ArticlePLoS genetics2023
Genomic instability caused by Arp2/3 complex inactivation results in micronucleus biogenesis and cellular senescence.
Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The biomedical application of inorganic metal nanoparticles in aging and aging-associated diseases.Journal of advanced research · 2025Pooled it
- Discovery of an Atypical Arp2/3 Complex in Malaria Parasites Sheds New Light on Nuclear Actin.Cytoskeleton (Hoboken, N.J.) · 2026Article
- From energy metabolic homeostasis to immune remodeling: the role and therapeutic potential of STING signaling in the tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- Synphilin-1 mitigates autophagy dysfusnction, modulates ubiquitinated protein aggregation, and promotes cell survival during proteotoxic stress.bioRxiv : the preprint server for biology · 2026Article
- Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Autophagosome turnover requires Arp2/3 complex-mediated maintenance of lysosomal integrity.Molecular biology of the cell · 2026Article
- ARP2/3 protein complex regulates myoblast proliferation, morphology, migration, and fusion during embryonic chick skeletal myogenesis.In vitro cellular & developmental biology. Animal · 2026Article
- Loss of Snhg5 disrupts cell-cycle regulation without altering cystogenesis in a mouse model of polycystic kidney disease.Scientific reports · 2026Article
- Revisiting osteoarthritis pathogenesis through the lens of cGAS-STING: Mitochondrial damage, pyroptosis, and inflammatory cascades.Journal of orthopaedic translation · 2026Review
- Targeting Cytoskeleton and Cell Motility: Past and Novel Strategies for Cancer Therapy.Oncology research · 2026Review
- A microexon in Arp2 alters tissue-specific Arp2/3-generated actin structures.bioRxiv : the preprint server for biology · 2025Article
- An atypical Arp2/3 complex is required for Plasmodium DNA segregation and malaria transmission.Nature microbiology · 2025Article
- GαInternational journal of molecular sciences · 2025Article
- YAP/TAZ-mediated nuclear membrane rupture in promoting senescence of skeletal muscle associated with COPD.Respiratory research · 2025Article
- Claudin-4 remodeling of nucleus-cell cycle crosstalk maintains ovarian tumor genome stability and drives resistance to genomic instability-inducing agents.bioRxiv : the preprint server for biology · 2024Article
- ANTXR1 deficiency promotes fibroblast senescence: implications for GAPO syndrome as a progeroid disorder.Scientific reports · 2024Article
- Proteomic analysis of mitochondria associated membranes in renal ischemic reperfusion injury.Journal of translational medicine · 2024Article
- Evolutionary diversification reveals distinct somatic versus germline cytoskeletal functions of the Arp2 branched actin nucleator protein.Current biology : CB · 2023Article
- At the Crossroads of the cGAS-cGAMP-STING Pathway and the DNA Damage Response: Implications for Cancer Progression and Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The Arp2/3 complex is an actin nucleator with well-characterized activities in cell morphogenesis and movement, but its roles in nuclear processes are relatively understudied. We investigated how the Arp2/3 complex affects genomic integrity and cell cycle progression using mouse fibroblasts containing an inducible knockout (iKO) of the ArpC2 subunit. We show that permanent Arp2/3 complex ablation results in DNA damage, the formation of cytosolic micronuclei, and cellular senescence. Micronuclei arise in ArpC2 iKO cells due to chromatin segregation defects during mitosis and premature mitotic exits. Such phenotypes are explained by the presence of damaged DNA fragments that fail to attach to the mitotic spindle, abnormalities in actin assembly during metaphase, and asymmetric microtubule architecture during anaphase. In the nuclei of Arp2/3-depleted cells, the tumor suppressor p53 is activated and the cell cycle inhibitor Cdkn1a/p21 mediates a G1 arrest. In the cytosol, micronuclei are recognized by the DNA sensor cGAS, which is important for stimulating a STING- and IRF3-associated interferon response. These studies establish functional requirements for the mammalian Arp2/3 complex in mitotic spindle organization and genome stability. They also expand our understanding of the mechanisms leading to senescence and suggest that cytoskeletal dysfunction is an underlying factor in biological aging.
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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.