ArticleProceedings of the National Academy of Sciences of the United States of America2025
Lineage tracing of both quiescent G0 and active Hoxb5+ LT-HSCs that actively contribute to homeostatic mouse hematopoiesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Unlocking the HOX: Homeobox Genes as Regulators of Hematopoietic Development.International journal of molecular sciences · 2026Review
- Lineage tracing of both quiescent G0 and active Hoxb5+ LT-HSCs that actively contribute to homeostatic mouse hematopoiesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
11 authors.
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Abstract
Studying the lineage commitment and differentiation potential of long-term hematopoietic stem cells (LT-HSCs) is important to understand the dynamics of hematopoiesis. A central question concerns which hematopoietic stem and progenitor cell populations are responsible for sustaining steady-state hematopoiesis in vivo without conditioning. Noninvasive HSC fate-mapping strategies to address this question require specific labeling of LT-HSCs only. In this study, we selectively labeled a subset of Hoxb5+ LT-HSCs-excluding short-term HSCs (ST-HSCs) and multipotent progenitors (MPPs)-to track the progeny of these cells. Hoxb5+ LT-HSCs comprise ~1 in 100,000 bone marrow cells. MPPs were not labeled until several months post-induction, indicating their derivation from LT-HSCs. At no time were MPPs labeled and LT-HSCs not, consistent with the origin and maintenance of MPPs from LT-HSCs. Hoxb5+ LT-HSCs are the principal contributors to steady-state in situ hematopoiesis, but only a fraction of LT-HSCs were labeled by the Cre/LoxP conversion to a lineage-tracing color. We tested whether quiescent HSCs could have incised the DNA at loxp sites, but did not finish the rearrangement. Analysis of phosphorylated H2AX (γ-H2AX) revealed that quiescent LT-HSCs retain Cre/LoxP-induced DNA incisions, which are repaired upon cell cycle entry, leading to the appearance of newly labeled LT-HSCs at later time points, mainly of the myeloid-biased HSC. Moreover, most LT-HSCs exhibit marked expansion in response to hematopoietic stress. With the age-related shift of blood formation from balanced to myeloid biased, the myeloid-biased HSCs expand preferentially after 6 mo of tracking.
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