Fig. 7: A working model of the roles of Prdm16 and Vcam1 cessation of neurogenesis and postnatal disappearance of embryonic radial glia. | Nature Communications

Fig. 7: A working model of the roles of Prdm16 and Vcam1 cessation of neurogenesis and postnatal disappearance of embryonic radial glia.

From: Prdm16 regulates the postnatal fate of embryonic radial glia via Vcam1-dependent mechanisms

Fig. 7: A working model of the roles of Prdm16 and Vcam1 cessation of neurogenesis and postnatal disappearance of embryonic radial glia.The alternative text for this image may have been generated using AI.

a Differentiation of radial glial cells in control and Prdm16 cKO mice. b A diagram shows embryonic slowly dividing radial glia become the adult type B cells postnatally. Vcam1 is highly expressed in the embryonic V-SVZ. In control mice, Prdm16 induces a reduction in Vcam1 levels postnatally, triggering the transition from embryonic radial glia to adult NSCs. In Prdm16 cKO mice, the expression of Vcam1 stays high postnatally, leading to the persistence of radial glia and the continuation of cortical neurogenesis. Created in BioRender. Zhang, Y. (2025) https://BioRender.com/r64e200.

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