Nuclear Actin: Transcription and Damage-Associated Filaments

Distinct evidence for initiation complexes and stress-associated actin assembly

A selective primary-evidence overview of transcription-associated actin and damage-associated nuclear filaments.

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Checked scientific scope

This HTML presents a selective primary-evidence overview. Every retained scientific paragraph and reference was appraised at the access depth listed below. Detailed Methods, raw data, exhaustive literature coverage and the associated source document remain outside the checked scope.

Actin in transcription-initiation evidence

Hofmann and colleagues detected beta-actin at two inducible promoters and in RNA-polymerase-II-associated preparations. Antibody inhibition and purified nuclear-component assays supported a contribution to transcription initiation and pre-initiation-complex formation. [hofmann2004]

This evidence concerns selected promoters and initiation systems. It does not establish that all nuclear actin must be filamentous, that every gene has identical dependence or that all RNA polymerases use the same mechanism. [hofmann2004]

Filaments observed during a damage response

Belin and colleagues observed damage-associated nuclear actin filaments in HeLa cells using live-cell probes and phalloidin in cells without the expressed probe. The structures included nucleoplasmic and nucleolus-associated patterns. [belin2015]

Formin-2 and combined Spire-1/Spire-2 dependence supported regulated assembly in the tested setting. Nuclear-actin and Formin-2-deficient models accumulated more 53BP1 or phosphorylated-H2AX damage foci. [belin2015]

The study reported probe-dependent visibility and filament stabilization, as well as limited overlap between filaments and damage foci. Foci are damage-signaling endpoints; these observations do not show a filament at every break or directly certify completed backbone repair. [belin2015]

Interpretation and corrected identity

Transcription-associated actin and damage-associated filaments are distinct observations. Together they support context-dependent nuclear functions, without establishing one universal actin structure for transcription and repair. [hofmann2004] [belin2015]

The primary correction replaces the title typography Spire-½ with Spire-1/2. It does not correct experimental results. The corrected article title is used in the bibliography. [belin2015correction]

The transcription study was inspected at primary Abstract depth; selected descriptive Results were inspected for the filament study, and the complete correction notice was read. Detailed Methods, all controls and disease extrapolations remain outside the checked scope. [hofmann2004] [belin2015] [belin2015correction]

Primary references and access depth

  1. Hofmann WA et al. (2004). Actin is part of pre-initiation complexes and is necessary for transcription by RNA polymerase II. Nature cell biology 6:1094-101. PMID 15502823. DOI 10.1038/ncb1182. Access: Abstract and citation record.
  2. Belin BJ et al. (2015). DNA damage induces nuclear actin filament assembly by Formin-2 and Spire-1/2 that promotes efficient DNA repair. eLife 4:e07735. PMID 26287480. DOI 10.7554/eLife.07735. Access: Abstract and selected descriptive Results.
  3. Belin BJ et al. (2015). Correction: DNA damage induces nuclear actin filament assembly by Formin-2 and Spire-1/2 that promotes efficient DNA repair. eLife 4:e11935. PMID 26437453. DOI 10.7554/eLife.11935. Access: Complete correction notice.

Actin-associated metabolism need not imply intranuclear filaments

The Ghose et al. (2025) reported actin-dependent mitochondrial repositioning around the nucleus and a nuclear ATP increase in its cell models. The actin-dependent organelle arrangement is a separate observation from the damage-induced intranuclear filaments of Belin and colleagues. It does not locate those filaments at every repair site or show that all nuclear ATP production uses an intranuclear actin network. Ghose et al. (2025).

Additional primary references

  1. Ghose et al. (2025). Mitochondria-derived nuclear ATP surge protects against confinement-induced proliferation defects. Nature Communications. DOI: 10.1038/s41467-025-61787-x. Primary study. Access in this reassessment: primary abstract and bibliographic record.

Reassessed 12 October 2026. Recent-source access is stated above; complete supplementary material and raw data were not reanalysed. The archived Word draft remains a separate, unreconciled document.