Somatosensory ganglia including dorsal root ganglion (DRG) and trigeminal ganglion (TG) are derived from a common pool of neural crest stem cells (NCCs), and are good systems to study the mechanisms of neurogenesis and gliogenesis.Notch signaling is known to play important roles in DRG and TG development, but the full scope of Notch functions in mammalian DRG and TG development remains poorly understood.In the present study, we used Wntl-Cre to conditionally inactivate the transcription factor Rbpj, a critical integrator of activation signals from all Notch receptors, in NCCs and their derived cells.Deletion of Rbpj caused the up-regulation of NeuroD1 and precocious neurogenesis in DRG early development but led to an eventual deficit of sensory neurons at later stages, due to reduced cell proliferation and abnormal cell death.In addition, gliogenesis was delayed initially, but a near-complete loss of glia was observed finally in Rbpj-deficient DRG.Interestingly, the phenotypes in TG show big differences compared with those in DRG in Rbpj CKO mice.Although deletion of Rbpj also resulted in a reduction of sensory neurons at E16.5 in the TG, the precocious neurogenesis was not observed in TG early development.Furthermore, the initial gliogenesis at E 10.0 in TG is also defective in the absence of Rbpj, but the normal distribution of glial ceils was observed at E16.5 in the TG which contrasts with the complete loss of glial cells in the DRG.The reason why the glial cells recover to the normal distribution density at later stages remained to be explored.Taken together, our data further elucidate the essential role of Rbpj in neurogenesis and gliogenesis during DRG and TG development.The differences in phenotypes between DRG and TG indicate the function of Rbpj is diversified and context-dependent.