Seeing the light: Combining a behavioural and genetic approach in unraveling the mysteries of the larval visual system of Drosophila melanogaster

Abstract

Using a behavioural and genetic approach, we employed single-gene mutations and photoreceptor cell ablations to study the molecules and cell-types underlying larval response to light Drosophila larvae modulate their locomotion in response to light In the Checker Assay the response to light is defined as an increased residence time in dark quadrants versus lit. In the ON/OFF Assay, it is in part defined as a decreased path length in the light. Previously, mutations in genes, which function in the adult phototransduction cascade were found to abolish fight perception as defined by a reduction in path length. This response to light was reported to be mediated by rhodopsins, other than Rh1, via a pathway similar to the one present in the adult visual system. After undertaking a similar genetic approach in the Checker Assay, the response to light measured in this assay appears also to be mediated through a similar pathway. Mutations in sine oculis (so), a homeobox gene necessary for proper visual system development, and targeted expression of the cell death gene head involution defective (hid), to larval photoreceptor neurons, abolished light response as measured in the Checker Assay. Thus, mutations affecting development oflarval visual system suggest that this response to light is also housed in the larva’s main photoreceptor organ, the BO. The modular GAL4 system was used to target expression of cell death genes, rpr and hid, to Rh5 and Rh6 expressing larval photoreceptor cells. In strains tested in the ON/OFF Assay, in which Rh5 cells are missing, the response to light is abolished, as measured by both decreased path length and increased head swinging behaviour in the light. In a strain in which Rh6 photoreceptor cells are ablated, this response to light is not abolished. This suggests that Rh5 mediates responses in the ON/OFF Assay, which were previously abolished by mutations in genes operating in the adult phototransduction cascade. Thus Rh5, not Rh6, appears to be necessary in mediating the response to light carried out via a pathway similar to the operating in adult phototransduction. In both ablated strains, Rh5-gal4xUAS-rpr and Rh5-gal4xUAS-hid, the integrity of remaining photoreceptor cells is not compromised, and in the latter strain, the extent of ablation appears to be complete. Previously in the ON/OFF assay, mutations and ablations of cell-types were found to disrupt only a subset of behaviours associated with the larval perception of light. Based upon this evidence it was surmised that Rh1 mediates a basic independent visual system, which operates in the larva. However, uncovering the possible roles in this system was hindered, as parental control strains did not respond.