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Background  Mutations in  spastin  are the most common cause of hereditary spastin paraplegia, a neurodegenerative disease. In this study, the role of  spastin  was examined in  Drosophila  photoreceptor development.    Methodology/Principal Findings  The  spastin  mutation in developing pupal eyes causes a mild mislocalization of the apical membrane domain at the distal section, but the apical domain was dramatically reduced at the proximal section of the developing pupal eye. Since the rhabdomeres in developing pupal eyes grow from distal to proximal, this phenotype strongly suggests that  spastin  is required for apical domain maintenance during rhabdomere elongation. This role of  spastin  in apical domain modulation was further supported by  spastin's  gain-of-function phenotype. Spastin overexpression in photoreceptors caused the expansion of the apical membrane domain from apical to basolateral in the developing photoreceptor. Although the localizations of the apical domain and adherens junctions (AJs) were severely expanded, there were no defects in cell polarity.    Conclusions/Significance  These results strongly suggest that  spastin  is essential for apical domain biogenesis during rhabdomere elongation in  Drosophila  photoreceptor morphogenesis.

Role of Spastin in Apical Domain Control along the Rhabdomere Elongation in Drosophila Photoreceptor