Figure 4. Acn genetically interacts with p38b MAP kinase and Cdk5/p35.

SEM images of eye expressing the indicated transgenes under GMR-Gal4 control at 28°C. (A) Expression of UAS-Acn^WT causes a rough eye. This eye-roughness is suppressed by knockdown of p38b MAPK (B) or co-expression of dominant-negative p38b MAPK^K53R (C). By contrast, co-expression of wild-type p38b MAPK enhances the roughness (D). Expression of Gal4 (E) or the indicated p38b MAPK transgenes in the absence of UAS-Acn^WT (F–H) causes little or no changes in eye morphology. Eye-roughness induced by UAS-Acn^WT is suppressed by knockdown of Cdk5 (I) or co-expression of dominant-negative Cdk5^K33A (J). By contrast, co-expression of wild-type Cdk5 (K) or the required cofactor p35 (L) enhance Acn^WT-induced roughness. Expression of the indicated Cdk5 and p35 transgene in the absence of UAS-Acn^WT (M–P) causes little or no changes in eye morphology. Scale bar in A-P: 50 µm. Quantification of genetic interactions is shown in Supplementary files 1 and 2. Detailed genotypes are listed in Supplementary file 3.

Figure 4—figure supplement 1. Knockdown efficiency of p38b MAPK, Cdk5 and p35 RNAi UAS-transgenes.

Indicated UAS-RNAi transgenes were expressed using Da-Gal4 or Arm-Gal4 drivers in adult flies. Transcript levels for the indicated genes were determined using RT-qPCR relative to the ribosomal protein RP49 and normalized to wild-type OreR flies. Bar graphs show mean ±SD from three biological replicas.

Figure 4—figure supplement 2. Expression of dominant-negative mutant Cdk5 and p38b MAP kinases.

FLAG-tagged dominant negative mutant Cdk5 or p38b kinases as used in Figure 4 were expressed in eye discs under control of the GMR-Gal4 driver and detected with anti-FLAG antibodies. Scale bar: 50 µm.