C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.

ABSTRACT: C1q levels in the CNS are elevated by inflammation and neurovascular trauma, yet the consequence of this increase for neural stem cell (NSC) regeneration response remain unknown. We have recently identified C1q receptor candidates that regulate NSC behavior. One of these is Brain Angiogenesis Inhibitor 1 (BAI1, ADGRB1), which has no previously discovered role in NSC. Here, we show that C1q acts in a BAI1-dependent manner to modulate NSC quiescence via two parallel mechanisms. First, negative regulation of MDM2, driving cell cycle suppression through p53. Second, endocytic internalization of C1q-BAI1-complex, driving regulation of p32 (C1qBP) and metabolic reprogramming towards aerobic glycolysis. We validated the biological significance of BAI1 in a male hNSC line in vivo using a female mo

SUBMITTER: Piltti KM 

PROVIDER: S-EPMC12738564 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature