During Drosophila retinal development, interommatidial pigment cells (IOPCs), photoreceptors and other specialist cell types are precisely arranged to produce a characteristic hexagonal lattice. This pattern must be maintained while the cells undergo terminal differentiation and cell shape changes, but it is unclear how these requirements are balanced. Here, Ilaria Rebay and colleagues show that loss of the cytoskeletal regulator Abelson (Abl) in the Drosophila pupal retina disrupts cell shape and cytoskeletal network organisation in both the IOPCs and the photoreceptors. At the tissue level, Abl knockout disrupts the organisation and integrity of the retina, with some photoreceptors falling through the retinal floor. The authors show that Abl is expressed in both the photoreceptors and the IOPCs, where it co-localises with F-actin. Depletion of Enabled, a protein that promotes linear F-actin assembly, partially rescues the Abl knockout phenotypes. Interestingly, restoring Abl function in the photoreceptors alone can partially restore proper cell morphology in both the photoreceptors and the neighbouring IOPCs, as well as improving overall tissue organisation. Similarly, restoring Abl function specifically in the IOPCs partially rescues both IOPC and photoreceptor morphology, thereby improving tissue-level patterns. Together, these data suggest that feedback between IOPCs and photoreceptors, coupled with Abl-dependent cytoskeletal arrangements, helps mediate proper retinal organisation in flies.
