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. Author manuscript; available in PMC: 2010 Oct 19.
Published in final edited form as: Development. 2007 Apr 11;134(10):1861–1871. doi: 10.1242/dev.002972

Fig. 8. Dpp signaling works together with DE-caderin and Rho1 to pattern the Drosophila pupal retina.

Fig. 8

(A,B) Removing one genomic copy of shg and either tkv (A) or Mad (B) resulted in a significant increase in the incidence of ectopic 2°/3°s (red arrows) and misplaced 3°s (green arrows). Most misplaced 3°s were accompanied by an extra cell; conversely, we observed many cases of extra cells without a misplaced tertiary (red arrow). (C) Quantification of 2°/3°s defects. The data are expressed as the percentage of ommatidia with defects out of the total number of ommatidia counted. n=number of ommatidia counted from at least four different animals for each genotype. (D,E) Removing one genomic copy of Rho1 in retinas expressing four copies of tkv-IR enhanced the frequency and severity of IPC patterning defects (arrows, compare D with E). The full genotypes were: (D) GMR-gal4/+; UAS-tkv-IR2(2X)/+; UAS-tkv-IR1(2X)/+; (E) GMR-gal4/+; UAS-tkv-IR2(2X)/Rho172F; UAS-tkv-IR1(2X)/+.