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Inverted Alu repeats in loop-out exon skipping across hominoid evolution.

Danielle Denisko1,2, Jeonghyeon Kim1,3, Jayoung Ku1,4,5

  • 1Division of Genetics and Genomics, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, United States.

Nucleic Acids Research
|March 26, 2026
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Summary
This summary is machine-generated.

Inverted Alu elements in RNA form structures that cause exon skipping, a mechanism driving genomic innovation in human evolution. This study reveals their prevalence and impact on primate genome diversification.

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Area of Science:

  • Genomics
  • Evolutionary Biology
  • Molecular Biology

Background:

  • RNA splicing diversifies the human genome's functional landscape.
  • Intronic Alu elements, when inverted, may form RNA stem-loop structures promoting exon skipping.

Purpose of the Study:

  • To systematically analyze inverted Alu pairs in the human genome.
  • To assess their impact on exon skipping and relevance to hominoid evolution.

Main Methods:

  • Genome-wide analysis of inverted Alu pairs.
  • Comparative genomic analysis across nine primate species.
  • Experimental validation of specific Alu pairs.

Main Results:

  • Inverted Alu pairs are enriched near skippable exons, particularly those with weak 3' splice sites.
  • Identified 67,126 hominoid-specific Alu insertions forming inverted pairs.
  • These pairs are enriched in ubiquitination pathway genes.

Conclusions:

  • Inverted Alu pairs contribute to exon skipping via RNA secondary structures.
  • Transposable elements, specifically Alu pairs, drive genomic innovation in hominoid evolution.