ArticleNucleus (Austin, Tex.)2016
Cervantes and Quijote protect heterochromatin from aberrant recombination and lead the way to the nuclear periphery.
Article in Nucleus (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- The Role of Arp2/3 in End-Resection During DNA Double-Strand Break Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Low YTHDC1 Expression Upregulates FSCN1 to Promote Nuclear F-Actin Formation and Facilitate Double-strand DNA Breaks Repair in TMZ-Resistant Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genome scale CRISPR screens identify actin capping proteins as key modulators of therapeutic responses to radiation and immunotherapy.bioRxiv : the preprint server for biology · 2025Article
- Nuclear and genome dynamics underlying DNA double-strand break repair.Nature reviews. Molecular cell biology · 2025Review
- Off-pore Nup98 condensates mobilize heterochromatic breaks and exclude Rad51.Molecular cell · 2025Article
- Interplay and Dynamics of Chromatin Architecture and DNA Damage Response: An Overview.Cancers · 2025Review
- The fission yeast SUMO-targeted ubiquitin ligase Slx8 functionally associates with clustered centromeres and the silent mating-type region at the nuclear periphery.Biology open · 2024Article
- DNA double-strand break movement in heterochromatin depends on the histone acetyltransferase dGcn5.Nucleic acids research · 2024Article
- "Off-pore" nucleoporins relocalize heterochromatic breaks through phase separation.bioRxiv : the preprint server for biology · 2024Article
- Nup153 is not required for anchoring heterochromatic DSBs to the nuclear periphery.microPublication biology · 2024Article
- The impact of chromatin on double-strand break repair: Imaging tools and discoveries.DNA repair · 2024Article
- A R-loop sensing pathway mediates the relocation of transcribed genes to nuclear pore complexes.Nature communications · 2023Article
- Review
- 53BP1 regulates heterochromatin through liquid phase separation.Nature communications · 2022Article
- TEX264 at the intersection of autophagy and DNA repair.Autophagy · 2022Review
- Multi-scale dynamics of heterochromatin repair.Current opinion in genetics & development · 2021Review
- The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks.Genes · 2021Review
- SUMO-Targeted Ubiquitin Ligases and Their Functions in Maintaining Genome Stability.International journal of molecular sciences · 2021Review
- Live Cell Imaging of Nuclear Actin Filaments and Heterochromatic Repair foci in Drosophila and Mouse Cells.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Repairing double-strand breaks (DSBs) is particularly challenging in heterochromatin, where the abundance of repeated sequences exacerbates the risk of ectopic recombination and chromosome rearrangements. In Drosophila cells, faithful homologous recombination (HR) repair of heterochromatic DSBs relies on a specialized pathway that relocalizes repair sites to the nuclear periphery before Rad51 recruitment. Here we show that HR progression is initially blocked inside the heterochromatin domain by SUMOylation and the coordinated activity of two distinct Nse2 SUMO E3 ligases: Quijote (Qjt) and Cervantes (Cerv). In addition, the SUMO-targeted ubiquitin ligase (STUbL) Dgrn, but not its partner dRad60, is recruited to heterochromatic DSBs at early stages of repair and mediates relocalization. However, Dgrn is not required to prevent Rad51 recruitment inside the heterochromatin domain, suggesting that the block to HR progression inside the domain and relocalization to the nuclear periphery are genetically separable pathways. Further, SUMOylation defects affect relocalization without blocking heterochromatin expansion, revealing that expansion is not required for relocalization. Finally, nuclear pores and inner nuclear membrane proteins (INMPs) anchor STUbL/RENi components and repair sites to the nuclear periphery, where repair continues. Together, these studies reveal a critical role of SUMOylation and nuclear architecture in the spatial and temporal regulation of heterochromatin repair and the protection of genome integrity.
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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.