Copper stress induces zebrafish central neural system myelin defects via WNT/NOTCH-hoxb5b signaling and pou3f1/fam168a/fam168b DNA methylation
文献类型：期刊论文
| 作者 | Zhang, Ting2,3; Guan, PengPeng1; Liu, WenYe2; Zhao, Guang2; Fang, YaPing1; Fu, Hui5; Gui, Jian-Fang4; Li, GuoLiang1; Liu, Jing-Xia2 |
| 刊名 | BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
 |
| 出版日期 | 2020-10-01 |
| 卷号 | 1863期号:10页码:16 |
| 关键词 | Copper Myelin hoxb5b fam168b/pou3f1 DNA methylation |
| ISSN号 | 1874-9399 |
| DOI | 10.1016/j.bbagrm.2020.194612 |
| 通讯作者 | Li, GuoLiang(guoliang.li@mail.hzau.edu.cn) ; Liu, Jing-Xia(ichliu@mail.hzau.edu.cn) |
| 英文摘要 | Unbalanced copper (Cu) homeostasis is associated with neurological development defects and diseases. However, the molecular mechanisms remain elusive. Here, central neural system (CNS) myelin defects and the down-regulated expression of WNT/NOTCH signaling and its down-stream mediator hoxb5b were observed in Cu2+ stressed zebrafish larvae. The loss/knockdown-of-function of hoxb5b phenocopied the myelin and axon defects observed in Cu2+ stressed embryos. Meanwhile, the activation of WNT/NOTCH signaling and ectopic expression of hoxb5b could rescue Cu induced myelin defects. Additionally, fam168b, similar to pou3f1/2, exhibited significant promoter hypermethylation and reduced expression in Cu2+ stressed embryos. The hypermethylated locus in fam168b promoter acted pivotally in its transcription, and the loss/knockdown of fam168b/pou3f1 also induced myelin defects. This study also demonstrated that fam168b/pou3f1 and hoxb5b axis acted in a seesaw manner during fish embryogenesis: Cu induced the down-regulated expression of the WNT &NOTCH-hoxb5b axis through the function of copper transporter cox17, coupled with the promoter methylation of genes fam168b/pou3f1, and its subsequent down-regulated expression through the function of another transporter atp7b, making joint contributions to myelin defects in embryos. |
| WOS关键词 | WHITE-MATTER ; MOTOR-NEURON ; WNT ; EXPRESSION ; OLIGODENDROCYTES ; DIFFERENTIATION ; ABNORMALITIES ; DEFICIENCY ; METABOLISM ; ACTIVATION |
| 资助项目 | National Key R&D Program of China[2018YFD0900101] ; Fundamental Research Funds for the Central University[2662018JC024] ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; National Natural Science Foundation of China[31771402] |
| WOS研究方向 | Biochemistry & Molecular Biology ; Biophysics |
| 语种 | 英语 |
| WOS记录号 | WOS:000574417000002 |
| 出版者 | ELSEVIER |
| 资助机构 | National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; National Key R&D Program of China ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; Fundamental Research Funds for the Central University ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; project of key laboratory of Biodiversity and Conservation of Aquatic Organisms ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China |
| 源URL | [http://ir.ihb.ac.cn/handle/342005/38946]  |
| 专题 | 水生生物研究所_鱼类生物学及渔业生物技术研究中心_期刊论文 |
| 通讯作者 | Li, GuoLiang; Liu, Jing-Xia |
| 作者单位 | 1.Huazhong Agr Univ, Coll Informat, Hubei Engn Technol Res Ctr Agr Big Data, Agr Bioinformat Key Lab Hubei Prov, Wuhan 430070, Peoples R China 2.Huazhong Agr Univ, Coll Fisheries, Key Lab Freshwater Anim Breeding, Minist Agr, Wuhan 430070, Peoples R China 3.Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, Guangdong Prov Key Lab Appl Marine Biol, Guangzhou 510301, Peoples R China 4.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China 5.Wuhan Univ, Sch Basic Med Sci, Dept Anat, Wuhan 430072, Peoples R China |
| 推荐引用方式 GB/T 7714 | Zhang, Ting,Guan, PengPeng,Liu, WenYe,et al. Copper stress induces zebrafish central neural system myelin defects via WNT/NOTCH-hoxb5b signaling and pou3f1/fam168a/fam168b DNA methylation[J]. BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS,2020,1863(10):16. |
| APA | Zhang, Ting.,Guan, PengPeng.,Liu, WenYe.,Zhao, Guang.,Fang, YaPing.,...&Liu, Jing-Xia.(2020).Copper stress induces zebrafish central neural system myelin defects via WNT/NOTCH-hoxb5b signaling and pou3f1/fam168a/fam168b DNA methylation.BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS,1863(10),16. |
| MLA | Zhang, Ting,et al."Copper stress induces zebrafish central neural system myelin defects via WNT/NOTCH-hoxb5b signaling and pou3f1/fam168a/fam168b DNA methylation".BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS 1863.10(2020):16. |
入库方式： OAI收割
来源：水生生物研究所
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