。在这里,我们研究了大西洋鲑在从吸收到分泌的预备性转换过程中硫酸盐转运体的调节及其潜在作用。在鲑鱼发育过程中,肾脏和鳃钠离子/钾离子-ATP 酶(Nka)酶活性的预备性增加表明了预备性渗透压调节变化。与鳃 Nka 活性相反,在直接暴露于 SW 后观察到肾脏 Nka 的短暂下降,这可能是肾小球滤过率降低和通过肾脏的管状流动减少的结果。计算机分析表明,大西洋鲑基因组包含单个 slc13a1 基因,以及 slc26a1 和 slc26a6a 的额外鲑鱼特异性重复,导致新的同源基因,即 slc26a1a 和 -b,以及 slc26a6a1 和 -a2。在鲑鱼变态和 SW 转移期间,肾脏中 slc26a6a1 和 slc26a1a 的特异性增加表明这些硫酸盐转运体在肾脏从吸收到分泌的调节转变中具有重要作用。FW 幼鲑的血浆硫酸盐浓度为 0.70 mM,随后在 SW 转移后 2 天短暂增加至 1.14 ± 0.33 mM,在 SW 中 1 个月后进一步降低至 0.69 ± 0.041 mM。我们的研究结果支持肾脏在通过上调的 slc26a6a1 排泄硫酸盐方面的重要作用,slc26a6a1 可能是鱼类中最有可能的分泌转运体候选物,它与 slc26a1a 转运体一起可能去除多余的硫酸盐,并最终使 SW 中正常的血浆硫酸盐水平得以调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/bb0ae89bd4af/PHY2-9-e15059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/82ad49b52780/PHY2-9-e15059-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/cf7c96167300/PHY2-9-e15059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/2fc10b648e3e/PHY2-9-e15059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/eab2fb668ead/PHY2-9-e15059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/bc45dbdf6f8d/PHY2-9-e15059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/fbd9e6e3ba97/PHY2-9-e15059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/0f717adf5949/PHY2-9-e15059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/ebc44b7dfd60/PHY2-9-e15059-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/bb0ae89bd4af/PHY2-9-e15059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/82ad49b52780/PHY2-9-e15059-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/cf7c96167300/PHY2-9-e15059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/2fc10b648e3e/PHY2-9-e15059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/eab2fb668ead/PHY2-9-e15059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/bc45dbdf6f8d/PHY2-9-e15059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/fbd9e6e3ba97/PHY2-9-e15059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/0f717adf5949/PHY2-9-e15059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/ebc44b7dfd60/PHY2-9-e15059-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6755/8495805/bb0ae89bd4af/PHY2-9-e15059-g001.jpg

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