MiR-200-3p Is Potentially Involved in Cell Cycle Arrest by Regulating Cyclin A during Aestivation in Apostichopus japonicus
MiR-200-3p Is Potentially Involved in Cell Cycle Arrest by Regulating Cyclin A during Aestivation in Apostichopus japonicus
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MiR-200-3p 可能通过调节仿刺参夏眠期间细胞周期蛋白 A 参与细胞周期停滞
DOI：
10.3390/cells8080843
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发表时间：
2019-08
期刊：
影响因子：
6
通讯作者：
Storey Kenneth B
中科院分区：
文献类型：
--
作者：
Wang Shanshan;Chen Muyan;Yin Yingchao;Storey Kenneth B
仿刺参（Apostichopus）是研究海洋无脊椎动物夏眠的良好模式生物。我们假设，机制，逮捕能源昂贵的细胞周期活动将有助于显着建立低代谢状态在夏眠。细胞周期蛋白A是一个核心和特别有趣的细胞周期调节因子，在S期和有丝分裂中发挥作用。在本研究中，miR-200- 3 p和AjCA的表达在转录和翻译水平上均呈负相关。- 是的双荧光素酶报告基因测定证实了AjCA基因转录物内miR-200- 3 p结合位点的靶向位置。此外，利用海参进行体内功能获得和丧失实验，以通过qRT-PCR和Western印迹验证肠组织中miR-200- 3 p和AjCA之间的相互作用。结果显示，在A.小肠。我们的研究结果表明，一个潜在的机制，可逆地阻止细胞周期进程在夏眠，这可能集中在miR-200- 3 p抑制控制翻译的细胞周期蛋白A mRNA转录。
The sea cucumber (Apostichopus japonicus) has become a good model organism for studying environmentally induced aestivation in marine invertebrates. We hypothesized that mechanisms that arrest energy-expensive cell cycle activity would contribute significantly to establishing the hypometabolic state during aestivation. Cyclin A is a core and particularly interesting cell cycle regulator that functions in both the S phase and in mitosis. In the present study, negative relationships between miR-200-3p and AjCA expressions were detected at both the transcriptional and the translational levels during aestivation in A. japonicus. Dual-luciferase reporter assays confirmed the targeted location of the miR-200-3p binding site within the AjCA gene transcript. Furthermore, gain- and loss-of-function experiments were conducted in vivo with sea cucumbers to verify the interaction between miR-200-3p and AjCA in intestine tissue by qRT-PCR and Western blotting. The results show that the overexpression of miR-200-3p mimics suppressed AjCA transcript levels and translated protein production, whereas transfection with a miR-200-3p inhibitor enhanced both AjCA mRNA and AjCA protein in A. japonicus intestine. Our findings suggested a potential mechanism that reversibly arrests cell cycle progression during aestivation, which may center on miR-200-3p inhibitory control over the translation of cyclin A mRNA transcripts.
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