Identification of possible signal transduction components mediating light induction of the Gsa gene for an early chlorophyll biosynthetic step in Chlamydomonas reinhardtii.
Light-induced expression of the Gsa gene encoding the heme and chlorophyll biosynthetic enzyme glutamate 1-semialdehyde aminotransferase in Chlamydomonas reinhardtii was previously shown to involve Ca2+ and calmodulin (CaM) (C. lm et al. 1996, Plant Cell 8: 2245-2253). To further analyze the signal transduction pathway for light-induced Gsa expression, the effects of several pharmacological agents were examined. Treatment of light-dark synchronized cells with the heterotrimeric G-protein agonist Mas-7 caused partial induction of Gsa in the dark. The phospholipase C inhibitor U73122 inhibited light induction of Gsa. Exposure of cells to light caused a sustained 3-fold increase in cellular D-inositol 1,4,5-trisphosphate (InsP3) concentration. KN-93, a specific inhibitor of Ca2+/CaM-dependent protein kinase II, inhibited light induction of Gsa. In contrast, cyclosporin A, a specific inhibitor of the Ca2+/CaM-dependent phosphoprotein phosphatase calcineurin, did not affect light induction of Gsa. These results, together with the earlier results, suggest the involvement of a canonical signal transduction pathway for light-regulated Gsa expression that involves a heterotrimeric G-protein activation, phospholipase C-catalyzed InsP3 formation, InsP3-dependent Ca2+ release, and activation of a downstream signaling pathway through a Ca2+/CaM-dependent protein kinase.
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Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.
Beale
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D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D015152:Blotting, Northern; D020013:Calcium Signaling; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism; D002478:Cells, Cultured; D016825:Chlamydomonas reinhardtii / Q000235:genetics / Q000378:metabolism*; D002734:Chlorophyll / Q000096:biosynthesis*; D016572:Cyclosporine / Q000494:pharmacology; D003624:Darkness; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004963:Estrenes / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000378:metabolism; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D019751:Intramolecular Transferases / Q000235:genetics / Q000378:metabolism*; D008027:Light; D010455:Peptides / Q000378:metabolism / Q000494:pharmacology; D011760:Pyrrolidinones / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism; D000096926:Benzenesulfonamides
D001596:Benzylamines; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D002147:Calmodulin; D002734:Chlorophyll; D016572:Cyclosporine; D004791:Enzyme Inhibitors; D004963:Estrenes; D019204:GTP-Binding Proteins; D015544:Inositol 1,4,5-Trisphosphate; D036341:Intercellular Signaling Peptides and Proteins; D019751:Intramolecular Transferases; D010455:Peptides; D011760:Pyrrolidinones; D013449:Sulfonamides; D010738:Type C Phospholipases; C084070:Mas7 protein, synthetic; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; C072105:KN 93; D000096926:Benzenesulfonamides; C061049:glutamate-1-semialdehyde 2,1-aminomutase