H4K20me3 and CTCF act reciprocally at TAD boundaries to regulate cell state transitions
H4K20me3, a mark associated with heterochromatin, and CTCF compete for chromatin boundary elementsCTCF and H4K20me3 play opposing roles, with increased CTCF in proliferating cells and elevated H4K20me3 in quiescent cellsModulating H4K20me3 or CTCF reversibly shifts cells between proliferative and quiescent stateMice with reduced H4K20me3 are larger, consistent with hyperproliferation.
Authors
- Kaiser Atai (ORCID: https://orcid.org/0000-0003-3520-5877)
- Kirthana Sarathy
- David Jelínek (ORCID: https://orcid.org/0000-0002-9234-311X)
- Hilary A. Coller (ORCID: https://orcid.org/0000-0003-0992-6494)
- Kenya Bonitto (ORCID: https://orcid.org/0000-0001-6269-8692)
- Mithun Mitra (ORCID: https://orcid.org/0000-0001-8056-8963)
- Aaron Ambrus
- Adriana Z. Corvalan
- Alex Dunkwu
- William Mason Sparks
- Richard Hu
- Laurent Voisin
- Eliana Bohn
Institutions
- University of California, Los Angeles (US)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-01-30
- DOI
- https://doi.org/10.64898/2026.01.29.702647
- Primary Topic
- Genomics and Chromatin Dynamics
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Institutes of Health
- National Cancer Institute
- National Institute of General Medical Sciences