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STEM CELLS

H3.3 safeguards haematopoietic ERV-quilibrium

Nature Cell Biology volume 24, pages 7–9 (2022)Cite this article

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Cell fate determination by H3.3 deposition in haematopoietic stem and progenitor cells is largely unexplored. Two studies jointly support the idea that H3.3 maintains haematopoiesis balance and prevents endogenous retroviral element (ERV) activation through chromatin marks and transcriptome alterations.

Guo et al. first questioned whether H3.3A and H3.3B, the two genes encoding H3.3, act redundantly. They found that double, but not single, H3.3 gene knockout caused differential changes in haematopoietic phenotypes. Specifically, loss of H3.3 resulted in a strong increase in the number of myeloid cells, whereas lymphocyte and erythroblast numbers were reduced. On the anatomical level, the mice showed splenomegaly, pale bones and a small thymus. In contrast, mice depleted of the H3.3 chaperone Hira showed only the reduced thymus size.

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Fig. 1: H3.3 and its chaperone Daxx are involved in maintaining a balance in haematopoiesis.

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Affiliations

  1. Cell Fate Engineering and Therapeutics Laboratory, A*STAR Institute of Molecular and Cell Biology, Singapore, Singapore

    Nadia Omega Cipta, Ying Chen & Yuin-Han Loh

  2. Department of Biological Sciences, National University of Singapore, Singapore, Singapore

    Nadia Omega Cipta & Yuin-Han Loh

  3. NUS Graduate School for Integrative Sciences and Engineering Programme, National University of Singapore, Singapore, Singapore

    Ying Chen & Yuin-Han Loh

  4. Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

    Yuin-Han Loh

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  1. Nadia Omega Cipta
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  2. Ying Chen
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  3. Yuin-Han Loh
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Correspondence to Yuin-Han Loh.

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Cipta, N.O., Chen, Y. & Loh, YH. H3.3 safeguards haematopoietic ERV-quilibrium. Nat Cell Biol 24, 7–9 (2022). https://doi.org/10.1038/s41556-021-00758-y

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