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Complementary Alu sequences mediate enhancer-promoter selectivity.

Liang Liang1, Changchang Cao1, Lei Ji1

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Alu elements mediate enhancer-promoter looping through complementary RNA interactions. This finding reveals a mechanism for gene regulation and links noncoding variants to molecular functions, including cancer risk.

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Area of Science:

  • Genomics
  • Molecular Biology
  • Epigenetics

Background:

  • Enhancers regulate gene expression by interacting with promoters.
  • The mechanism by which enhancers find their cognate promoters remains largely unknown.

Purpose of the Study:

  • To investigate the role of RNA interactions in enhancer-promoter connectivity.
  • To map enhancer-promoter RNA interactions and identify associated genomic elements.
  • To link noncoding genetic variants to their molecular functions.

Main Methods:

  • RNA in situ conformation sequencing (RICS) technology was applied to generate enhancer-promoter RNA interaction maps.
  • Analysis of Alu element overlap with enhancer-promoter RNA interaction sites.
  • Functional experiments involving Alu element knockout and tethering.
  • Mapping of noncoding risk variants to enhancer-promoter interaction maps.

Main Results:

  • 37.9% of enhancer-promoter RNA interaction sites overlapped with Alu sequences.
  • Alu and non-Alu RNA sequences showed complementarity, suggesting duplex formation.
  • Alu element manipulation (knockout, insertion, tethering) affected enhancer-promoter looping.
  • A framework was established to link noncoding variants to gene functions, identifying thousands of variants within Alu elements impacting protein-coding genes.
  • Polymorphic Alu insertion at the PTK2 enhancer was linked to tumorigenesis.

Conclusions:

  • Alu elements play a crucial role in mediating enhancer-promoter pairing specificity through RNA duplex formation.
  • This study provides a method to interpret the molecular functions of noncoding risk variants.
  • The findings offer a new understanding of gene regulation and its implications in disease.