Recent studies in Drosophila melanogaster retina indicate that absorption of light causes the translocation of signaling molecules and actin from the photoreceptor's signaling membrane to the cytosol, but the underlying mechanisms are not fully understood. As ezrin-radixin-moesin (ERM) proteins are known to regulate actin–membrane interactions in a signal-dependent manner, we analyzed the role of Dmoesin, the unique D. melanogaster ERM, in response to light. We report that the illumination of dark-raised flies triggers the dissociation of Dmoesin from the light-sensitive transient receptor potential (TRP) and TRP-like channels, followed by the migration of Dmoesin from the membrane to the cytoplasm. Furthermore, we show that light-activated migration of Dmoesin results from the dephosphorylation of a conserved threonine in Dmoesin. The expression of a Dmoesin mutant form that impairs this phosphorylation inhibits Dmoesin movement and leads to light-induced retinal degeneration. Thus, our data strongly suggest that the light- and phosphorylation-dependent dynamic association of Dmoesin to membrane channels is involved in maintenance of the photoreceptor cells.
Light-regulated interaction of Dmoesin with TRP and TRPL channels is required for maintenance of photoreceptors
I. Chorna-Ornan and V. Tzarfaty contributed equally to this paper.
Abbreviations used in this paper: EBP50, ezrin binding phosphoprotein 50; ERM, ezrin-radixin-moesin; INAD, inactivation-no-afterpotential D; NIS, nonimmune serum; PDZ, PSD95/DlgA/ZO-1 homology; PIP2, phosphatidylinositol 4,5-bisphosphate; T559, threonine 559; TRP, transient receptor potential; TRPL, TRP-like; WT, wild-type.
Irit Chorna-Ornan, Vered Tzarfaty, Galit Ankri-Eliahoo, Tamar Joel-Almagor, Nina E. Meyer, Armin Huber, François Payre, Baruch Minke; Light-regulated interaction of Dmoesin with TRP and TRPL channels is required for maintenance of photoreceptors . J Cell Biol 10 October 2005; 171 (1): 143–152. doi: https://doi.org/10.1083/jcb.200503014
Download citation file:
Sign in
Client Account
Sign in via your Institution
Sign in via your InstitutionSuggested Content
Email alerts
Advertisement
Advertisement