ArticleNucleic acids research2026
TRF2-RAP1 inhibits homology-directed repair of telomeres by promoting BLM-mediated removal of telomere R-loops.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Multi-omics profiling reveals homologous recombination repair hyperactivation as a therapeutic vulnerability in neuroendocrine cervical carcinoma.Signal transduction and targeted therapy · 2026Article
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2 authors.
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Abstract
The telomere long noncoding RNA TERRA forms R-loops in vitro at telomeres in a RAD51AP1-dependent manner. In classic DNA double-strand break repair, RAD51AP1 promotes R-loop formation and enables RAD51 to form D-loops by promoting the invasion of local RNA transcripts into donor DNA to form DNA-RNA (DR)-loops. We have previously shown that cells lacking the basic domain of TRF2 and functional RAP1 accumulate telomere D-loops, resulting in homology-directed repair (HDR)-mediated telomere-telomere clustering and formation of ultrabright telomeres (UTs). TRF2B also cooperates with RAP1 to repress telomere R-loop formation in UTs. TERRA has been shown to promote telomere HDR, associating telomeres during R-loop formation. However, the mechanism behind TERRA-mediated telomere HDR and how the TRF2-RAP1 complex regulates telomere R-loops remain unclear. Using reconstituted biochemical systems, we found that RAD51AP1 and TERRA-dependent R-loops promote RAD51-mediated telomere D-loop formation in a TERRA length- and sequence-dependent manner. Specifically, RAD51-ssDNA filaments capture telomere R-loops preferentially over dsDNA. We also discovered that BLM's interaction with the TRF2-RAP1 complex is required to promote BLM helicase-mediated unwinding of telomere R-loops. Importantly, BLM-deficient cells and cells reconstituted with BLM mutants unable to interact with TRF2 accumulate telomere R-loops in UTs. Our findings highlight a novel mechanism revealing that the TRF2-RAP1-BLM complex removes R-loops at telomeres to inhibit the generation of telomere D-loops, thus repressing telomere HDR and UT formation.
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