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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).
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