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在海胆中,与miR-2013-3p相互作用的低氧诱导因子-1α(HIF-1α)通过靶向谷氨酸脱氢酶来调节病原体诱导的能量产生变化。

HIF-1α interacting with miR-2013-3p regulates pathogen-induced energy production changes via targeting glutamate dehydrogenase in the sea urchin .

作者信息

Ning Bingyu, Sun Jingxian, Cui Dongyao, Zhang Shuxin, Zhan Yaoyao, Chang Yaqing

机构信息

Key Laboratory of Mariculture & Stock Enhancement in North China's Sea, Ministry of Agriculture and Rural Affairs, Dalian Ocean University, Dalian, Liaoning, P. R. China.

College of Life Science, Liaoning Normal University, Dalian, Liaoning, P. R. China.

出版信息

Virulence. 2024 Dec;15(1):2367660. doi: 10.1080/21505594.2024.2367660. Epub 2024 Jun 18.

Abstract

To investigate the functions of hypoxia inducible factor-1α (HIF-1α) homologs, we cloned and characterized the full-length cDNA of a novel homolog () from the sea urchin . We then explored the functions of and its regulatory factor (miR-2013-3p) in the pathogen-induced metabolic response of . The results showed the following: 1) The full-length cDNA of was 4265 bp, with a high level of sequence conservation across the phylum Echinodermata. 2) MiR-2013-3p could bind to the 3'-UTR of and negatively regulate the expression of in . 3) Both silencing and miR-2013-3p overexpression suppressed the relative content of adenosine triphosphate (ATP) in coelomocytes as well as the relative expression (mRNA and protein) and total enzyme activity of glutamate dehydrogenase (GDH) in . 4) The miR-2013-3p/ axis may regulate ATP production at 6-24 h and 48-72 h post-pathogen infection through accompanied by alterations in the relative expression and enzyme activity of GDH in . In summary, all observations from this study indicated that the pathogen utilizes the miR-2013-3p/SinHIF-1α axis to reduce ATP production and thereby attenuate the antimicrobial capability of the host via targeting GDH.

摘要

为了研究缺氧诱导因子-1α(HIF-1α)同源物的功能,我们克隆并鉴定了来自海胆的一种新型同源物()的全长cDNA。然后,我们探讨了和其调控因子(miR-2013-3p)在病原体诱导的的代谢反应中的功能。结果如下:1)的全长cDNA为4265 bp,在棘皮动物门中具有高度的序列保守性。2)MiR-2013-3p可以与的3'-UTR结合,并负向调节中的表达。3)沉默和miR-2013-3p过表达均抑制了体腔细胞中三磷酸腺苷(ATP)的相对含量,以及中的谷氨酸脱氢酶(GDH)的相对表达(mRNA和蛋白质)和总酶活性。4)miR-2013-3p/轴可能通过伴随着中的GDH相对表达和酶活性的改变,在病原体感染后6-24小时和48-72小时调节ATP的产生。总之,本研究的所有观察结果表明,病原体利用miR-2013-3p/SinHIF-1α轴来减少ATP的产生,从而通过靶向GDH来削弱宿主的抗菌能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8550/11188814/bd0e618b61b8/KVIR_A_2367660_F0001_OC.jpg

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