Extreme disruption of heterochromatin is required for accelerated hematopoietic aging
Abstract
Loss of heterochromatin has been proposed as a universal mechanism of aging across different species and cell types. However, a comprehensive analysis of hematopoietic changes caused by heterochromatin loss is lacking. Moreover, there is conflict in the literature around the role of the major heterochromatic histone methyltransferase Suv39h1 in the aging process. Here, we use individual and dual deletion of Suv39h1 and Suv39h2 enzymes to examine the causal role of heterochromatin loss in hematopoietic cell development. Loss of neither Suv39h1 nor Suv39h2 individually had any effect on hematopoietic stem cell function or the development of mature lymphoid or myeloid lineages. However, deletion of both enzymes resulted in characteristic changes associated with aging such as reduced hematopoietic stem cell function, thymic involution and decreased lymphoid output with a skewing toward myeloid development, and increased memory T cells at the expense of naive T cells. These cellular changes were accompanied by molecular changes consistent with aging, including alterations in nuclear shape and increased nucleolar size. Together, our results indicate that the hematopoietic system has a remarkable tolerance for major disruptions in chromatin structure and reveal a role for Suv39h2 in depositing sufficient H3K9me3 to protect the entire hematopoietic system from changes associated with premature aging.
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Global disruption of heterochromatin by deletion of both H3K9me3 methyltransferases SUV39H1 and SUV39H2 has a pro-ageing effect on HSCs and the immune system.
“The global disruption of heterochromatin by deletion of both H3K9me3 methyltransferases SUV39H1 and SUV39H2 has a ‘pro-ageing’ effect on HSCs and the immune system102.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [102]
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- Authors
- Keenan, C. R., Iannarella, N., Naselli, G., Bediaga, N. G., Johanson, T. M., Harrison, L. C., & Allan, R. S.
- Affiliations
- The University of Melbourne (AU)
- Walter and Eliza Hall Institute of Medical Research (AU)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2020-06-04
- Volume
- 135
- Issue
- 23
- Pages
- 2049-2058
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W3016656062
- Cited by
- 34
- References
- 42
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 7 · 2023: 4 · 2022: 7 · 2021: 3 · 2020: 5
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- heterochromatin loss, hematopoietic aging, SUV39H1, SUV39H2, H3K9me3, hematopoietic stem cells, thymic involution, myeloid skewing, memory T cells, nucleolar size, nuclear shape, chromatin structure
- MeSH terms
- Aged, Animals, Cell Differentiation, Cell Nucleus, Female, Hematopoiesis, Hematopoietic Stem Cells, Heterochromatin, Humans, Male, Methyltransferases, Histone-Lysine N-Methyltransferase, Repressor Proteins, T-Lymphocytes, Mice, Knockout, Aging, Premature, Mice
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