ttk loss of function phenotypes are suppressed in a lzmr2 mutant background. A. Scanning Electron Microscopy (SEM) of a wild-type (wt) adult eye. B. SEM shows that the lzmr2 mutation results in a mild eye phenotype, with ommatidial disorganisation observed at the posterior rim of the adult eye. Insets represent higher magnification images in this and subsequent panels, and posterior is to the right in all images. C. SEM of ttk1e11 mutant adult retina (loss of Ttk69; tissue generated using the Flp/FRT clonal system) shows severe retinal degeneration, with severely disrupted ommatidia. Severe scarring across the retina and failure of bristle formation is shown. Micrographs were taken from flies where clones were generated across nearly all the eye (w- tissue; not shown). E. When ttk1e11 mutant clones were generated in a lzmr2 background, the ttk1e11 mutant phenotype was partially suppressed, with the degree of ommatidial scarring reduced, and bristle formation restored. D. The eye phenotype caused by the generation of ttkrm730 mutant tissue (loss of Ttk69 and ttk88) across the majority of the eye results in a severely deformed ommatidia and a lack of bristle development. F. The ttkrm730 eye phenotype can be partially rescued when clones are generated in a lzmr2 mutant background, with the degree of ommatidial scarring reduced, and the restoration of ommatidial structure and bristle formation observed.
Siddall et al. BMC Developmental Biology 2009 9:64 doi:10.1186/1471-213X-9-64