4.8 Article

TRF2 promotes, remodels and protects telomeric Holliday junctions

Journal

EMBO JOURNAL
Volume 28, Issue 6, Pages 641-651

Publisher

WILEY
DOI: 10.1038/emboj.2009.11

Keywords

recombination; resolvase; telomere; TRF2

Funding

  1. Ligue Nationale contre le Cancer (Eric Gilson equipe labellisee)
  2. Cancer Research UK
  3. Institut National du Cancer (INCa)
  4. Ligue Contre le Cancer de Haute Savoie
  5. Association pour la Recherche sur le Cancer
  6. Biotechnology and Biological Sciences Research Council [BB/E001777/1] Funding Source: researchfish
  7. BBSRC [BB/E001777/1] Funding Source: UKRI

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The ability of the telomeric DNA-binding protein, TRF2, to stimulate t-loop formation while preventing t-loop deletion is believed to be crucial to maintain telomere integrity in mammals. However, little is known on the molecular mechanisms behind these properties of TRF2. In this report, we show that TRF2 greatly increases the rate of Holliday junction (HJ) formation and blocks the cleavage by various types of HJ resolving activities, including the newly identified human GEN1 protein. By using potassium permanganate probing and differential scanning calorimetry, we reveal that the basic domain of TRF2 induces structural changes to the junction. We propose that TRF2 contributes to t-loop stabilisation by stimulating HJ formation and by preventing resolvase cleavage. These findings provide novel insights into the interplay between telomere protection and homologous recombination and suggest a general model in which TRF2 maintains telomere integrity by controlling the turnover of HJ at t-loops and at regressed replication forks.

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