Evidence map›Paper›PMID 39134516›Full record

ArticleNature communications2024

HMGA1 orchestrates chromatin compartmentalization and sequesters genes into 3D networks coordinating senescence heterogeneity.

Ioana Olan, Masami Ando-Kuri, Aled J Parry, Tetsuya Handa, Stefan Schoenfelder, Peter Fraser, Yasuyuki Ohkawa, Hiroshi Kimura, Masako Narita, Masashi Narita

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Past, Present and Future of Regenerative Gene Therapy for Ischemic Heart Failure.Journal of cardiovascular translational research · 2026
    Review
  7. The role of HMGA1 in genome stability: Implications in human cancer.Cellular and molecular life sciences : CMLS · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. The states of senescent cells.Biochemical Society transactions · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Ioana Olan *Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID 0000-0003-0692-1831
Masami Ando-Kuri *Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.
Aled J Parry *Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.
Tetsuya HandaCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID 0000-0001-7707-0195
Stefan SchoenfelderEpigenetics Programme, The Babraham Institute, Cambridge, UK.ORCID 0000-0002-3200-8133
Peter FraserNuclear Dynamics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, UK.
Yasuyuki OhkawaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi, Fukuoka, 812-0054, Japan.ORCID 0000-0001-6440-9954
Hiroshi KimuraCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, Japan.ORCID 0000-0003-0854-083X
Masako NaritaCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID 0000-0002-9774-4908
Masashi NaritaCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK. Masashi.Narita@cruk.cam.ac.uk.ORCID 0000-0001-7764-577X

Funding

Babraham Institute BBS/E/B/000C0421Babraham Institute Career Progression FellowshipCancer Research UK (CRUK) C63389/A30462Cancer Research UK (CRUK) C9545/A29580MEXT | Japan Society for the Promotion of Science (JSPS) JP23H00372MEXT | Japan Society for the Promotion of Science (JSPS) JP24H02323RCUK | Biotechnology and Biological Sciences Research Council (BBSRC) BB/S013466/1RCUK | Medical Research Council (MRC) MR/T016787/1
6 · The paper itself

Abstract

HMGA1 is an abundant non-histone chromatin protein that has been implicated in embryonic development, cancer, and cellular senescence, but its specific role remains elusive. Here, we combine functional genomics approaches with graph theory to investigate how HMGA1 genomic deposition controls high-order chromatin networks in an oncogene-induced senescence model. While the direct role of HMGA1 in gene activation has been described previously, we find little evidence to support this. Instead, we show that the heterogeneous linear distribution of HMGA1 drives a specific 3D chromatin organization. HMGA1-dense loci form highly interactive networks, similar to, but independent of, constitutive heterochromatic loci. This, coupled with the exclusion of HMGA1-poor chromatin regions, leads to coordinated gene regulation through the repositioning of genes. In the absence of HMGA1, the whole process is largely reversed, but many regulatory interactions also emerge, amplifying the inflammatory senescence-associated secretory phenotype. Such HMGA1-mediated fine-tuning of gene expression contributes to the heterogeneous nature of senescence at the single-cell level. A similar 'buffer' effect of HMGA1 on inflammatory signalling is also detected in lung cancer cells. Our study reveals a mechanism through which HMGA1 modulates chromatin compartmentalization and gene regulation in senescence and beyond.

Indexed as

Cellular SenescenceChromatinHMGA1a ProteinCell Line, TumorGene Expression RegulationGene Regulatory NetworksHumansLung NeoplasmsChromatinHMGA1a ProteinHMGA1 protein, human

Identifiers

PMID39134516
PMCPMC11319441

What OpenQuestion holds

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Registered trials

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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.