A model of Ft-mediated regulation of Ex. Graphical illustration of findings (not to scale). In wild-type conditions, Ft regulates Ex independently of Crb and there is a homeostasis of Ex levels. Ft promotes apical localization of Ex. Degradation of Ex is stimulated by Dlish, which is balanced by Ft-mediated inhibition of Dlish. Loss of Ds increases the amount of apical Dlish available to interact with and degrade Ex, however this is counteracted by Ft actively inhibiting this process. Upon loss of Ft, or the conserved E region responsible for Ft–Ex interaction, Dlish is derepressed, increasing Ex degradation. Ft and Ds cis interaction may act to antagonize Ft-mediated inhibition of Dlish, which may also promote mutual antagonism between Ft and Ds to support PCP. TM, transmembrane domain.