Ligand-independent EPHA2 signaling sustains neural progenitors via ECSIT and NAD+

ABSTRACT: Embryonic neural stem and progenitor cells occupy a specialized niche along the lateral ventricles, where receptors on their apical membrane sense extracellular cues essential for preserving progenitor identity. How such surface signals are coupled to mitochondrial metabolism remains unclear. Here, we identify EPHA2 as a receptor enriched in cortical progenitors and show that disruption of its non-canonical, ligand-independent signaling compromises progenitor maintenance in vivo. EPHA2 perturbation reduces mitochondrial respiration, Complex I activity, and mitochondrial NAD+ regeneration, and is accompanied by lower mitochondrial abundance of the Complex I assembly factor ECSIT. Restoring mitochondrial NAD+ regeneration with MTS-LbNOX, or restoring mitochondrial ECSIT with ECSIT WT-but not

SUBMITTER: Sang Ki Park 

PROVIDER: S-SCDT-10_1038-S44319-026-00858-6 | biostudies-other |

REPOSITORIES: biostudies-other