Fertility Enhancement but Premature Ovarian Failure in esr1-Deficient Female Zebrafish.

Fertility Enhancement but Premature Ovarian Failure in esr1-Deficient Female Zebrafish.
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esr1缺陷雌性斑马鱼的生育能力增强但卵巢早衰

DOI:
10.3389/fendo.2018.00567
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发表时间:
2018
影响因子:
5.2
通讯作者:
Lin H
Lin H
中科院分区:
医学2区
文献类型:
--
作者:
Chen Y;Tang H;Wang L;He J;Guo Y;Liu Y;Liu X;Lin H

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雌激素通过卵巢中的雌激素受体(ER)调节雌性生殖。然而,雌激素/ER信号在生殖过程中的确切生理作用在斑马鱼中仍然不清楚。本研究通过转录激活因子样效应子核酸酶(TALENs)在斑马鱼中成功构建了雌激素受体α(esr 1)突变株。结果表明,突变体雌虫在受精后90天(dpf),其生育能力增强,卵巢组织学正常。然而,有生育能力的女性数量随着年龄的增长而减少。到180 dpf时,esr 1突变雌性不育,卵巢退化,而年龄匹配的野生型雌性仍然具有生育能力。此外,在90 dpf的完全生长(FG)卵泡中可以发现很少的大卵黄颗粒,并且在esr 1突变体斑马鱼中,vtg基因的表达在90和180 dpf都下调。此外,类固醇生成途径和mTOR信号通路在90 dpf时过度激活,但在esr 1突变体斑马鱼中在180 dpf时过早下降。总的来说,本研究提供的证据表明esr 1是斑马鱼卵巢维持的基础。
It is well established that estrogens regulate female reproduction through estrogen receptors (ERs) in the ovary. However, the precise physiological role of estrogen/ER signaling in reproduction processes remains poorly defined in zebrafish. In this study, we successfully generated an ERα (esr1) mutant line in zebrafish via transcription activator-like effectors nucleases (TALENs). It was found in the mutant females that the fertility was enhanced and the ovarian histology was normal at 90 days post-fertilization (dpf). However, the number of fertile females decreased with age. By 180 dpf, esr1 mutant females were infertile with degenerated ovaries, while the age-matched wild-type females were still fertile. Additionally, few large vitellogenic granules can be found in full grown (FG) follicles at 90 dpf and the expression of vtg genes were down-regulated at both 90 and 180 dpf in esr1 mutant zebrafish. Moreover, steroidogenesis pathway and mTOR signaling pathway were over-activated at 90 dpf, but declined prematurely in esr1 mutant zebrafish by 180 dpf. Collectively, the present study provides evidence that esr1 is fundamental for ovarian maintenance in zebrafish.
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