Fig. 6: Three-step model of posterior specification.

Our data supports a working model in which after an amputation, foxG is expressed at early stages of regeneration in the posterior-facing wounds. The FOXG transcription factor activates wnt1 expression in the organizer cells, possibly by interacting with an enhancer located in its first intron. Because of this interaction, these cells express and secret wnt1. In the 3-step model, the wnt1 responding cells, through the β-catenin-1/TCF pathway, will induce the expression of chromatin remodelers (1) and TFs (i.e. sp5, tsh, Homeobox) (2). Consequently, the chromatin will be accessible for the TFs regulating the expression of crucial genes for posterior specification (i.e. Wnt11s, fzd4-1) (3).