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鼠 B2 串联重复元件可作为 IFN 诱导增强子发挥作用。

Mouse B2 SINE elements function as IFN-inducible enhancers.

机构信息

Department of Molecular, Cellular, and Developmental Biology and BioFrontiers Institute, University of Colorado Boulder, Boulder, United States.

出版信息

Elife. 2023 May 9;12:e82617. doi: 10.7554/eLife.82617.

DOI:10.7554/eLife.82617
PMID:37158599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10229128/
Abstract

Regulatory networks underlying innate immunity continually face selective pressures to adapt to new and evolving pathogens. Transposable elements (TEs) can affect immune gene expression as a source of inducible regulatory elements, but the significance of these elements in facilitating evolutionary diversification of innate immunity remains largely unexplored. Here, we investigated the mouse epigenomic response to type II interferon (IFN) signaling and discovered that elements from a subfamily of B2 SINE (B2_Mm2) contain STAT1 binding sites and function as IFN-inducible enhancers. CRISPR deletion experiments in mouse cells demonstrated that a B2_Mm2 element has been co-opted as an enhancer driving IFN-inducible expression of . The rodent-specific B2 SINE family is highly abundant in the mouse genome and elements have been previously characterized to exhibit promoter, insulator, and non-coding RNA activity. Our work establishes a new role for B2 elements as inducible enhancer elements that influence mouse immunity, and exemplifies how lineage-specific TEs can facilitate evolutionary turnover and divergence of innate immune regulatory networks.

摘要

先天免疫的调控网络不断面临着适应新出现和不断进化的病原体的选择压力。转座元件（TEs）可以作为诱导性调控元件的来源影响免疫基因表达，但这些元件在促进先天免疫的进化多样化方面的意义在很大程度上仍未得到探索。在这里，我们研究了小鼠对 II 型干扰素（IFN）信号的表观基因组反应，发现 B2 SINE（B2_Mm2）亚家族的元件含有 STAT1 结合位点，并作为 IFN 诱导增强子发挥作用。在小鼠细胞中的 CRISPR 缺失实验表明，B2_Mm2 元件已被选为增强子，驱动 IFN 诱导表达。 啮齿动物特异性 B2 SINE 家族在小鼠基因组中高度丰富，先前的研究表明其元件具有启动子、绝缘子和非编码 RNA 活性。我们的工作为 B2 元件作为影响小鼠免疫的诱导增强子元件确立了一个新的角色，并例证了谱系特异性 TEs 如何促进先天免疫调控网络的进化更替和分化。

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