| Literature DB >> 33159854 |
Stylianos Lefkopoulos1, Aikaterini Polyzou2, Marta Derecka3, Veronica Bergo4, Thomas Clapes3, Pierre Cauchy3, Carolina Jerez-Longres3, Megumi Onishi-Seebacher5, Na Yin3, Natalia-Adriana Martagon-Calderón3, Kathryn S Potts6, Lhéanna Klaeylé3, Feng Liu7, Teresa V Bowman6, Thomas Jenuwein5, Maria Caterina Mione8, Eirini Trompouki9.
Abstract
Inflammatory signaling is required for hematopoietic stem and progenitor cell (HSPC) development. Here, we studied the involvement of RIG-I-like receptors (RLRs) in HSPC formation. Rig-I or Mda5 deficiency impaired, while Lgp2 deficiency enhanced, HSPC emergence in zebrafish embryos. Rig-I or Mda5 deficiency reduced HSPC numbers by inhibiting inflammatory signals that were in turn enhanced in Lgp2 deficient embryos. Simultaneous reduction of Lgp2 and either Rig-I or Mda5 rescued inflammatory signals and HSPC numbers. Modulating the expression of the signaling mediator Traf6 in RLR deficient embryos restored HSPC numbers. Repetitive element transcripts could be detected in hemogenic endothelial cells and HSPCs, suggesting a role as RLR ligands. Indeed, ectopic expression of repetitive elements enhanced HSPC formation in wild-type, but not in Rig-I or Mda5 deficient embryos. Manipulation of RLR expression in mouse fetal liver HSPCs indicated functional conservation among species. Thus, repetitive elements transcribed during development drive RLR-mediated inflammatory signals that regulate HSPC formation.Entities:
Keywords: HSCs; RIG-I-like receptors; development; hematopoiesis; hematopoietic stem cells; inflammation; innate immune receptors; repetitive elements; transposable elements; zebrafish
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Year: 2020 PMID: 33159854 DOI: 10.1016/j.immuni.2020.10.007
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745