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Updated: Dec 1, 2025

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TRF2 Mediates Replication Initiation within Human Telomeres to Prevent Telomere Dysfunction.

William C Drosopoulos1, Zhong Deng2, Shyam Twayana1

  • 1Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.

Cell Reports
|November 11, 2020
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Summary
This summary is machine-generated.

Telomeric repeat-binding factor 2 (TRF2) recruits origin recognition complex (ORC) to telomeres, forming functional DNA replication origins. This process is crucial for rescuing compromised telomere replication and preventing telomere dysfunction.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Telomeres protect chromosome ends but pose replication challenges.
  • Telomeric repeat-binding factor 2 (TRF2) is a key shelterin component at telomeres.
  • Origin recognition complex (ORC) proteins initiate DNA replication.

Purpose of the Study:

  • To investigate if TRF2-recruited ORC proteins form functional replication origins at telomeres.
  • To understand the role of telomeric origins in resolving replication stress.

Main Methods:

  • Utilized a TRF2 mutant defective in ORC interaction.
  • Assessed telomeric initiation events, telomere repeat length, and aberrations in human cells.
  • Induced replication stress to study telomeric origin activation.
  • Investigated the role of chromatin remodeler SNF2H.

Main Results:

  • Reducing ORC2 recruitment to telomeres decreased initiation events and caused telomere loss and dysfunction.
  • Telomeric origins are activated under replication stress, acting as a rescue mechanism.
  • SNF2H facilitates ORC2 access, promoting telomeric initiation.

Conclusions:

  • TRF2 actively recruits ORC to establish functional telomeric origins.
  • These origins are vital for rescuing compromised telomere replication and maintaining telomere stability.
  • TRF2-mediated ORC recruitment is a critical mechanism against telomere dysfunction.