NF-κB signaling controls H3K9me3 levels at intronic LINE-1 and hematopoietic stem cell genes in cis.
Journal
The Journal of experimental medicine
ISSN: 1540-9538
Titre abrégé: J Exp Med
Pays: United States
ID NLM: 2985109R
Informations de publication
Date de publication:
01 08 2022
01 08 2022
Historique:
received:
23
06
2021
revised:
23
12
2021
accepted:
21
06
2022
entrez:
8
7
2022
pubmed:
9
7
2022
medline:
14
7
2022
Statut:
ppublish
Résumé
Ionizing radiations (IR) alter hematopoietic stem cell (HSC) function on the long term, but the mechanisms underlying these effects are still poorly understood. We recently showed that IR induces the derepression of L1Md, the mouse young subfamilies of LINE-1/L1 retroelements. L1 contributes to gene regulatory networks. However, how L1Md are derepressed and impact HSC gene expression are not known. Here, we show that IR triggers genome-wide H3K9me3 decrease that occurs mainly at L1Md. Loss of H3K9me3 at intronic L1Md harboring NF-κB binding sites motifs but not at promoters is associated with the repression of HSC-specific genes. This is correlated with reduced NFKB1 repressor expression. TNF-α treatment rescued all these effects and prevented IR-induced HSC loss of function in vivo. This TNF-α/NF-κB/H3K9me3/L1Md axis might be important to maintain HSCs while allowing expression of immune genes during myeloid regeneration or damage-induced bone marrow ablation.
Identifiants
pubmed: 35802137
pii: 213343
doi: 10.1084/jem.20211356
pmc: PMC9274146
pii:
doi:
Substances chimiques
Histones
0
NF-kappa B
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Institut National de la Santé et de la Recherche Médicale
Organisme : La Ligue Nationale contre le Cancer
Organisme : Institut National Du Cancer
ID : PLBIO no. 2020-095
Organisme : Fondation ARC pour la Recherche sur le Cancer
ID : N° 20161204988
Organisme : Agence Nationale de la Recherche
ID : ANRJCJC20-CE14-0018-01
Informations de copyright
© 2022 Pelinski et al.
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