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Mouse B2 SINE elements function as IFN-inducible enhancers.

Isabella Horton1, Conor J Kelly1, Adam Dziulko1

  • 1Department of Molecular, Cellular, and Developmental Biology and BioFrontiers Institute, University of Colorado Boulder, Boulder, United States.

Elife
|May 9, 2023
PubMed
Summary
This summary is machine-generated.

Transposable elements called B2 SINEs act as immune system enhancers. These elements are inducible by interferon signaling, driving gene expression and influencing innate immunity evolution in mice.

Keywords:
chromosomesgene expressiongene regulationgeneticsgenomicsinterferonmousetransposon

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Area of Science:

  • Genetics
  • Immunology
  • Evolutionary Biology

Background:

  • Innate immunity requires adaptation to evolving pathogens.
  • Transposable elements (TEs) can regulate immune genes but their evolutionary role is unclear.
  • Type II interferon (IFN) signaling is crucial for innate immune responses.

Purpose of the Study:

  • Investigate the role of TEs in the epigenomic response to IFN signaling.
  • Determine if TEs can act as inducible regulatory elements in innate immunity.
  • Explore the contribution of TEs to the evolutionary diversification of immune networks.

Main Methods:

  • Analysis of mouse epigenomic response to type II IFN signaling.
  • Identification of STAT1 binding sites within TEs.
  • CRISPR-Cas9 mediated deletion of specific TE elements in mouse cells.
  • Assay of IFN-inducible gene expression.

Main Results:

  • A subfamily of B2 SINEs (B2_Mm2) contains STAT1 binding sites and functions as IFN-inducible enhancers.
  • CRISPR deletion confirmed a B2_Mm2 element acts as an enhancer for IFN-inducible Dicer1 expression.
  • B2 SINE elements are abundant in the mouse genome and have diverse regulatory activities.

Conclusions:

  • B2 SINE elements serve as inducible enhancers in mouse innate immunity.
  • Lineage-specific TEs can drive evolutionary changes in immune gene regulation.
  • TEs facilitate the evolutionary turnover and divergence of innate immune regulatory networks.