Gene Molecular Function Mutant Phenotype DOWN- up PATTERN

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Gene Molecular Function Mutant Phenotype DOWN- up PATTERN

DOWN- UP PATTERN Supplementary Fig.3. Talylor et al Gene Molecular Function Mutant Phenotype Arrestin 1 Deactivation of rhodopsin-mediated signaling, disrupts the interaction of Rhodopsin Light-dependent eye degeneration with the G-protein, transducin Deactivation of rhodopsin-mediated signaling, disrupts the interaction of Rhodopsin Arrestin 2 Light-dependent eye degeneration with the G-protein, transducin inaD Deactivation of rhodopsin-mediated signaling Light-dependent eye degeneration inaF Deactivation of rhodopsin-mediated signaling Defect. LAVG Ca2+ channel function inaC Deactivation of rhodopsin-mediated signaling, Diacylglycerol-binding protein kinase C Defect. Rhodopsin-mediated signaling Gb 76C Deactivation of rhodopsin-mediated signaling, b-subunit of heterotrimeric G-protein GTPase Light-dependent eye degeneration (Transducin) Gg 30A Heterotrimeric G-protein GTPase involved in rhodopsin-mediated signaling Unknown 2+ trp Light-activated voltage-gated Ca channel Defect. Rhod-mediated signaling, eye degen. trp-like Light-activated voltage-gated Ca2+ channel Defect. Rhod-mediated signaling, eye degen. ninaE Long-wave sensitive opsin in R1-R6, mediates G-protein-coupled signaling Defect. Rhod-mediated signaling, rhabdomere degen. Rhodopsin 3 UV-sensitive opsin in R7-8, mediates G-protein-coupled signaling Defect. Rhod-mediated signaling Rhodopsin 4 UV-sensitive opsin in R7, mediates G-protein-coupled signaling Defect. Rhodopsin-mediated signaling Rhodopsin 5 Blue-sensitive in R8, mediates G-protein-coupled signaling Defect. Rhod-mediated signaling Rab-RP1 Rab-like GTPase involved in intracellular signaling Unknown oxidoreductase Short-chain dehydrogenase/reductase, implicated in repulsive axon guidance Unknown CG4979 Phosphatidylserine-specific phospholipase A1 Unknown chaoptic Extracellular membrane glycoprotein, mediates homophilic photoreceptor cell adhesion Rhabdomeres highly deranged ninaC Deactivation of rhodopsin-mediated signaling, calmodulin-binding serine/threonine Defect. Rhod-mediated signaling, kinase reduced Rhodopsin levels. msta Unknown, expressed in photoreceptor cells Unknown PIP82 Unknown, expressed in photoreceptor cells Unknown CG13077 Unknown Unknown CG1561 Unknown Unknown CG4468 Unknown Unknown.

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ADP-Ribosylation Factor, a Small GTP-Binding Protein, Is Required for Binding of the Coatomer Protein Fl-COP to Golgi Membranes JULIE G
Proc. Natl. Acad. Sci. USA Vol. 89, pp. 6408-6412, July 1992 Biochemistry ADP-ribosylation factor, a small GTP-binding protein, is required for binding of the coatomer protein fl-COP to Golgi membranes JULIE G. DONALDSON*, DAN CASSEL*t, RICHARD A. KAHN*, AND RICHARD D. KLAUSNER* *Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, and tLaboratory of Biological Chemistry, Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 Communicated by Marc Kirschner, April 20, 1992 (receivedfor review February 11, 1992) ABSTRACT The coatomer is a cytosolic protein complex localized to the Golgi complex, although their functions have that reversibly associates with Golgi membranes and is Impli- not been defined. Distinct among these proteins is the ADP- cated in modulating Golgi membrane transport. The associa- ribosylation factor (ARF), originally identified as a cofactor tion of 13-COP, a component of coatomer, with Golgi mem- required for in vitro cholera toxin-catalyzed ADP- branes is enhanced by guanosine 5'-[v-thioltriphosphate ribosylation of the a subunit of the trimeric GTP-binding (GTP[yS]), a nonhydrolyzable analogue of GTP, and by a protein G, (G,.) (19). ARF is an abundant cytosolic protein mixture of aluminum and fluoride ions (Al/F). Here we show that reversibly associates with Golgi membranes (20, 21). that the ADP-ribosylation factor (ARF) is required for the ARF has been shown to be present on Golgi coated vesicles binding of (-COP. Thus, 13-COP contained in a coatomer generated in the presence of GTP[yS], but it is not a com- fraction that has been resolved from ARF does not bind to Golgi ponent of the cytosolic coatomer (22).
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