ArticleMolecular cell2010
The MMS22L-TONSL complex mediates recovery from replication stress and homologous recombination.
Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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94 citing papers in PubMed, 141 citations in OpenAlex.
- Identification of novel genes with enriched expression in human intermediate progenitors reveals a key role for CDKN3 in cortical development.Stem cell reports · 2026Article
- Pathogenic variants in the human TONSL protein associated with SPONASTRIME dysplasia impair protein dimerization and DNA repair.Science advances · 2026Article
- TONSL Promotes Hepatocellular Carcinoma Progression by Inhibiting Apoptosis Through Homologous Recombination Repair.Cancer science · 2026Article
- TONSL emerges as a key barrier to prevent large tandem duplications.Nature structural & molecular biology · 2026Article
- Treatment Response and Outcomes of Prostate Cancer Patients Carrying the Germline MMS22L F722fs Mutation.The Prostate · 2026Article
- TONSOKU prevents the formation of large tandem duplications and restrains ATR-WEE1 checkpoint activation.Nature communications · 2026Article
- TONSL suppresses polymerase theta-dependent tandem duplications through chromatin-guided repair.Nature communications · 2026Article
- Article
- A case report of SPONASTRIME dysplasia with novel TONSL mutation: genetic analysis, clinical manifestations, and the effect of growth hormone treatment.Human molecular genetics · 2025Article
- Cancer histone mutations impact protein binding and DNA repair with possible links to genomic instability.Nucleic acids research · 2025Article
- H3.1K27M-induced misregulation of the TONSOKU-H3.1 pathway causes genomic instability.Nature communications · 2025Article
- Predictomes, a classifier-curated database of AlphaFold-modeled protein-protein interactions.Molecular cell · 2025Article
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- MulNet: a scalable framework for reconstructing intra- and intercellular signaling networks from bulk and single-cell RNA-seq data.Briefings in bioinformatics · 2025Article
- Carboplatin-resistance-related DNA damage repair prognostic gene signature and its association with immune infiltration in breast cancer.Frontiers in immunology · 2025Article
- Knockout ofBiomedicines · 2024Article
- CRISPR/Cas9 Technology Providing the Therapeutic Landscape of Metastatic Prostate Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The multifaceted roles of the Ctf4 replisome hub in the maintenance of genome integrity.DNA repair · 2024Review
- Comparative DNA methylation reveals epigenetic adaptation to high altitude in snub-nosed monkeys.Zoological research · 2024Article
34 more citing papers are in PubMed but not listed here.
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25 authors at 8 institutions in 4 countries.
Funding
Abstract
Genome integrity is jeopardized each time DNA replication forks stall or collapse. Here we report the identification of a complex composed of MMS22L (C6ORF167) and TONSL (NFKBIL2) that participates in the recovery from replication stress. MMS22L and TONSL are homologous to yeast Mms22 and plant Tonsoku/Brushy1, respectively. MMS22L-TONSL accumulates at regions of ssDNA associated with distressed replication forks or at processed DNA breaks, and its depletion results in high levels of endogenous DNA double-strand breaks caused by an inability to complete DNA synthesis after replication fork collapse. Moreover, cells depleted of MMS22L are highly sensitive to camptothecin, a topoisomerase I poison that impairs DNA replication progression. Finally, MMS22L and TONSL are necessary for the efficient formation of RAD51 foci after DNA damage, and their depletion impairs homologous recombination. These results indicate that MMS22L and TONSL are genome caretakers that stimulate the recombination-dependent repair of stalled or collapsed replication forks.
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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.