ArticleScience advances2020
Mus81-Eme1-dependent aberrant processing of DNA replication intermediates in mitosis impairs genome integrity.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Asymmetric attrition and secondary chromosome destabilization after double-strand breaks in human embryonic development.Nature communications · 2026Article
- Integrating genomic structural equation modeling and experimental validation to unravel the genetic basis of male genital lichen sclerosus.Frontiers in immunology · 2026Article
- Decoding nucleoside supplementation: how thymidine outperforms ribonucleosides in accelerating mammalian replication forks.Nucleic acids research · 2025Article
- Oncogenic EME1 promotes tumor progression and immune modulation in human cancers with therapeutic targeting potential.Discover oncology · 2025Article
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- Targeting the Werner syndrome protein in microsatellite instability cancers: mechanisms and therapeutic potential.Clinical and experimental medicine · 2025Review
- Versatile enhancement of the killing potential of anti-cancer agents achieved by peptide mimetics of the PCNA interface towards specialized DNA polymerases.Cell death & disease · 2025Article
- Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe.Science advances · 2025Article
- Buenos Aires Breast Cancer Symposium (BA-BCS 2024) A Second Successful "Trial" for Bringing Together both World Hemispheres To Debate the Future of Translational Breast Cancer Research.Journal of mammary gland biology and neoplasia · 2025Article
- TDP1 phosphorylation by CDK1 in mitosis promotes MUS81-dependent repair of trapped Top1-DNA covalent complexes.The EMBO journal · 2024Article
- Novel molecular typing reveals the risk of recurrence in patients with early-stage papillary thyroid cancer.Thyroid research · 2024Article
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- Polymerase iota (Pol ι) prevents PrimPol-mediated nascent DNA synthesis and chromosome instability.Science advances · 2023Article
- FIBP interacts with transcription factor STAT3 to induce EME1 expression and drive radioresistance in lung adenocarcinoma.International journal of biological sciences · 2023Article
- Multiple DNA repair pathways contribute to MMS-induced post-replicative DNA synthesis inmicroPublication biology · 2023Article
- Sister chromatid exchanges induced by perturbed replication can form independently of BRCA1, BRCA2 and RAD51.Nature communications · 2022Article
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- Metnase and EEPD1: DNA Repair Functions and Potential Targets in Cancer Therapy.Frontiers in oncology · 2022Review
- Homologous Recombination Related Signatures Predict Prognosis and Immunotherapy Response in Metastatic Urothelial Carcinoma.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome instability (CIN) underpins cancer evolution and is associated with drug resistance and poor prognosis. Understanding the mechanistic basis of CIN is thus a priority. The structure-specific endonuclease Mus81-Eme1 is known to prevent CIN. Intriguingly, however, here we show that the aberrant processing of late replication intermediates by Mus81-Eme1 is a source of CIN. Upon depletion of checkpoint kinase 1 (Chk1), Mus81-Eme1 cleaves under-replicated DNA engaged in mitotic DNA synthesis, leading to chromosome segregation defects. Supplementing cells with nucleosides allows the completion of mitotic DNA synthesis, restraining Mus81-Eme1-dependent DNA damage in mitosis and the ensuing CIN. We found no correlation between CIN arising from nucleotide shortage in mitosis and cell death, which were selectively linked to DNA damage load in mitosis and S phase, respectively. Our findings imply the possibility of optimizing Chk1-directed therapies by inducing cell death while curtailing CIN, a common side effect of chemotherapy.
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