Figure 2. Synergy between Notch and Src in the eye and wing causes hyperplastic phenotypes and activates JNK.
(A–H) Various UAS-Src constructs were driven by E1Gal4 along with UAS-Nact in the developing eye. When d10338, an Exelixis allele that causes Gal4-dependent overexpression of Src42A, and Nact are coexpressed (A), the Nact large eye phenotype (C) is enhanced; in addition, occasional outgrowths of eye tissue can be seen (arrow). Note that d10338 alone (B) results in decreased eye size, whereas Nact alone (C) results in increased eye size compared to the control (D). Src42ACA and Src64B both cause a similar phenotype (E, G) when coexpressed with Nact under E1Gal4, and both also result in decreased eye size in the absence of Nact (F, H). (I–L) UAS-Nact and UAS-Src42ACA were driven in the developing wing using the vgGal4 driver. When Nact and Src42ACA are co-expressed (I), wing discs are overgrown compared to either Src42ACA (J) or Nact (K) alone and display a characteristic ‘crumpled ball’ phenotype indicative of tissue disorganization and cell migration. Note that Src42ACA alone (J) causes disorganization but not overgrowth. (M–P) Puc-LacZ reporter assay for JNK signal activation in wing discs expressing UAS constructs as indicated under the vgGal4 driver in a pucE69/+ background. Coexpression of Nact and Src42ACA (M) causes strong, global activation of the pucLacZ reporter. In contrast, expression of either gene alone (N, O) causes weaker activation that is limited in scope. Scale bars: 100 μm.
Figure 2—figure supplement 1. d10338 is a UAS allele of Src42A.
Figure 2—figure supplement 2. Src64B also synergizes with Nact in the wing disc.
