Chromatin remodeler Fun30 facilitates the relocation of persistent <scp>DNA</scp> double‐strand breaks to the nuclear periphery

DNA double-strand break (DSB) repair is critical for genome stability and requires chromatin remodeling for efficient processing. Fun30, an ATP-dependent chromatin remodeler, promotes long-range DNA end resection to generate 3' overhangs, a key step in homologous recombination. Persistent DSBs relocate to the nuclear periphery, particularly through interactions with the inner nuclear membrane protein Mps3 and the nuclear pore complex component Nup84. By tracking a single irreparable break, we show that Fun30 facilitates this relocation. In fun30Δ cells, Mps3 and Nup84 enrichment at DSBs was reduced, indicating impaired tethering. We further demonstrate that Fun30 promotes deposition of the histone variant H2A.Z at DSBs. Thus, Fun30 favors relocation of persistent DSBs to the nuclear periphery by supporting resection and H2A.Z incorporation.

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Publication Details

Journal
FEBS Letters
Published
2026-02-01
DOI
https://doi.org/10.1002/1873-3468.70295
Primary Topic
DNA Repair Mechanisms
Type
article
Field-Weighted Citation Impact
0.00

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article

Chromatin remodeler Fun30 facilitates the relocation of persistent DNA double‐strand breaks to the nuclear periphery

Amira Bekdash, Mehwish Iqbal, Jisha Chalissery, Amna Hassan et al.
FEBS Letters
DNA Repair Mechanisms
article

Chromatin remodeler Fun30 facilitates the relocation of persistent DNA double‐strand breaks to the nuclear periphery

Amira Bekdash, Mehwish Iqbal, Jisha Chalissery, Amna Hassan, Asma Alnuaimi
article en

Abstract

DNA double-strand break (DSB) repair is critical for genome stability and requires chromatin remodeling for efficient processing. Fun30, an ATP-dependent chromatin remodeler, promotes long-range DNA end resection to generate 3' overhangs, a key step in homologous recombination. Persistent DSBs relocate to the nuclear periphery, particularly through interactions with the inner nuclear membrane protein Mps3 and the nuclear pore complex component Nup84. By tracking a single irreparable break, we show that Fun30 facilitates this relocation. In fun30Δ cells, Mps3 and Nup84 enrichment at DSBs was reduced, indicating impaired tethering. We further demonstrate that Fun30 promotes deposition of the histone variant H2A.Z at DSBs. Thus, Fun30 favors relocation of persistent DSBs to the nuclear periphery by supporting resection and H2A.Z incorporation.

FEBS LettersVol. 600(4)
United Arab Emirates University (AE), Zayed University (AE)
Brandeis University, United Arab Emirates University
Openalex Percentile: Top 70%
DNA Repair Mechanisms
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