ArticleNature communications2026
TONSL suppresses polymerase theta-dependent tandem duplications through chromatin-guided repair.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- TONSL emerges as a key barrier to prevent large tandem duplications.Nature structural & molecular biology · 2026Article
- TONSOKU prevents the formation of large tandem duplications and restrains ATR-WEE1 checkpoint activation.Nature communications · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Tandem duplications (TDs) are a common form of genomic rearrangements with both adaptive and pathogenic consequences. While prevalent in genomically unstable cancer genomes, TDs are rarely detected in normal tissues, suggesting the existence of robust protective mechanisms. Here, we identify the histone chaperone TONSL/TONSOKU (tnsl-1 in C. elegans) as a critical suppressor of TD formation. Loss of tnsl-1 results in the accumulation of TDs in two distinct size classes (~25 kb and ~300 kb), arising from different developmental contexts: small TDs emerge in rapidly dividing embryonic cells, whereas large TDs form in slower-dividing germline progenitors. Both classes depend on polymerase theta-mediated end joining (TMEJ), implicating DNA double-strand breaks in their genesis. Inhibition of break-induced replication (BIR) via Pif1 helicase loss reduces TD size, revealing a role for BIR in TD expansion. Remarkably, TONSL-deficient Arabidopsis thaliana exhibit an identical TD signature, highlighting the evolutionary conservation of this genome surveillance mechanism. These findings position TONSL as a cross-kingdom guardian of genome integrity through suppression of TD formation.
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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 OpenQuestion graph.