ArticleCell death & disease2025
Rb substantially compensates for the double loss of p130 and p107 in adult but not embryonic neural stem cell lineages.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Mettl8 Regulates Hippocampal Neural Stem Cell Proliferation and Neurogenesis via mTOR/4E-BP1 Signaling.CNS neuroscience & therapeutics · 2026Article
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10 authors.
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Abstract
The Retinoblastoma (Rb) family of pocket proteins (p107, Rb, and p130) controls all aspects of neurogenesis from stem cell activation to long-term neuronal survival in the brain. Previous studies have reported non-overlapping, often complementary, roles for these cell cycle regulators with possibility for functional compensation. Yet the extent to which each protein might compensate for other family members and whether synergistic effects exist during neural stem cell (NSC) lineage development remain unclear. Fong et al. recently revealed that a triple knock-out (TKO) of all pocket proteins results in a transcriptomic switch from NSC quiescence to activation, followed by niche depletion in the adult hippocampus. Here, we investigated whether pocket proteins are equally critical in NSC fate regulation in the adult subventricular zone (aSVZ) and during embryogenesis. We report that TKO of these proteins results in NSC activation coupled to ectopic progenitor proliferation and massive apoptosis, leading to niche depletion and premature loss of neurogenesis inside the olfactory bulb (OB). Notably, a p107-p130 double knockout carrying a single wild-type Rb allele (DKO) substantially rescues the above defects and maintains adult neurogenesis. In comparison, TKO embryos display severe disruptions in all stages of neurogenesis at E14.5, leading to embryonic lethality. Similar defects are detected when any five out of the six alleles of pocket proteins are lost, with only partial rescue of the proliferation defects observed in DKO embryos. The above TKO phenotypes are partially mediated by opposed deregulations in the Notch-Hes signaling pathway in the embryonic versus the adult brain. Such deregulation is linked to opposite changes in E2F3a and E2F3b embryonic gene expressions. Our data identifies Rb as a critical pocket protein in the control and maintenance of adult OB neurogenesis, and uncovers interchangeable, dose-dependent roles for pocket proteins in the control of neuronal differentiation and survival during development.
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