H3F3A K27M mutations drive a repressive transcriptome by modulating chromatin accessibility independent of H3K27me3 in Diffuse Midline Glioma
Our findings reveal that the H3.3K27M mutation alters chromatin accessibility and uniquely deregulates gene expression independent of H3K27 methylation loss. These PRC2-independent functions of K27M contribute to changes in biological pathway activity and are necessary for tumor development, highlighting novel mechanisms of K27M-driven gliomagenesis.
Authors
- Alyssa Langfald
- Igor Entin (ORCID: https://orcid.org/0000-0002-4870-1274)
- Charles Day (ORCID: https://orcid.org/0000-0001-6277-2004)
- James P. Robinson (ORCID: https://orcid.org/0000-0002-6585-0116)
- Faruck Lukmanul Hakkim (ORCID: https://orcid.org/0000-0002-1194-0933)
- Florina Grigore (ORCID: https://orcid.org/0000-0002-5621-9939)
- Edward H. Hinchcliffe (ORCID: https://orcid.org/0000-0003-0091-3814)
- Suraj Bhattarai (ORCID: https://orcid.org/0000-0003-0458-8617)
Institutions
- University of Minnesota (US)
- Mayo Clinic (US)
- Hormel (United States) (US)
- Mayo Clinic in Arizona (US)
- University of Minnesota Medical Center (US)
- Mayo Clinic in Florida (US)
Publication Details
- Journal
- Epigenetics & Chromatin
- Published
- 2025-04-26
- DOI
- https://doi.org/10.1186/s13072-025-00585-7
- Citations
- 3
- Primary Topic
- Glioma Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 4.88
Funders
- U.S. Department of Defense
- University of Minnesota
- University of California, Davis
- National Heart, Lung, and Blood Institute