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. 2017 Aug 1;10(8):993–1003. doi: 10.1242/dmm.026179

Fig. 4.

Fig. 4.

Expression of expanded (CCUG)n causes severe disruption of eye morphology, which can be modified by loss or gain of MBNL. (A) The eye of a GMR-Gal4-only fly. (B) Expression of the control N-16 transgene under the GMR-Gal4 driver shows a very mild eye roughening, which is caused by GMR-Gal4. (C) Disruption of the external eye morphology of a fly that expresses DM2-106 using GMR-Gal4. (D) Expression of a UAS control transgene, UAS-GFP, does not rescue the eye phenotype of GMR-Gal4>DM2-106 flies. (E) Heterozygosity for a null allele of muscleblind (mblKG08885), resulting in functional hemizygosity, severely enhances the DM2-106 eye phenotype owing to the 50% reduction in MBL protein levels. (F) Expression of human MBNL1 rescues the eye phenotype of DM2-106 flies under GMR-Gal4 control. (G) Co-expression of a CUGBP1 transgene using GMR-Gal4 does not rescue or provides only very little rescue of the external eye morphology of DM2-106 flies. (H) Expression levels of control (N-16) and experimental (DM2-106) transgenes under GMR-Gal4 control in eye imaginal discs. Statistical analysis was by two-tailed, non-paired t-test (P=0.222). (I-I″) MBNL1 protein (green) accumulates in CCUG foci (red) in GMR-Gal4>DM2-106 eye imaginal discs (arrows). Interestingly, MBNL1 also aggregates in foci independently of CCUG repeats (arrowheads). Nuclei are labeled with DAPI (blue).