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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Dev Biol. 2017 Apr 12;432(1):72–85. doi: 10.1016/j.ydbio.2017.04.002

Fig. 9. A model of the roles of Spop in spinal cord patterning.

Fig. 9

(A) In the lateral region of the spinal cord (long range) including p0-pMN, low to intermediate levels of Shh reduce the production of Gli3R from Gli3FL by antagonizing the repressive function of Sufu, allowing the expression of genes such as Olig2 and Nkx6.1. In pFP and p3, high levels of Shh promote the production of Gli2A and Gli3A, which then activate the expression of Foxa2 and Nkx2.2. Gli2A plays a more predominant role than Gli3A in this context. Spop targets Gli3 for degradation, preventing over activation of the Shh pathway. (B) The levels of both Gli3A and Gli3R increase in the absence of Spop, but the effect of the increased Gli3A on the formation of pFP and p3 is only revealed in Spop;Gli2 double mutants, in which the much more potent Gli2A is absent. In Gli1;Sufu double mutants, the reduced levels of Gli2A and Gli3A are insufficient to support pFP and p3 formation. Loss of Spop increases Gli3A and rescues the formation of pFP and p3 in Sufu;Gli1;Spop triple mutants. The moderate increase in Gli3R in the absence of Spop does not show apparent effect in ventral spinal cord patterning in various single and compound mutants.