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Repeats mimic pathogen-associated patterns across a vast evolutionary landscape.

Petr Šulc1, Andrea Di Gioacchino2, Alexander Solovyov3

  • 1School of Molecular Sciences and Center for Molecular Design and Biomimetics, The Biodesign Institute, Arizona State University, Tempe, AZ, USA; School of Natural Sciences, Department of Bioscience, TU Munich, Garching, Germany.

Cell Genomics
|September 25, 2025
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Summary
This summary is machine-generated.

Diseased cells can activate innate immunity by transcribing silenced DNA. Our framework quantifies this viral mimicry, revealing evolutionary pressures that maintain these genetic elements.

Keywords:
cancergenome evolutioninnate immunitymathematical modelsnon-coding RNApathogen-associated molecular patternsrepetitive elementsstatistical physicsviral mimicry

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Area of Science:

  • Genomics and Molecular Biology
  • Immunology
  • Evolutionary Biology
  • Statistical Physics

Background:

  • Many human diseases involve the transcription of repetitive DNA elements that are usually silenced.
  • These transcribed elements contain pathogen-associated molecular patterns (PAMPs) that activate the innate immune system through pattern recognition receptors (PRRs), a process termed viral mimicry.
  • Understanding the evolutionary forces driving the emergence and retention of these PAMPs is crucial.

Purpose of the Study:

  • To develop a statistical physics framework for quantifying viral mimicry.
  • To identify specific repetitive DNA elements that act as potential viral mimics across eukaryotic genomes.
  • To propose evolutionary hypotheses explaining the enrichment and maintenance of PAMPs within repetitive DNA.

Main Methods:

  • Developed a statistical physics framework to measure 'selective forces' enriching PAMPs.
  • Compared PAMP enrichment against genome-wide reference distributions.
  • Validated predictions by identifying specific repeats binding to different PRRs in eukaryotic genomes.

Main Results:

  • Identified potential viral mimics within various repeat families across eukaryotic genomes.
  • Demonstrated that shared evolutionary mechanisms likely drive the emergence and retention of these PAMPs.
  • Showed that PAMPs can be enriched due to selection acting on repetitive DNA.

Conclusions:

  • Viral mimicry is an emerging hallmark of disease, driven by transcribed repetitive DNA.
  • Two evolutionary hypotheses, 'repeat-centric' and 'organism-centric', are proposed to explain PAMP maintenance.
  • The findings suggest PAMPs are integral to repeat expansion or serve as a cell-intrinsic regulatory mechanism against transcriptional dysregulation.