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Record W7115892702 · doi:10.64898/2025.12.16.694654

Clastogenesis by nucleotide lesions requires the completion of two cell cycles

2025· article· W7115892702 on OpenAlexaff

Bibliographic record

VenuebioRxiv (Cold Spring Harbor Laboratory) · 2025
Typearticle
Language
FieldBiochemistry, Genetics and Molecular Biology
TopicDNA Repair Mechanisms
Canadian institutionsInstitute of Cancer Research
FundersOffice of the Higher Education Commission
KeywordsDNA repairGenome instabilityDNA replicationMitosisDNADNA damageSomatic cellNucleotide excision repairNucleotide

Abstract

fetched live from OpenAlex

Abstract Damaged DNA nucleotides can trigger genome rearrangements through clastogenesis, a process driven by erroneous repair of double-strand breaks (DSBs) and associated with cancer development. While DSBs are known to arise from endonuclease activity at stalled replication forks, the clastogenic potential of such DSBs has remained uncertain. Here, we identify a previously unrecognized mechanism of clastogenesis using wild-type, nucleotide excision repair (NER)-deficient and translesion synthesis (TLS)-deficient cells, combined with advanced cytogenetic analyses. We demonstrate that, single-stranded DNA (ssDNA) tracts harboring unrepaired lesions rather than DSBs at collapsed replication forks can persist through mitosis. Only during the subsequent S phase, these tracts are converted into a new class of, highly clastogenic, DSBs. Consistent with a role of this mechanism in carcinogenesis, prostate cancers exhibiting extensive genomic rearrangements frequently harbor somatic defects in NER or in error-free homologous recombination-mediated DSB repair. These findings provide critical mechanistic insight and highlight potential implications for routine clastogenicity testing. Graphical abstract Nucleotide lesions (light blue triangle) can trigger double-strand breaks (DSBs) through endonucleolytic cleavage at stalled or reversed replication forks. Traditionally, these DSBs were assumed to drive genome rearrangements, a process termed clastogenesis. Here we describe a distinct, delayed, mechanism of clastogenesis. Thus, unreplicated nucleotide lesions within single-stranded (ss) DNA regions persist through mitosis into the next cell cycle. During the subsequent S phase, these ssDNA tracts collapse into DSBs, presumably via replication runoff. These delayed DSBs then promote extensive genomic reshuffling. Supporting this model, prostate cancers with high levels of genomic rearrangements are frequently associated with somatic defects in nucleotide excision repair (NER)—a pathway that normally prevents lesion-induced clastogenesis.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.004
Threshold uncertainty score0.014

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0040.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.009
GPT teacher head0.227
Teacher spread0.218 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

Explore more

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