Light-regulated expression of the gsa gene encoding the chlorophyll biosynthetic enzyme glutamate 1-semialdehyde aminotransferase in carotenoid-deficient Chlamydomonas reinhardtii cells

• Published in: Plant molecular biology 1999-01, Vol.39 (2), p.289-297
• Main Authors: Herman, C.A, Im, C.S, Beale, S.I
• Format: Article
• Language: English
• Subjects: Animals; Carotenoids; Carotenoids - deficiency; Chlamydomonas reinhardtii; Chlamydomonas reinhardtii - enzymology; Chlamydomonas reinhardtii - radiation effects; Chlorophyll; Chlorophyll - biosynthesis; deficiency; Enzyme Inhibitors - pharmacology; Freshwater; gene expression; Gene Expression Regulation, Plant - radiation effects; genetic regulation; green light; Intramolecular Transferases - genetics; Light; messenger RNA; mutants; Onium Compounds - pharmacology; photoreceptors; phototaxis; Proteins; Signal transduction; structural genes; transaminases
• ISSN: 0167-4412; 1573-5028
• DOI: 10.1023/A:1006100822721

Expression of the Chlamydomonas reinhardtii gsa gene encoding the chlorophyll biosynthetic enzyme glutamate 1-semialdehyde aminotransferase was previously shown to be induced by blue light. Possible blue light photoreceptors include flavins and carotenoids. Light induction of gsa was investigated in carotenoid-deficient mutant C. reinhardtii cells. Strain CC-2682 cells are sensitive to light, produce only small amounts of chlorophyll, and do not exhibit phototaxis. Solvent extracts show the absence of carotenoids and carotenoid precursors beyond phytoene in dark-grown mutant cells. Although apparently devoid of carotenoids, the cells did show light induction of gsa. The gsa transcript level was very low in dark-grown cells but increased significantly after 2 h of exposure to dim (1.5 X 10(-5) mol m-2 s-1) green (480-585 nm) light. This light regime was previously determined not to injure these photosensitive cells and to fully induce gsa in wild-type cells. Exposure to this light did not cause the mutant cells to produce measurable carotenoids or to become phototactic. Growth of the mutant cells in the presence of exogenous beta-carotene or all-trans retinol restored phototaxis but did not affect the degree of gsa induction by light. The induction of gsa by light in the absence of carotenoids, and the fact that incorporation of physiologically usable carotenoids (as indicated by the restoration of phototaxis) did not affect the degree of light induction, indicate that the photoreceptor for light induction of gsa in C. reinhardtii is not a carotenoid. The flavin antagonist diphenyleneiodonium blocked light induction of gsa in both wild-type and mutant cells under conditions where respiration was not inhibited. These results suggest that the photoreceptor or a signal transduction effector for light induction of the C. reinhardtii gsa gene is a flavoprotein.