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Article ; Online: Increased iron uptake by splenic hematopoietic stem cells promotes TET2-dependent erythroid regeneration.

Tseng, Yu-Jung / Kageyama, Yuki / Murdaugh, Rebecca L / Kitano, Ayumi / Kim, Jong Hwan / Hoegenauer, Kevin A / Tiessen, Jonathan / Smith, Mackenzie H / Uryu, Hidetaka / Takahashi, Koichi / Martin, James F / Samee, Md Abul Hassan / Nakada, Daisuke

Nature communications

2024 Volume 15, Issue 1, Page(s) 538

Abstract: Hematopoietic stem cells (HSCs) are capable of regenerating the blood system, but the instructive cues that direct HSCs to regenerate particular lineages lost to the injury remain elusive. Here, we show that iron is increasingly taken up by HSCs during ... ...

Abstract	Hematopoietic stem cells (HSCs) are capable of regenerating the blood system, but the instructive cues that direct HSCs to regenerate particular lineages lost to the injury remain elusive. Here, we show that iron is increasingly taken up by HSCs during anemia and induces erythroid gene expression and regeneration in a Tet2-dependent manner. Lineage tracing of HSCs reveals that HSCs respond to hemolytic anemia by increasing erythroid output. The number of HSCs in the spleen, but not bone marrow, increases upon anemia and these HSCs exhibit enhanced proliferation, erythroid differentiation, iron uptake, and TET2 protein expression. Increased iron in HSCs promotes DNA demethylation and expression of erythroid genes. Suppressing iron uptake or TET2 expression impairs erythroid genes expression and erythroid differentiation of HSCs; iron supplementation, however, augments these processes. These results establish that the physiological level of iron taken up by HSCs has an instructive role in promoting erythroid-biased differentiation of HSCs.
MeSH term(s)	Humans ; Spleen ; Hematopoietic Stem Cells/metabolism ; Cell Differentiation ; Iron/metabolism ; Anemia/metabolism ; Erythroid Cells ; DNA-Binding Proteins/metabolism ; Dioxygenases/metabolism
Chemical Substances	Iron (E1UOL152H7) ; TET2 protein, human (EC 1.13.11.-) ; DNA-Binding Proteins ; Dioxygenases (EC 1.13.11.-)
Language	English
Publishing date	2024-01-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-44718-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: An oncogenic enhancer encodes selective selenium dependency in AML.

Eagle, Kenneth / Jiang, Yajian / Shi, Xiangguo / Li, Minhua / Obholzer, Nikolaus D / Hu, Tianyuan / Perez, Monika W / Koren, Jošt Vrabič / Kitano, Ayumi / Yi, Joanna S / Lin, Charles Y / Nakada, Daisuke

Cell stem cell

2022 Volume 29, Issue 4, Page(s) 650

Language	English
Publishing date	2022-04-08
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2022.03.006
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Article ; Online: An oncogenic enhancer encodes selective selenium dependency in AML.

Eagle, Kenneth / Jiang, Yajian / Shi, Xiangguo / Li, Minhua / Obholzer, Nikolaus P / Hu, Tianyuan / Perez, Monika W / Koren, Jošt Vrabič / Kitano, Ayumi / Yi, Joanna S / Lin, Charles Y / Nakada, Daisuke

Cell stem cell

2022 Volume 29, Issue 3, Page(s) 386–399.e7

Abstract: Deregulation of transcription is a hallmark of acute myeloid leukemia (AML) that drives oncogenic expression programs and presents opportunities for therapeutic targeting. By integrating comprehensive pan-cancer enhancer landscapes with genetic ... ...

Abstract	Deregulation of transcription is a hallmark of acute myeloid leukemia (AML) that drives oncogenic expression programs and presents opportunities for therapeutic targeting. By integrating comprehensive pan-cancer enhancer landscapes with genetic dependency mapping, we find that AML-enriched enhancers encode for more selective tumor dependencies. We hypothesized that this approach could identify actionable dependencies downstream of oncogenic driver events and discovered a MYB-regulated AML-enriched enhancer regulating SEPHS2, a key component of the selenoprotein production pathway. Using a combination of patient samples and mouse models, we show that this enhancer upregulates SEPHS2, promoting selenoprotein production and antioxidant function required for AML survival. SEPHS2 and other selenoprotein pathway genes are required for AML growth in vitro. SEPHS2 knockout and selenium dietary restriction significantly delay leukemogenesis in vivo with little effect on normal hematopoiesis. These data validate the utility of enhancer mapping in target identification and suggest that selenoprotein production is an actionable target in AML.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Enhancer Elements, Genetic/genetics ; Humans ; Leukemia, Myeloid, Acute/pathology ; Mice ; Oncogenes ; Selenium/therapeutic use
Chemical Substances	Selenium (H6241UJ22B)
Language	English
Publishing date	2022-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2022.01.003
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Article: Highly efficient gene disruption of murine and human hematopoietic progenitor cells by crispr/cas9

Brunetti, Lorenzo / Gundry, Michael C / Kitano, Ayumi / Nakada, Daisuke / Goodell, Margaret A

Journal of visualized experiments. 2018 Apr. 10, , no. 134

2018

Abstract: Advances in the hematopoietic stem cell (HSCs) field have been aided by methods to genetically engineer primary progenitor cells as well as animal models. Complete gene ablation in HSCs required the generation of knockout mice from which HSCs could be ... ...

Abstract	Advances in the hematopoietic stem cell (HSCs) field have been aided by methods to genetically engineer primary progenitor cells as well as animal models. Complete gene ablation in HSCs required the generation of knockout mice from which HSCs could be isolated, and gene ablation in primary human HSCs was not possible. Viral transduction could be used for knock-down approaches, but these suffered from variable efficacy. In general, genetic manipulation of human and mouse hematopoietic cells was hampered by low efficiencies and extensive time and cost commitments. Recently, CRISPR/Cas9 has dramatically expanded the ability to engineer the DNA of mammalian cells. However, the application of CRISPR/Cas9 to hematopoietic cells has been challenging, mainly due to their low transfection efficiencies, the toxicity of plasmid-based approaches and the slow turnaround time of virus-based protocols. A rapid method to perform CRISPR/Cas9-mediated gene editing in murine and human hematopoietic stem and progenitor cells with knockout efficiencies of up to 90% is provided in this article. This approach utilizes a ribonucleoprotein (RNP) delivery strategy with a streamlined three-day workflow. The use of Cas9-sgRNA RNP allows for a hit-and-run approach, introducing no exogenous DNA sequences in the genome of edited cells and reducing off-target effects. The RNP-based method is fast and straightforward: it does not require cloning of sgRNAs, virus preparation or specific sgRNA chemical modification. With this protocol, scientists should be able to successfully generate knockouts of a gene of interest in primary hematopoietic cells within a week, including downtimes for oligonucleotide synthesis. This approach will allow a much broader group of users to adapt this protocol for their needs.
Keywords	DNA ; animal models ; gene editing ; gene targeting ; genes ; hematopoietic stem cells ; humans ; knockout mutants ; mice ; nucleotide sequences ; oligonucleotides ; rapid methods ; ribonucleoproteins ; toxicity ; transfection ; viruses
Language	English
Dates of publication	2018-0410
Size	p. e57278.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/57278
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Clonal expansion and myeloid leukemia progression modeled by multiplex gene editing of murine hematopoietic progenitor cells.

Shi, Xiangguo / Kitano, Ayumi / Jiang, Yajian / Luu, Victor / Hoegenauer, Kevin A / Nakada, Daisuke

Experimental hematology

2018 Volume 64, Page(s) 33–44.e5

Abstract: Recent advances in next-generation sequencing have identified novel mutations and revealed complex genetic architectures in human hematological malignancies. Moving forward, new methods to quickly generate animal models that recapitulate the complex ... ...

Abstract	Recent advances in next-generation sequencing have identified novel mutations and revealed complex genetic architectures in human hematological malignancies. Moving forward, new methods to quickly generate animal models that recapitulate the complex genetics of human hematological disorders are needed to transform the genetic information to new therapies. Here, we used a ribonucleoprotein-based CRISPR/Cas9 system to model human clonal hematopoiesis of indeterminate potential and acute myeloid leukemia (AML). We edited multiple genes recurrently mutated in hematological disorders, including those encoding epigenetic regulators, transcriptional regulators, and signaling components in murine hematopoietic stem/progenitor cells. Tracking the clonal dynamics by sequencing the indels induced by CRISPR/Cas9 revealed clonal expansion in some recipient mice that progressed to AML initiated by leukemia-initiating cells. Our results establish that the CRISPR/Cas9-mediated multiplex mutagenesis can be used to engineer a variety of murine models of hematological malignancies with complex genetic architectures seen in human disease.
MeSH term(s)	Animals ; Bone Marrow Transplantation ; CRISPR-Associated Protein 9 ; CRISPR-Cas Systems ; Clone Cells/pathology ; Disease Models, Animal ; Disease Progression ; Female ; Gene Editing/methods ; Genes, Neoplasm ; Hematopoietic Stem Cells/pathology ; Humans ; INDEL Mutation ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Neoplastic Stem Cells/pathology ; Preleukemia/genetics ; Preleukemia/pathology ; Ribonucleoproteins/genetics ; Specific Pathogen-Free Organisms
Chemical Substances	Ribonucleoproteins ; CRISPR-Associated Protein 9 (EC 3.1.-)
Language	English
Publishing date	2018-05-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2018.04.009
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Article ; Online: Highly Efficient Gene Disruption of Murine and Human Hematopoietic Progenitor Cells by CRISPR/Cas9.

Brunetti, Lorenzo / Gundry, Michael C / Kitano, Ayumi / Nakada, Daisuke / Goodell, Margaret A

Journal of visualized experiments : JoVE

2018 , Issue 134

Abstract	Advances in the hematopoietic stem cell (HSCs) field have been aided by methods to genetically engineer primary progenitor cells as well as animal models. Complete gene ablation in HSCs required the generation of knockout mice from which HSCs could be isolated, and gene ablation in primary human HSCs was not possible. Viral transduction could be used for knock-down approaches, but these suffered from variable efficacy. In general, genetic manipulation of human and mouse hematopoietic cells was hampered by low efficiencies and extensive time and cost commitments. Recently, CRISPR/Cas9 has dramatically expanded the ability to engineer the DNA of mammalian cells. However, the application of CRISPR/Cas9 to hematopoietic cells has been challenging, mainly due to their low transfection efficiencies, the toxicity of plasmid-based approaches and the slow turnaround time of virus-based protocols. A rapid method to perform CRISPR/Cas9-mediated gene editing in murine and human hematopoietic stem and progenitor cells with knockout efficiencies of up to 90% is provided in this article. This approach utilizes a ribonucleoprotein (RNP) delivery strategy with a streamlined three-day workflow. The use of Cas9-sgRNA RNP allows for a hit-and-run approach, introducing no exogenous DNA sequences in the genome of edited cells and reducing off-target effects. The RNP-based method is fast and straightforward: it does not require cloning of sgRNAs, virus preparation or specific sgRNA chemical modification. With this protocol, scientists should be able to successfully generate knockouts of a gene of interest in primary hematopoietic cells within a week, including downtimes for oligonucleotide synthesis. This approach will allow a much broader group of users to adapt this protocol for their needs.
MeSH term(s)	Animals ; CRISPR-Cas Systems/genetics ; Gene Editing ; Hematopoietic Stem Cells/metabolism ; Humans ; Mice ; Stem Cells/metabolism
Language	English
Publishing date	2018-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/57278
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Article ; Online: Bmi1 Suppresses Adipogenesis in the Hematopoietic Stem Cell Niche.

Hu, Tianyuan / Kitano, Ayumi / Luu, Victor / Dawson, Brian / Hoegenauer, Kevin A / Lee, Brendan H / Nakada, Daisuke

Stem cell reports

2019 Volume 13, Issue 3, Page(s) 545–558

Abstract: Bone marrow stromal cells (BMSCs) that express high levels of stem cell factor (SCF) and CXC chemokine ligand 12 (CXCL12) are one crucial component of the hematopoietic stem cell (HSC) niche. While the secreted factors produced by BMSCs to support HSCs ... ...

Abstract	Bone marrow stromal cells (BMSCs) that express high levels of stem cell factor (SCF) and CXC chemokine ligand 12 (CXCL12) are one crucial component of the hematopoietic stem cell (HSC) niche. While the secreted factors produced by BMSCs to support HSCs have been well described, little is known regarding the transcriptional regulators controlling the cell fate of BMSCs and thus indirectly maintaining HSCs. BMI1 is a polycomb group protein that regulates HSCs both cell intrinsically and extrinsically, but it is unknown in which cell type and how BMI1 functions to maintain HSCs extrinsically. Here we show that Bmi1 maintains HSCs by preventing adipogenic differentiation of BMSCs. Bmi1 is highly expressed in BMSCs but becomes downregulated upon adipogenic differentiation and during aging. Deleting Bmi1 from BMSCs increased marrow adipocytes, induced HSC quiescence and depletion, and impaired hematopoiesis. We found that BMI1 repressed multiple developmental programs in BMSCs by safeguarding the repressive epigenetic marks histone H2A ubiquitylation and H3 lysine 27 trimethylation. We identified a novel adipogenic program governed by Pax3, which BMI1 repressed in BMSCs. Our results establish Bmi1 as a critical regulator of BMSC cell fate that suppresses marrow adipogenesis to create a supportive niche for HSCs.
MeSH term(s)	Adipocytes/cytology ; Adipocytes/metabolism ; Adipogenesis ; Animals ; Cell Differentiation ; Cellular Senescence ; Female ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Histones/metabolism ; Male ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Methylation ; Mice ; Mice, Inbred C57BL ; PAX3 Transcription Factor/genetics ; PAX3 Transcription Factor/metabolism ; Polycomb Repressive Complex 1/genetics ; Polycomb Repressive Complex 1/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; RNA Interference ; RNA, Small Interfering/metabolism ; Stem Cell Niche
Chemical Substances	Bmi1 protein, mouse ; Histones ; PAX3 Transcription Factor ; Proto-Oncogene Proteins ; RNA, Small Interfering ; Pax3 protein, mouse (138016-91-8) ; Polycomb Repressive Complex 1 (EC 2.3.2.27)
Language	English
Publishing date	2019-06-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2019.05.027
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Article ; Online: Nuclear NAD

Shi, Xiangguo / Jiang, Yajian / Kitano, Ayumi / Hu, Tianyuan / Murdaugh, Rebecca L / Li, Yuan / Hoegenauer, Kevin A / Chen, Rui / Takahashi, Koichi / Nakada, Daisuke

Science advances

2021 Volume 7, Issue 30

Abstract: Metabolic dysregulation underlies malignant phenotypes attributed to cancer stem cells, such as unlimited proliferation and differentiation blockade. Here, we demonstrate that ... ...

Abstract	Metabolic dysregulation underlies malignant phenotypes attributed to cancer stem cells, such as unlimited proliferation and differentiation blockade. Here, we demonstrate that NAD
MeSH term(s)	Animals ; Apoptosis/genetics ; Homeostasis ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mice ; NAD/metabolism ; Neoplastic Stem Cells/metabolism ; Nicotinamide-Nucleotide Adenylyltransferase/genetics ; Nicotinamide-Nucleotide Adenylyltransferase/metabolism
Chemical Substances	NAD (0U46U6E8UK) ; NMNAT1 protein, human (EC 2.7.7.1) ; Nicotinamide-Nucleotide Adenylyltransferase (EC 2.7.7.1) ; Nmnat1 protein, mouse (EC 2.7.7.1)
Language	English
Publishing date	2021-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abf3895
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Article ; Online: The histone H3.3 chaperone HIRA restrains erythroid-biased differentiation of adult hematopoietic stem cells.

Murdaugh, Rebecca L / Hoegenauer, Kevin A / Kitano, Ayumi / Holt, Matthew V / Hill, Matthew C / Shi, Xiangguo / Tiessen, Jonathan F / Chapple, Richard / Hu, Tianyuan / Tseng, Yu-Jung / Lin, Angelique / Martin, James F / Young, Nicolas L / Nakada, Daisuke

Stem cell reports

2021 Volume 16, Issue 8, Page(s) 2014–2028

Abstract: Histone variants contribute to the complexity of the chromatin landscape and play an integral role in defining DNA domains and regulating gene expression. The histone H3 variant H3.3 is incorporated into genic elements independent of DNA replication by ... ...

Abstract	Histone variants contribute to the complexity of the chromatin landscape and play an integral role in defining DNA domains and regulating gene expression. The histone H3 variant H3.3 is incorporated into genic elements independent of DNA replication by its chaperone HIRA. Here we demonstrate that Hira is required for the self-renewal of adult hematopoietic stem cells (HSCs) and to restrain erythroid differentiation. Deletion of Hira led to rapid depletion of HSCs while differentiated hematopoietic cells remained largely unaffected. Depletion of HSCs after Hira deletion was accompanied by increased expression of bivalent and erythroid genes, which was exacerbated upon cell division and paralleled increased erythroid differentiation. Assessing H3.3 occupancy identified a subset of polycomb-repressed chromatin in HSCs that depends on HIRA to maintain the inaccessible, H3.3-occupied state for gene repression. HIRA-dependent H3.3 incorporation thus defines distinct repressive chromatin that represses erythroid differentiation of HSCs.
MeSH term(s)	Adult Stem Cells/metabolism ; Age Factors ; Animals ; Animals, Newborn ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Differentiation/genetics ; Cell Self Renewal/genetics ; Erythroid Cells/metabolism ; Gene Expression Profiling/methods ; Gene Ontology ; Hematopoiesis/genetics ; Hematopoietic Stem Cells/metabolism ; Histone Chaperones/genetics ; Histone Chaperones/metabolism ; Histones/genetics ; Histones/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; RNA-Seq/methods ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Mice
Chemical Substances	Cell Cycle Proteins ; Hira protein, mouse ; Histone Chaperones ; Histones ; Transcription Factors
Language	English
Publishing date	2021-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2021.06.009
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Article ; Online: Lineage tracing of murine adult hematopoietic stem cells reveals active contribution to steady-state hematopoiesis.

Chapple, Richard H / Tseng, Yu-Jung / Hu, Tianyuan / Kitano, Ayumi / Takeichi, Makiko / Hoegenauer, Kevin A / Nakada, Daisuke

Blood advances

2018 Volume 2, Issue 11, Page(s) 1220–1228

Abstract: Characterization of hematopoietic stem cells (HSCs) has advanced largely owing to transplantation assays, in which the developmental potential of HSCs is assessed generally in nonhomeostatic conditions. These studies established that adult HSCs ... ...

Abstract	Characterization of hematopoietic stem cells (HSCs) has advanced largely owing to transplantation assays, in which the developmental potential of HSCs is assessed generally in nonhomeostatic conditions. These studies established that adult HSCs extensively contribute to multilineage hematopoietic regeneration upon transplantation. On the contrary, recent studies performing lineage tracing of HSCs under homeostatic conditions have shown that adult HSCs may contribute far less to steady-state hematopoiesis than would be anticipated based on transplantation assays. Here, we used 2 independent HSC-lineage-tracing models to examine the contribution of adult HSCs to steady-state hematopoiesis. We show that adult HSCs contribute robustly to steady-state hematopoiesis, exhibiting faster efflux toward the myeloid lineages compared with lymphoid lineages. Platelets were robustly labeled by HSCs, reaching the same level of labeling as HSCs by 1 year of chase. Our results support the view that adult HSCs contribute to the continuous influx of blood cells during steady-state hematopoiesis.
MeSH term(s)	Adult Stem Cells/cytology ; Adult Stem Cells/metabolism ; Animals ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Mice ; Mice, Transgenic
Language	English
Publishing date	2018-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2876449-3
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2018016295
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