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暴露于有毒甲藻的扇贝中谷胱甘肽过氧化物酶()基因的组织偏向性和物种特异性调控

Tissue-Biased and Species-Specific Regulation of Glutathione Peroxidase () Genes in Scallops Exposed to Toxic Dinoflagellates.

作者信息

Hlaing Sein Moh Moh, Lou Jiarun, Cheng Jie, Xun Xiaogang, Li Moli, Lu Wei, Hu Xiaoli, Bao Zhenmin

机构信息

Key Laboratory of Marine Genetics and Breeding, College of Marine Life Sciences, Ocean University of China, Ministry of Education, 5 Yushan Road, Qingdao 266003, China.

Laboratory for Marine Fisheries Science and Food Production Processes, Pilot National Laboratory for Marine Science and Technology (Qingdao), 1 Wenhai Road, Qingdao 266237, China.

出版信息

Toxins (Basel). 2020 Dec 31;13(1):21. doi: 10.3390/toxins13010021.

DOI:10.3390/toxins13010021
PMID:33396547
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7824116/
Abstract

Marine bivalves could accumulate paralytic shellfish toxins (PSTs) produced by toxic microalgae, which might induce oxidative stress. Glutathione peroxidases (GPxs) are key enzymes functioning in the antioxidant defense, whereas our understanding of their roles in PST challenge in bivalves is limited. Herein, through genome-wide screening, we identified nine () and eight () genes in Zhikong scallop () and Yesso scallop (), respectively, and revealed the expansion of GPx3 sub-family in both species. RNA-Seq analysis revealed high expression of scallop s after D stage larva during early development, and in adult hepatopancreas. However, in scallops exposed to PST-producing dinoflagellates, no was significantly induced in the hepatopancreas. In scallop kidneys where PSTs were transformed to higher toxic analogs, most s were up-regulated, with s being acutely and chronically induced by and . exposure, respectively, but only one from subfamily was up-regulated by . exposure. Our results suggest the function of scallop s in protecting kidneys against the oxidative stresses by PST accumulation or transformation. The tissue-, species-, and toxin-dependent expression pattern of scallop s also implied their functional diversity in response to toxin exposure.

摘要

海洋双壳贝类可积累由有毒微藻产生的麻痹性贝类毒素(PSTs),这可能会引发氧化应激。谷胱甘肽过氧化物酶(GPxs)是在抗氧化防御中起作用的关键酶,然而我们对其在双壳贝类应对PST挑战中的作用了解有限。在此,通过全基因组筛选,我们分别在栉孔扇贝(Chlamys farreri)和虾夷扇贝(Patinopecten yessoensis)中鉴定出9个(Chlamys farreri)和8个(Patinopecten yessoensis)GPx基因,并揭示了两个物种中GPx3亚家族的扩张。RNA测序分析显示,扇贝的GPx在D期幼虫后的早期发育阶段以及成年肝胰腺中高表达。然而,在暴露于产生PST的甲藻的扇贝中,肝胰腺中没有GPx被显著诱导。在PSTs转化为毒性更高类似物的扇贝肾脏中,大多数GPx被上调,其中某些GPx分别被okadaic acid(OA)和dinophysistoxin-1(DTX1)急性和慢性诱导,但只有来自GPx3亚家族的一个GPx被DTX3暴露上调。我们的结果表明扇贝GPx在保护肾脏免受PST积累或转化引起的氧化应激方面的功能。扇贝GPx的组织、物种和毒素依赖性表达模式也暗示了它们在响应毒素暴露时的功能多样性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/2eea2be08f87/toxins-13-00021-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/ba31042b3e50/toxins-13-00021-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/a80cfa15b727/toxins-13-00021-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/230223ea5793/toxins-13-00021-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/2eea2be08f87/toxins-13-00021-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/ba31042b3e50/toxins-13-00021-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/a80cfa15b727/toxins-13-00021-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/230223ea5793/toxins-13-00021-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ce/7824116/2eea2be08f87/toxins-13-00021-g004.jpg

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