Mutation in rugose gene locus affects the pigment cell number and alters the optic lobe phenotype in the Drosophila visual system.

In the Drosophila melanogaster, developmental signals orchestrate cell differentiation in a sequential manner which lead to precise neural and cellular patterns. The previous work demonstrated that the rugose (rg) gene is required for proper differentiation of the cone and pigment cells in the Drosophila compound eye. In this study, the pigment cell number in several ommatidia in rugose mutant eyes was analyzed and showed multiplication of secondary pigment cells in the null mutation.

rugose (rg), a Drosophila A kinase anchor protein, is required for retinal pattern formation and interacts genetically with multiple signaling pathways.

In the developing Drosophila eye, cell fate determination and pattern formation are directed by cell-cell interactions mediated by signal transduction cascades. Mutations at the rugose locus (rg) result in a rough eye phenotype due to a disorganized retina and aberrant cone cell differentiation, which leads to reduction or complete loss of cone cells. The cone cell phenotype is sensitive to the level of rugose gene function.

Neuronal development in the Drosophila compound eye: photoreceptor cells R1, R6, and R7 fail to differentiate in the retina aberrant in pattern (rap) mutant.

The compound eye of Drosophila is a reiterated pattern of 800 unit eyes known as ommatidia. In each ommatidium there are eight photoreceptor neurons (R1-R8) and an invariant number of accessory cells organized in a precise manner. In the developing eye, specification of cell fates is triggered by sequential inductive events mediated by cell-cell interactions.