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Multiple signals control the balance between proliferation and differentiation of neural progenitor cells during corticogenesis. A key point of this regulation is the control of G1 phase length, which is regulated by the Cyclin/Cdks complexes. Using genome-wide chromatin immunoprecipitation assay and mouse genetics, we have explored the transcriptional regulation of  Cyclin D1  ( Ccnd1 ) during the early developmental stages of the mouse cerebral cortex. We found evidence that SP8 binds to the  Ccnd1  locus on exon regions.  In vitro  experiments show SP8 binding activity on  Ccnd1  gene 3′-end, and point to a putative role for SP8 in modulating PAX6-mediated repression of  Ccnd1  along the dorso-ventral axis of the developing pallium, creating a medial Low -lateral High  gradient of neuronal differentiation. Activation of  Ccnd1  through the promoter/5′-end of the gene does not depend on SP8, but on βcatenin (CTNNB1). Importantly, alteration of the  Sp8  level of expression  in vivo  affects  Ccnd1  expression during early corticogenesis. Our results indicate that  Ccnd1  regulation is the result of multiple signals and that SP8 is a player in this regulation, revealing an unexpected and potentially novel mechanism of transcriptional activation.

SP8 Transcriptional Regulation of Cyclin D1 During Mouse Early Corticogenesis