IκBα controls dormancy in hematopoietic stem cells via retinoic acid during embryonic development

Nat Commun. 2024 Jun 1;15(1):4673. doi: 10.1038/s41467-024-48854-5.

Abstract

Recent findings suggest that Hematopoietic Stem Cells (HSC) and progenitors arise simultaneously and independently of each other already in the embryonic aorta-gonad mesonephros region, but it is still unknown how their different features are established. Here, we uncover IκBα (Nfkbia, the inhibitor of NF-κB) as a critical regulator of HSC proliferation throughout development. IκBα balances retinoic acid signaling levels together with the epigenetic silencer, PRC2, specifically in HSCs. Loss of IκBα decreases proliferation of HSC and induces a dormancy related gene expression signature instead. Also, IκBα deficient HSCs respond with superior activation to in vitro culture and in serial transplantation. At the molecular level, chromatin regions harboring binding motifs for retinoic acid signaling are hypo-methylated for the PRC2 dependent H3K27me3 mark in IκBα deficient HSCs. Overall, we show that the proliferation index in the developing HSCs is regulated by a IκBα-PRC2 axis, which controls retinoic acid signaling.

MeSH terms

  • Animals
  • Cell Proliferation*
  • Embryonic Development / genetics
  • Female
  • Gene Expression Regulation, Developmental
  • Hematopoietic Stem Cells* / cytology
  • Hematopoietic Stem Cells* / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • NF-KappaB Inhibitor alpha* / genetics
  • NF-KappaB Inhibitor alpha* / metabolism
  • Polycomb Repressive Complex 2 / genetics
  • Polycomb Repressive Complex 2 / metabolism
  • Signal Transduction*
  • Tretinoin* / metabolism

Substances

  • Tretinoin
  • NF-KappaB Inhibitor alpha
  • Polycomb Repressive Complex 2
  • Nfkbia protein, mouse