Skip to main content
. Author manuscript; available in PMC: 2022 May 3.
Published in final edited form as: Dev Cell. 2021 Apr 13;56(9):1268–1282.e6. doi: 10.1016/j.devcel.2021.03.024

Figure 7. Model for position-dependent regulation of the neural crest identity by canonical Wnt signaling.

Figure 7.

(A) NC genes are regulated by multiple enhancers that contact promoters in a tissue-specific manner. Essential components of the NC GRN are regulated by at least one Wnt-associated element.

(B) Wnt-associated elements act as genomic sensors that respond to environmental inputs. These enhancers possess multiple TCF/LEF binding motifs that allow response to levels of signaling. As cells migrate away from the stem cell niche, these elements lose their interactions with nuclear effectors, resulting in loss of gene expression and inactivation of the GRN.

(C-D) Models for the role of Wnt signaling in the control of the NC GRN. Instead of acting as an upstream regulator (C), our results indicate canonical Wnts simultaneously control multiple components the GRN in a hub-and-spoke architecture (D).