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. 2010 Nov 2;5:28. doi: 10.1186/1749-8104-5-28

Figure 2.

Figure 2

Double mutations of ihog and boi severely disrupt eye development. (A) Normal morphology of an ihogDC1 mosaic eye in a boiC1/+ heterozygote (genotype: boiC1 /+; ihogDC1, FRT40A/FRT40A, l(2)CL-L1; ey-FLP/+). Ommatidia composed of ihogDC1/DC1 homozygous cells are pigmented orange, while the dark red patches mark ommatidia with ihogDC1/+ heterozygous cells. (B) Eye morphology is severely disrupted in an ihogDC1 mosaic eye in a boiC1/- mutant (genotype: boiC1/Y; ihogDC1, FRT40A/FRT40A, l(2)CL-L1; ey-FLP/+). The eye is small, poorly shaped, and many ommatidia are missing. Some double mutant ommatidia appear to differentiate in these mosaics but have a roughened appearance, which is consistent with smo mutations. (C) Addition of Ihog rescues viability and eye morphology in a double mutant (genotype: boiC1/Y; ihogDC1/DC1; UAS-ihog::myc/+). (D) RT-PCR to demonstrate loss of ihog transcripts in ihogDC1/DC1 mutants, and to characterize a transgenic line with low-level, constitutive expression of UAS-ihog::myc in the absence of a Gal4 driver.