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Updated: Jul 3, 2026
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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
Published on: January 26, 2018
Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development
Sakshi Chauhan1, Fuki Kudoh1,2, Anup Dey1
1Division of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Iscience
|July 2, 2026
Summary
Variant histone H3.3 is essential for myeloid progenitor cell proliferation and DNA integrity. While its absence hinders early development, H3.3 is not indispensable for later bone marrow-derived macrophage differentiation.
Area of Science:
- Cell Biology
- Genetics
- Immunology
Background:
- Variant histone H3.3 is crucial for gene expression and cellular survival.
- H3.3 deletion causes embryonic lethality in mice, but its role in later development is unclear.
- The myeloid lineage is vital for innate immunity.
Purpose of the Study:
- To investigate the role of H3.3 in myeloid lineage development.
- To understand H3.3's function in bone marrow-derived macrophage differentiation.
Main Methods:
- Conditional knockout of H3.3 genes in myeloid progenitor cells.
- Analysis of cell proliferation, DNA damage, and apoptosis.
- Assessment of gene expression, chromatin accessibility, and histone modifications in H3.3-deficient cells.
Main Results:
- H3.3-deficient myeloid progenitor cells showed impaired replication, DNA damage, and apoptosis.
- Surviving H3.3-deficient cells upregulated interferon-stimulated genes.
- H3.3-deficient macrophages maintained accessible chromatin and general nucleosomal structure.
Conclusions:
- H3.3 is required for myeloid progenitor cell proliferation.
- H3.3 is not essential for the differentiation of bone marrow-derived macrophages.
- H3.3 plays a critical role in maintaining genomic stability during myeloid development.
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