Loss of Dnmt3a Immortalizes Hematopoietic Stem Cells In Vivo
Open accessAbstract
Somatic mutations in DNMT3A are recurrent events across a range of blood cancers. Dnmt3a loss of function in hematopoietic stem cells (HSCs) skews divisions toward self-renewal at the expense of differentiation. Moreover, DNMT3A mutations can be detected in the blood of aging individuals, indicating that mutant cells outcompete normal HSCs over time. It is important to understand how these mutations provide a competitive advantage to HSCs. Here we show that Dnmt3a-null HSCs can regenerate over at least 12 transplant generations in mice, far exceeding the lifespan of normal HSCs. Molecular characterization reveals that this in vivo immortalization is associated with gradual and focal losses of DNA methylation at key regulatory regions associated with self-renewal genes, producing a highly stereotypical HSC phenotype in which epigenetic features are further buttressed. These findings lend insight into the preponderance of DNMT3A mutations in clonal hematopoiesis and the persistence of mutant clones after chemotherapy.
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DNMT3A loss-of-function does not lead to global DNA methylation changes.
“This reinforces previous findings that DNMT3A loss-of-function does not lead to global DNA methylation changes (15,16,19)”
From <i>Txnip</i> Enhances Fitness of <i>Dnmt3a</i> -Mutant Hematopoietic Stem Cells via <i>p21</i> (2022) · cites this paper as [19]
In the Results section, “Dnmt3a Controls DNA Methylation at HSC Regulatory Elements” (page not provided), the paper reports that Dnmt3aKO HSCs retained an overall methylation profile but displayed hypomethylation compared with controls. The “Molecular Analysis” Results section also describes hypomethylation throughout the genome in mutant HSCs, more pronounced in Dnmt3aKO HSCs. Thus, retained overall methylation does not mean an absence of global changes. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredIn serially transplanted Dnmt3a−/− HSCs compared with WT HSCs, these genes are also differentially suppressed in the Dnmt3a−/− cells.
“In a recently published study examining gene expression differences between serially transplanted Dnmt3a−/− HSCs and WT HSCs, these genes are also differentially suppressed in the Dnmt3a−/− cells”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Jeong et al., 2018
The Results section, “Dnmt3a Controls DNA Methylation at HSC Regulatory Elements” (page unavailable), reports RNA-seq comparisons of control and serially transplanted Dnmt3aKO HSCs and says genes in bivalent canyons showed repression with extended passage. The citing sentence does not identify what “these genes” refers to, so our copy cannot establish that the particular genes intended were suppressed. (LLM, conf=0.78)
Experimental — accuracy not yet measuredHypermethylation in the setting of a Dnmt3a deletion may be related to compensatory effects of alternative methyltransferases.
“and may be related to compensatory effects of alternative methyltransferases (Jeong et al., 2018).”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Jeong et al., 2018
The Results section, “Dnmt3a Controls DNA Methylation at HSC Regulatory Elements” (page unavailable), reports hypermethylated regions in Dnmt3a-knockout HSCs, including increased methylation in bivalent and inactive canyons. It does not attribute that hypermethylation to compensatory activity by alternative methyltransferases, so the proposed explanation is unsupported by our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredDnmt3a−/− HSCs demonstrate defective differentiation and enhanced self-renewal.
“prior studies showed that Dnmt3a−/− HSCs demonstrate defective differentiation and enhanced self-renewal (Challen et al., 2011; Jeong et al., 2018)”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Jeong et al., 2018
Hypermethylation in the setting of a Dnmt3a deletion has also been reported in other studies.
“While hypermethylation in the setting of a Dnmt3a deletion seems counterintuitive, it has also been reported in other studies”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Jeong et al., 2018
The competitive advantage of Dnmt3a-mutant hematopoietic stem cells is exacerbated by hematopoietic stress such as serial transplantation and microbial infection.
“The competitive advantage of Dnmt3a-mutant HSCs is exacerbated by hematopoietic stress such as serial transplantation (19) and microbial infection (20).”
From <i>Txnip</i> Enhances Fitness of <i>Dnmt3a</i> -Mutant Hematopoietic Stem Cells via <i>p21</i> (2022) · cites this paper as [19]
Infection is likely not the only chronic stress or source of chronic inflammation that contributes to regulation of these genes.
“suggesting that infection is likely not the only chronic stress or source of chronic inflammation that contributes to their regulation (Jeong et al., 2018).”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Jeong et al., 2018
The Results section on HSC regulatory elements describes gene-expression changes after Dnmt3a loss, but does not link those changes to infection or other chronic inflammatory stresses. Searches for infection, chronic inflammation, and chronic stress found no passage in our copy addressing whether such stresses regulate the genes. (LLM, conf=0.74)
Experimental — accuracy not yet measuredThe presence of clonal haematopoiesis was reported to negatively impact clinical outcomes in patients receiving treatment for non-haematological cancers.
“However, the presence of clonal haematopoiesis was reported to negatively impact clinical outcomes in patients receiving treatment for non-haematological cancers 86 .”
From The roles of DNA, RNA and histone methylation in ageing and cancer (2019) · cites this paper as [86]
Stem cells that are expanded in clonal haematopoiesis often have somatic mutations in genes encoding epigenetic regulators such as DNA methyltransferase 3A (DNMT3A).
“Stem cells that are expanded in clonal haematopoiesis often have somatic mutations in genes encoding epigenetic regulators such DNA methyltransferase 3A (DNMT3A)50,51.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [50]
Even partial loss of function of these epigenetic regulators biases the stem cells towards self-renewal and reduced differentiation.
“Broadly, even partial loss of function of these epigenetic regulators biases the stem cells towards self-renewal and reduced differentiation50,51.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [50]
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Base editor scanning charts the DNMT3A activity landscape
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- Authors
- Jeong, M., Park, H. J., Celik, H., Ostrander, E. L., Reyes, J. M., Guzman, A., Rodriguez, B., Lei, Y., Lee, Y., Ding, L., Guryanova, O. A., Li, W., Goodell, M. A., & Challen, G. A.
- Affiliations
- Baylor College of Medicine (US)
- Washington University in St. Louis (US)
- Columbia University Irving Medical Center (US)
- University of Florida (US)
- Corresponding author
- Goodell, Margaret A.
- Challen, Grant A.
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-04
- Volume
- 23
- Issue
- 1
- Pages
- 1-10
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC5908249
- OpenAlex
- W2796241254
- Cited by
- 243
- References
- 36
- Citations by year
- 2026: 17 · 2025: 26 · 2024: 30 · 2023: 25 · 2022: 33 · 2021: 51 · 2020: 30 · 2019: 23 · 2018: 8
- FWCI
- 20.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion, cc-by-nc-nd)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- NIH (DK102428, HG007538, CA193466, HL132074, CA178191, DK092883, CA183252, AG036695, CPRIT RP140053, 5T32DK60445, 5T32CA113275)
- American Society of Hematology
- NYSTEM (GM056929)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- DNMT3A, DNMT3A mutation, hematopoietic stem cells, DNA methylation loss, self-renewal, clonal hematopoiesis, hematologic malignancies, epigenetic regulation, chemoresistance, aging
- MeSH terms
- DNA Methyltransferase 3A, Animals, DNA (Cytosine-5-)-Methyltransferases, Female, Hematopoiesis, Hematopoietic Stem Cells, Male, Mice, Inbred C57BL, Gene Deletion, Cell Lineage, DNA Methylation, Epigenesis, Genetic, Mice
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