ArticleCell reports2025
Translesion-synthesis-mediated bypass of DNA lesions occurs predominantly behind replication forks restarted by PrimPol.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Understanding single stranded DNA gaps: from formation to fate.The Biochemical journal · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- The need for speed: drivers and consequences of accelerated replication forks.Communications biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The bypass of DNA lesions by translesion synthesis (TLS) polymerases is a critical step for DNA damage tolerance, allowing the completion of DNA synthesis. It has been under debate whether TLS-mediated bypass restarts stalled forks or occurs post-replicationally. We developed cell imaging techniques based on proximity ligation to monitor the recruitment of TLS polymerases Polκ and Polη to DNA adducts. We show that this recruitment is adduct specific, with Polκ being preferentially recruited to benzo[a]pyrene diol epoxide (BPDE) lesions and Polη to cisplatin lesions. The recruitment depends on the primase-polymerase PrimPol, which reprimes downstream of stalled forks to restart DNA synthesis. TLS polymerase deficiency results in the accumulation of single-stranded DNA (ssDNA) gaps in an adduct-specific manner, which are processed into double-strand breaks (DSBs). Our findings argue that TLS occurs mainly behind the restarted replication fork in order to fill PrimPol-derived gaps and is essential to suppress the nucleolytic conversion of ssDNA gaps into cytotoxic DSBs in a lesion-specific manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.