NuMA promotes constitutive heterochromatin compaction by stabilizing linker histone H1 on chromatin
Heterochromatin exerts pivotal functions of silencing specific genes and maintenance of genome stability. However, its formation and maintenance mechanisms remain unclear. Here, we discover that the mitotic regulator NuMA, as a nucleoskeleton protein, is required for constitutive heterochromatin organization at the nucleosome level in interphase. NuMA depletion results in shortened nucleosome repeat length, dispersed nucleosome clutches, increased chromatin accessibility, and disrupted transcription repression of long terminal repeats in heterochromatin regions. Such functions of NuMA rely on its interaction with linker histone H1, which stabilizes H1's binding to chromatin and facilitates nucleosome stacking, as directly visualized by in situ cryo-ET. Notably, NuMA oligomerizes into quasi-meshwork in the nucleoplasm, providing its organization basis as a nucleoskeleton protein. Collectively, our findings illuminate the concerted effect of nucleoskeleton and linker histone on chromatin compaction at the nucleosome level, unveiling a previously unexplored mechanism by which nucleoskeleton regulates heterochromatin formation and maintenance.
Authors
- Aibin He
- Wolfgang Baumeister (ORCID: https://orcid.org/0000-0001-8154-8809)
- Jiahao Niu (ORCID: https://orcid.org/0000-0003-4273-4398)
- Weihong Yuan
- Guohong Li (ORCID: https://orcid.org/0000-0003-2137-0783)
- Peng Xu
- Yujie Sun
- Shanshan Ai
- Yao Wang
- Wenxue Zhao
- Cheng Li
- Xiaotian Wang
- Cuifang Liu
Institutions
- Chinese Academy of Sciences (CN)
- Peking University (CN)
- Hubei University of Chinese Medicine (CN)
- Zhujiang Hospital (CN)
- Ministry of Education (ET)
- Max Planck Institute of Biochemistry (DE)
- Center for Life Sciences (CN)
- Southern Medical University (CN)
Publication Details
- Journal
- Cell Reports
- Published
- 2026-01-23
- DOI
- https://doi.org/10.1016/j.celrep.2025.116901
- Primary Topic
- Genomics and Chromatin Dynamics
- Type
- article
- Field-Weighted Citation Impact
- 0.00