{
  "abstract": "DNA double-strand breaks (DSBs) require rapid signalling and physical stabilisation of broken DNA ends to preserve genome integrity. Here, we identify myosin VI (MVI) as an ATM-regulated component of the DSB response. DNA damage induces rapid nuclear accumulation and nanoscale reorganisation of MVI across multiple cell models, in an ATM-dependent manner. Pharmacological or genetic perturbation of MVI attenuates {gamma}H2AX signalling and disrupts Ku80 organisation, while DNA damage persists. This leads to increased sensitivity to cisplatin and bleomycin. Super-resolution imaging reveals spatial association of MVI with Ku80-containing repair structures, implicating MVI in non-homologous end joining (NHEJ). In a minimal reconstituted system, MVI and actin enhance the proximity of Ku70/80-bound DNA ends. Together, our findings identify MVI as a regulator of DSB repair that links ATM signalling to Ku-associated DNA-end stabilisation and suggest that targeting MVI may sensitise tumour cells to genotoxic therapy.",
  "abstract_shown": true,
  "affiliations": [
    "University of Sheffield"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 13,
  "authors": [
    {
      "name": "A. Alanazi"
    },
    {
      "name": "A. Cook"
    },
    {
      "name": "I. Shahid-Fuente"
    },
    {
      "name": "N. Fili"
    },
    {
      "name": "T. Venit"
    },
    {
      "name": "A.-M. Gherghelas"
    },
    {
      "name": "N. B. Hitchcock"
    },
    {
      "name": "A. Moreno Mitchell"
    },
    {
      "name": "J. Arron"
    },
    {
      "name": "T. L. Chew"
    },
    {
      "name": "L. Wang"
    },
    {
      "name": "P. Percipalle"
    },
    {
      "affs": [
        0
      ],
      "name": "C. P. Toseland"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/3qzg7etqnmtkq.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.09.01.748478",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748478v1.full",
  "id": "3qzg7etqnmtkq",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748478v1",
  "language": null,
  "licence": "CC-BY-ND",
  "licence_label": "CC BY-ND",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "cancer biology"
    ],
    [
      "openalex",
      "1312|DNA Repair Mechanisms"
    ]
  ],
  "openalex": "W7207694258",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748478v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-01",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/3qzg7etqnmtkq.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:18:37Z",
      "native_id": "10.64898/2026.09.01.748478",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748478v1"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "biorxiv:cancer biology",
      "subfield": "oncology"
    }
  ],
  "title": "Nuclear Myosin VI stabilises Ku-associated DNA ends during non-homologous end joining",
  "title_text": "Nuclear Myosin VI stabilises Ku-associated DNA ends during non-homologous end joining",
  "type": "preprint",
  "updated_at": "2026-10-30T12:18:37Z",
  "url": "https://research.draconitic.com/paper/3qzg7etqnmtkq",
  "venue": "bioRxiv",
  "versions": []
}