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. 2002 Sep 9;99(19):12208–12213. doi: 10.1073/pnas.192138799

Fig 2.

Fig 2.

Providencia stuartii AarA can activate EGFr signaling in developing wings. (a) Wild-type wing, the names of the major longitudinal veins are indicated to facilitate comparison with developing wings (g and h). (b) Wing-directed expression of AarA results in ectopic wing vein tissue formation and wing blistering. (c) This phenotype is very similar, for example, to mild RHO-1 overexpression achieved by an heat-shock promoter. (d) Halving the dosage of SPI, an endogenous EGFr ligand normally expressed in the wing, consistently suppressed the AarA induced phenotype (compare with b). (e and f) In addition, the AarA-induced phenotype is (e) partially suppressed in an heterozygote EGFr mutant background, and (f) completely suppressed by coexpression of a dominant-negative EGFr construct (resulting in wings indistinguishable to DN-EGFr expressing ones). (g and h), Activation of EGFr signaling is also confirmed by activated MAPK staining. (g) In wild-type developing wings, activated MAPK is restricted to vein-precursor territories. (h) After AarA expression, ectopic signal is typically detected in the regions most affected in the adult wing (arrowheads).

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