The human fetal brain shows extensive somatic mosaicism with each embryonic neuronal progenitor cell (NPC) accumulating five mutations daily, whereas postnatal mature neurons accumulate 23 mutations yearly. Somatic mosaicism can contribute to neurodevelopmental disorders like schizophrenia and play a role in interindividual phenotypic differences. Rapid NPC proliferation may cause the high mutation rate, and somatic mutations can alter NPC survival, proliferation, or differentiation, causing clonal selection. Little is known about the mechanisms driving clonal evolution in neurotypical brains due to model limitations and scarce biopsy availability. I developed a mouse model to explore whether NPC replication speed can influence somatic mosaicism. Previous research showed that telencephalic NPCs can compensate for diphtheria toxin A-mediated ablation of 50% of their pool, suggesting a shortened cell cycle. My model similarly targets NPCs of the entire CNS, reducing their pool by 30-50% before embryonic day (E) 12.5. Single-cell transcriptomics and histology revealed that the remaining NPCs successfully generated all neuronal populations at E17.5, despite a 15% reduction in isocortical cellularity. As hypothesized, NPCs shortened their S phase by 50%. Deep whole-genome sequencing of neuronal cells derived from fast-cycling NPCs identified positively selected clones without known driver mutations and a single-nucleotide substitution profile dominated by C>T and C>A transitions. We are further investigating the implications of this clonally enriched mutational spectrum and model expansion and competition of fast-proliferative NPCs in silico.In conclusion, we aim to explore the connection between somatic mutations and cell proliferation rate, suggesting positive selection of fast-proliferating clones in early neurodevelopment.