ArticleNature communications2018
53BP1 can limit sister-chromatid rupture and rearrangements driven by a distinct ultrafine DNA bridging-breakage process.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Myelin Dynamics at the Axon-Oligodendrocyte Interface: Adaptive Conduction Homeostasis in Demyelination, Remyelination and White Matter Repair.International journal of molecular sciences · 2026Review
- ANKLE1 processes chromatin bridges by cleaving mechanically stressed DNA.Nature communications · 2025Article
- Centromere protection requires strict mitotic inactivation of the Bloom syndrome helicase complex.Nature communications · 2025Article
- A homozygous TRIP13 pathogenic variant associated with familiar oocyte arrest and prematurely condensed sperm chromosomes.Molecular cytogenetics · 2025Article
- RECQ4-MUS81 interaction contributes to telomere maintenance with implications to Rothmund-Thomson syndrome.Nature communications · 2025Article
- The interplay of the translocase activity and protein recruitment function of PICH in ultrafine anaphase bridge resolution and genomic stability.Nucleic acids research · 2025Article
- Human AAA+ ATPase FIGNL1 suppresses RAD51-mediated ultra-fine bridge formation.Nucleic acids research · 2024Article
- DNA strand breaks at centromeres: Friend or foe?Seminars in cell & developmental biology · 2024Review
- Biochemical and mechanistic analysis of the cleavage of branched DNA by human ANKLE1.Nucleic acids research · 2023Article
- Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.Nature communications · 2023Article
- Incorporation of 53BP1 into phase-separated bodies in cancer cells during aberrant mitosis.Journal of cell science · 2023Article
- Article
- Processing DNA lesions during mitosis to prevent genomic instability.Biochemical Society transactions · 2022Review
- Genome-Protective Topoisomerase 2a-Dependent G2 Arrest Requires p53 in hTERT-Positive Cancer Cells.Cancer research · 2022Article
- Mechanistic origins of diverse genome rearrangements in cancer.Seminars in cell & developmental biology · 2022Review
- 53BP1-ACLY-SLBP-coordinated activation of replication-dependent histone biogenesis maintains genomic integrity.Nucleic acids research · 2022Article
- Review
- Regulation of mitotic chromosome architecture and resolution of ultrafine anaphase bridges by PICH.Cell cycle (Georgetown, Tex.) · 2021Article
- Mind the replication gap.Royal Society open science · 2021Review
- Shaping the BRCAness mutational landscape by alternative double-strand break repair, replication stress and mitotic aberrancies.Nucleic acids research · 2021Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Chromosome missegregation acts as one of the driving forces for chromosome instability and cancer development. Here, we find that in human cancer cells, HeLa and U2OS, depletion of 53BP1 (p53-binding protein 1) exacerbates chromosome non-disjunction resulting from a new type of sister-chromatid intertwinement, which is distinct from FANCD2-associated ultrafine DNA bridges (UFBs) induced by replication stress. Importantly, the sister DNA intertwinements trigger gross chromosomal rearrangements through a distinct process, named sister-chromatid rupture and bridging. In contrast to conventional anaphase bridge-breakage models, we demonstrate that chromatid axes of the intertwined sister-chromatids rupture prior to the breakage of the DNA bridges. Consequently, the ruptured sister arms remain tethered and cause signature chromosome rearrangements, including whole-arm (Robertsonian-like) translocation/deletion and isochromosome formation. Therefore, our study reveals a hitherto unreported chromatid damage phenomenon mediated by sister DNA intertwinements that may help to explain the development of complex karyotypes in tumour cells.
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