The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Histone H1 loss drives lymphoma by disrupting 3D chromatin architecture
Open accessAbstract
Linker histone H1 proteins bind to nucleosomes and facilitate chromatin compaction1, although their biological functions are poorly understood. Mutations in the genes that encode H1 isoforms B–E (H1B, H1C, H1D and H1E; also known as H1-5, H1-2, H1-3 and H1-4, respectively) are highly recurrent in B cell lymphomas, but the pathogenic relevance of these mutations to cancer and the mechanisms that are involved are unknown. Here we show that lymphoma-associated H1 alleles are genetic driver mutations in lymphomas. Disruption of H1 function results in a profound architectural remodelling of the genome, which is characterized by large-scale yet focal shifts of chromatin from a compacted to a relaxed state. This decompaction drives distinct changes in epigenetic states, primarily owing to a gain of histone H3 dimethylation at lysine 36 (H3K36me2) and/or loss of repressive H3 trimethylation at lysine 27 (H3K27me3). These changes unlock the expression of stem cell genes that are normally silenced during early development. In mice, loss of H1c and H1e (also known as H1f2 and H1f4, respectively) conferred germinal centre B cells with enhanced fitness and self-renewal properties, ultimately leading to aggressive lymphomas with an increased repopulating potential. Collectively, our data indicate that H1 proteins are normally required to sequester early developmental genes into architecturally inaccessible genomic compartments. We also establish H1 as a bona fide tumour suppressor and show that mutations in H1 drive malignant transformation primarily through three-dimensional genome reorganization, which leads to epigenetic reprogramming and derepression of developmentally silenced genes. Mutations in histone H1 induce the remodelling of chromatin architecture to a more relaxed state, which leads to malignant transformation through changes in histone modifications and the expression of stem cell genes.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping
Rao, S. S. P., Huntley, M. H., Durand, N. C., Stamenova, E. K., Bochkov, I. D., Robinson, J. T., Sanborn, A. L., Machol, I., Omer, A. D., Lander, E. S., et al. (2014) · Cell · doi:10.1016/j.cell.2014.11.021 · Cited by 9,212
Chapuy, B., Stewart, C., Dunford, A. J., Kim, J., Kamburov, A., Redd, R. A., Lawrence, M. S., Roemer, M. G. M., Li, A. J., Ziepert, M., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0016-8 · Cited by 1,941
Wright, G. W., Huang, D. W., Phelan, J. D., Coulibaly, Z. A., Roulland, S., Young, R. M., Wang, J. Q., Schmitz, R., Morin, R. D., Tang, J., et al. (2020) · Cancer Cell · doi:10.1016/j.ccell.2020.03.015 · Cited by 1,169
Self-citationGerminal Center B Cell Dynamics
Mesin, L., Ersching, J., & Victora, G. D. (2016) · Immunity · doi:10.1016/j.immuni.2016.09.001 · Cited by 994
Béguelin, W., Popovic, R., Teater, M., Jiang, Y., Bunting, K. L., Rosen, M., Shen, H., Yang, S. N., Wang, L., Ezponda, T., et al. (2013) · Cancer Cell · doi:10.1016/j.ccr.2013.04.011 · Cited by 846
Self-citationOkosun, J., Bödör, C., Wang, J., Araf, S., Yang, C.-Y., Pan, C., Boller, S., Cittaro, D., Bozek, M., Iqbal, S., et al. (2014) · Nature Genetics · doi:10.1038/ng.2856 · Cited by 734
Module Map of Stem Cell Genes Guides Creation of Epithelial Cancer Stem Cells
Wong, D. J., Liu, H., Ridky, T. W., Cassarino, D., Segal, E., & Chang, H. Y. (2008) · Cell Stem Cell · doi:10.1016/j.stem.2008.02.009 · Cited by 720
Fan, Y., Nikitina, T., Zhao, J., Fleury, T. J., Bhattacharyya, R., Bouhassira, E. E., Stein, A., Woodcock, C. L., & Skoultchi, A. I. (2005) · Cell · doi:10.1016/j.cell.2005.10.028 · Cited by 572
Self-citationEmerging roles of linker histones in regulating chromatin structure and function
Fyodorov, D. V., Zhou, B.-R., Skoultchi, A. I., & Bai, Y. (2018) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.94 · Cited by 485
Self-citationEminli, S., Foudi, A., Stadtfeld, M., Maherali, N., Ahfeldt, T., Mostoslavsky, G., Hock, H., & Hochedlinger, K. (2009) · Nature Genetics · doi:10.1038/ng.428 · Cited by 442
Cited by
Nicheformer: a foundation model for single-cell and spatial omics
Tejada-Lapuerta, A., Schaar, A. C., Gutgesell, R., Palla, G., Halle, L., Minaeva, M., Vornholz, L., Dony, L., Drummer, F., Richter, T., et al. (2025) · Nature Methods · doi:10.1038/s41592-025-02814-z · Cited by 100
Structural features of nucleosomes in interphase and metaphase chromosomes
Arimura, Y., Shih, R. M., Froom, R., & Funabiki, H. (2021) · Molecular Cell · doi:10.1016/j.molcel.2021.08.010 · Cited by 59
Spatial promoter–enhancer hubs in cancer: organization, regulation, and function
Zhao, J., & Faryabi, R. B. (2023) · Trends in Cancer · doi:10.1016/j.trecan.2023.07.017 · Cited by 28
Arimura, Y., Konishi, H. A., & Funabiki, H. (2025) · eLife · doi:10.7554/elife.103486.3 · Cited by 4
Metadata
- Authors
- Yusufova, N., Kloetgen, A., Teater, M., Osunsade, A., Camarillo, J. M., Chin, C. R., Doane, A. S., Venters, B. J., Portillo-Ledesma, S., Conway, J., Phillip, J. M., Elemento, O., Scott, D. W., Béguelin, W., Licht, J. D., Kelleher, N. L., Staudt, L. M., Skoultchi, A. I., Keogh, M.-C., Apostolou, E., Mason, C. E., Imielinski, M., Schlick, T., David, Y., Tsirigos, A., Allis, C. D., Soshnev, A. A., Cesarman, E., & Melnick, A. M.
- Venue
- Nature
- Published
- 2020-12-09
- Volume
- 589
- Issue
- 7841
- Pages
- 299-305
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W3110786706
- Cited by
- 253
- References
- 33
- FWCI
- 10.23
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Histone H1 loss drives lymphoma by disrupting 3D chromatin architecture. https://app.cochat.ai/papers/10.1038/s41586-020-3017-y
- The paper
- Yusufova, N., Kloetgen, A., Teater, M., Osunsade, A., Camarillo, J. M., Chin, C. R., Doane, A. S., Venters, B. J., Portillo-Ledesma, S., Conway, J., Phillip, J. M., Elemento, O., Scott, D. W., Béguelin, W., Licht, J. D., Kelleher, N. L., Staudt, L. M., Skoultchi, A. I., Keogh, M.-C., . . . Melnick, A. M. (2021). Histone H1 loss drives lymphoma by disrupting 3D chromatin architecture. Nature. https://doi.org/10.1038/s41586-020-3017-y
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
