ArticleCommunications biology2025
Continuous nuclear envelope surveillance is required for DNA double strand break repair.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Physiological and pathological roles of ANXA11: a multifunctional regulator in neurodegeneration and other disorders.Cell communication and signaling : CCS · 2026Review
- Continuous nuclear envelope surveillance is required for DNA double strand break repair.Communications biology · 2025Article
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Authors and funding
2 authors.
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Abstract
Precise double-strand break (DSB) repair is paramount for genome stability. Homologous recombination (HR) is preferred to repair DSBs when a nearby sister chromatid ensures an error-free template. In Saccharomyces cerevisiae, this preference extends into anaphase and telophase (late mitosis; late-M) despite sister chromatids having been pulled apart. Previously, we identified the nuclear envelope (NE) protein Msc1 as important for late-M DSB repair. Here, we report that Msc1 faces the NE lumen, and its depletion leads to DSB-independent over-compartmentalization of the nucleus and nuclear pore complex (NPC) mislocation. These phenotypes are partly shared by the highly conserved NE healing complex ESCRT-III. Finally, we show that these abnormal NE phenotypes are found throughout the cell cycle and in the DSB-driven G2/M arrest. These findings highlight the essential role of NE homeostasis in DSB repair.
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