Fig. 6. (A-C) Schematic models of the effects of Wg and Egfr activities in the PE. (A) The squamous morphology and genetic specification of peripodial cells (A) is transformed by ectopic Wg (B) or Egfr (C) signalling. (D-G) Different mechanisms that could account for the absence of Wg and Egfr signalling in the PE (see Discussion). The decay in the concentration of the ligands from their sources in the wing-notum side could lower this concentration down to zero (D) or below a hypothetical activation threshold (E). Alternatively, peripodial cells could be refractory to Wg and Egfr activities because of repression of the signals downstream of the receptor level (F) or decreased diffusive ability of the ligands in peripodial cells (G). These two latter possibilities imply a previous genetic heterogeneity that sets the limits of the peripodial developmental field from early larval stages and implements suppression of Wg and Egfr signalling (H).