Defective ommatidial cell assembly leads to defective morphogenesis: a phenotypic analysis of the E(spl) D mutation of Drosophila melanogaster

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Abstract
The spl mutation of the N gene causes, among other phenotypic traits, the lack of a few ommatidia, roughness and a general reduction in the size of the compound eye; these defects are drastically enhanced by the dominant mutation E(spl)D. We have studied cellular and developmental aspects of the phenotypic interaction between spl and E(spl)D. We found that the initial clustering of photoreceptor cells is affected in eye imaginal discs of spl larvae causing the defects visible in the adult eye. The degree of disorganization of the spl/Y; E(spl)D/ + eye disc is much higher, only a few photoreceptor cells are able to group with representatives of the other cell types and differentiate normally. BrdU incorporation shows that the proliferation pattern of the spl/Y; E(spl)D/ + disc cells during the third instar is normal. Abundant cell death occurs posteriorly in the mutant discs, which accounts for their small size. Finally, we found that in the eye imaginal disc the transcription of m8, the E(spl) gene, responsible for the enhancement of the spl phenotype caused by the E(spl)D mutation, is restricted to the morphogenetic furrow, where the ommatidial cells start grouping with each other to take on their future developmental fates; the m8 transcription rate is highly increased in E(spl)D eye discs. All these observations indicate that the assembly of the ommatidial cells is affected in the spl/Y; E(spl)D/ + disc and that the other abnormalities are morphogenetic consequences of the defective cell grouping.