ArticleNature2011
Aberrant chromosome morphology in human cells defective for Holliday junction resolution.
Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 217 citations in OpenAlex.
- Centrosome-related gene SPHK1 drives bladder cancer progression and therapeutic vulnerability.Translational oncology · 2026Article
- The ultrafine-bridge-associated endonuclease ANKLE1 is stimulated by tension in DNA to process branch-points.Nucleic acids research · 2026Article
- Real-time visualization of spatial and temporal coordination in resolvase-mediated Holliday junction binding.iScience · 2026Article
- Discovery of Two Structurally Distinct Classes of Inhibitors Targeting the Nuclease MUS81 and Enhancing Efficacy of Chemotherapy in Cancer Cells.Journal of medicinal chemistry · 2026Article
- ANKLE1 processes chromatin bridges by cleaving mechanically stressed DNA.Nature communications · 2025Article
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- Mechanism of structure-specific DNA binding by the FANCM branchpoint translocase.Nucleic acids research · 2024Article
- The anti-tumor effect of trifluridine via induction of aberrant mitosis is unaffected by mutations modulating p53 activity.Cell death discovery · 2024Article
- TFIP11 promotes replication fork reversal to preserve genome stability.Nature communications · 2024Article
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- FIRRM/C1orf112 mediates resolution of homologous recombination intermediates in response to DNA interstrand crosslinks.Science advances · 2023Article
- Human Endonuclease ANKLE1 Localizes at the Midbody and Processes Chromatin Bridges to Prevent DNA Damage and cGAS-STING Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- NCAPH Stabilizes GEN1 in Chromatin to Resolve Ultra-Fine DNA Bridges and Maintain Chromosome Stability.Molecules and cells · 2022Article
- Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy.Nature communications · 2022Article
- Article
- DNA Holliday Junction: History, Regulation and Bioactivity.International journal of molecular sciences · 2022Review
- Single-cell transcription profiles in Bloom syndrome patients link BLM deficiency with altered condensin complex expression signatures.Human molecular genetics · 2022Article
- New twists to the ALTernative endings at telomeres.DNA repair · 2022Review
- Holliday junction resolution by At-HIGLE: an SLX1 lineage endonuclease from Arabidopsis thaliana with a novel in-built regulatory mechanism.Nucleic acids research · 2022Article
- Generation of double Holliday junction DNAs and their dissolution/resolution within a chromatin context.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In somatic cells, Holliday junctions can be formed between sister chromatids during the recombinational repair of DNA breaks or after replication fork demise. A variety of processes act upon Holliday junctions to remove them from DNA, in events that are critical for proper chromosome segregation. In human cells, the BLM protein, inactivated in individuals with Bloom's syndrome, acts in combination with topoisomerase IIIα, RMI1 and RMI2 (BTR complex) to promote the dissolution of double Holliday junctions. Cells defective for BLM exhibit elevated levels of sister chromatid exchanges (SCEs) and patients with Bloom's syndrome develop a broad spectrum of early-onset cancers caused by chromosome instability. MUS81-EME1 (refs 4-7), SLX1-SLX4 (refs 8-11) and GEN1 (refs 12, 13) also process Holliday junctions but, in contrast to the BTR complex, do so by endonucleolytic cleavage. Here we deplete these nucleases from Bloom's syndrome cells to analyse human cells compromised for the known Holliday junction dissolution/resolution pathways. We show that depletion of MUS81 and GEN1, or SLX4 and GEN1, from Bloom's syndrome cells results in severe chromosome abnormalities, such that sister chromatids remain interlinked in a side-by-side arrangement and the chromosomes are elongated and segmented. Our results indicate that normally replicating human cells require Holliday junction processing activities to prevent sister chromatid entanglements and thereby ensure accurate chromosome condensation. This phenotype was not apparent when both MUS81 and SLX4 were depleted from Bloom's syndrome cells, suggesting that GEN1 can compensate for their absence. Additionally, we show that depletion of MUS81 or SLX4 reduces the high frequency of SCEs in Bloom's syndrome cells, indicating that MUS81 and SLX4 promote SCE formation, in events that may ultimately drive the chromosome instabilities that underpin early-onset cancers associated with Bloom's syndrome.
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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.