Cited by 127DNA Repair MechanismsNuclear Structure and FunctionCellular Mechanics and Interactions

Nuclear actin filaments in DNA repair dynamics

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Caridi, Christopher Patrick, Plessner, Matthias, Grosse, Robert, Chiolo, Irene·2019·Nature Cell Biology

Abstract

Actin filaments (F-actin) have well-known functions in the cytoplasm, including generating forces for cell movement and enabling myosin-driven dynamics of vesicles and mRNAs. In addition, the recent development of innovative tools for F-actin detection have revealed dynamic and transient filaments in the nuclei, which form in response to specific stimuli. Here we provide an overview of the functions of F-actin and myosins in nuclei, with a focus on their role in DNA repair and genome stability. We emphasize recent discoveries of nuclear F-actin driving the relocalization of heterochromatic repair sites to the nuclear periphery for ‘safe' homologous recombination (HR) repair of double-strand breaks (DSBs). F-actin also promotes repair focus clustering and DSB resection in euchromatin, facilitating HR progression. We highlight regulatory mechanisms specialized for actin polymerization during DNA replication and repair, and emphasize recent studies revealing alternative motors for the directional movement of repair sites. Together, these discoveries challenge previous models that actin is substantially monomeric in the nucleus and that DSBs move via Brownian motion, revealing a complex network of dynamic filaments, motors and regulators, coordinating chromatin dynamics with repair progression.

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  • When double strands of DNA break, nuclear F-actin is required for the non-homologous end joining and homologous recombination repair pathways.

    “In contrast, when double strands of DNA break, nuclear F-actin is required for the non-homologous end joining and homologous recombination repair pathways92.”

    From The WAVE complex in developmental and adulthood brain disorders (2025) · cites this paper as [92]

    The section “Nuclear F-actin is required for DSB repair” identifies NHEJ and HR as the two major DSB repair pathways and reports that components of both bind F-actin. It also reports defective repair when nuclear actin polymerization is inhibited, but describes F-actin’s direct roles as suggested and enigmatic; it does not establish that F-actin is required for each pathway individually. No page number is available in our copy. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Caridi, C. P., Plessner, M., Grosse, R., & Chiolo, I.
Affiliations
  • University of Southern California (US)
  • University of Freiburg (DE)
Corresponding author
Chiolo, Irene
Venue
Nature Cell Biology
Published
2019-09
Volume
21
Issue
9
Pages
1068-1077
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
OpenAlex
W2971986416
Cited by
127
References
6
Citations by year
2026: 9 · 2025: 15 · 2024: 16 · 2023: 28 · 2022: 21 · 2021: 25 · 2020: 10 · 2019: 3
FWCI
1.32
Type
journal article
Language
en
Open access
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Deutsche Forschungsgemeinschaft (GR 2111/7-1)
  • U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (R01GM117376)
  • National Science Foundation (CAREER1751197)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
Keywords
F-actin, DNA double-strand break repair, chromatin dynamics
MeSH terms
Actins, Animals, Cell Nucleus, Chromatin, DNA Repair, Humans, Actin Cytoskeleton, DNA Breaks, Double-Stranded

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