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Redox-dependent Igfbp2 signaling controls Brca1 DNA damage response to govern neural stem cell fate
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Redox-dependent Igfbp2 signaling controls Brca1 DNA damage response to govern neural stem cell fate
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Journal Article
Redox-dependent Igfbp2 signaling controls Brca1 DNA damage response to govern neural stem cell fate
2023
Overview
Neural stem cell (NSC) maintenance and functions are regulated by reactive oxygen species (ROS). However, the mechanisms by which ROS control NSC behavior remain unclear. Here we report that ROS-dependent Igfbp2 signaling controls DNA repair pathways which balance NSC self-renewal and lineage commitment.
Ncf1
or
Igfbp2
deficiency constrains NSCs to a self-renewing state and prevents neurosphere formation. Ncf1-dependent oxidation of Igfbp2 promotes neurogenesis by NSCs in vitro and in vivo while repressing Brca1 DNA damage response genes and inducing DNA double-strand breaks (DDSBs). By contrast,
Ncf1
–/–
and
Igfbp2
–/–
NSCs favor the formation of oligodendrocytes in vitro and in vivo. Notably, transient repression of Brca1 DNA repair pathway genes induces DDSBs and is sufficient to rescue the ability of
Ncf1
–/–
and
Igfbp2
–/–
NSCs to lineage-commit to form neurospheres and neurons. NSC lineage commitment is dependent on the oxidizable cysteine-43 residue of Igfbp2. Our study highlights the role of DNA damage/repair in orchestrating NSC fate decisions downstream of redox-regulated Igfbp2.
How reactive oxygen species regulate neuronal stem cell (NSC) behavior is poorly understood. Here, the authors report that Ncf1-dependent oxidation of Igfbp2 cystines represses DNA repair networks to regulate NSC self-renewal and cell fate decisions.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14/35
/ 38/1
/ 38/77
/ 38/91
/ 42/100
/ 42/109
/ 42/89
/ 49/88
/ 64/60
/ 82/29
/ 82/58
/ 96/106
/ 96/35
/ Cell Differentiation - genetics
/ Damage
/ DNA
/ Genes
/ Humanities and Social Sciences
/ Insulin-like growth factor-binding protein 2
/ Neural Stem Cells - metabolism
/ Oxygen
/ Reactive Oxygen Species - metabolism
/ Repair
/ Science
