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Plant Physiology 56:313-317 (1975) © 1975 American Society of Plant Biologists Events Surrounding the Early Development of Euglena ChloroplastsV. Control of Paramylum Degradation 1a Department of Biology, Brandeis University, Waltham, Massachusetts 02154
The degradation of the storage carbohydrate, paramylum, is induced by light in wild-type Euglena gracilis Klebs var. bacillaris Pringsheim and in a mutant, W3BUL, which lacks detectable plastid DNA. Treatment of wild type with cycloheximide in the dark produces 60% as much paramylum breakdown as light, whereas treatment with levulinic acid in the dark yields a slightly greater response than light. Both cycloheximide and levulinic acid produce a greater paramylum breakdown in the light than they do in the dark. Treatment of W3BUL with levulinic acid in darkness produces a larger paramylum degradation than light, with values similar to wild type in the light. Treatment of W3BUL with cycloheximide induces paramylum degradation in darkness, and as with wild type, light is slightly stimulatory in the presence of both cycloheximide or levulinic acid. Streptomycin brings about only a very small amount of paramylum breakdown in the dark and only slightly inhibits breakdown in the light. Thus paramylum breakdown induced by light does not require the synthesis of proteins on cytoplasmic or plastid ribosomes. A model which explains these results postulates the existence of a protein which inhibits paramylum breakdown. When the synthesis of this protein is prevented either by light, cycloheximide, or by levulinic acid acting as a regulatory analog of delta amino levulinic acid, paramylum breakdown takes place. Because levulinic acid is a better inducer than light in W3BUL, W3BUL may not be able to form as much delta amino levulinic acid in light as wild type. The small amount of induction by streptomycin is viewed as a secondary regulatory effect attributable to interference with plastid protein synthesis which affects regulatory signals from the plastid to the rest of the cell.
2 Microbiology trainee of the National Institutes of Health, Grant Number GM1586. Portions of the material in this paper were taken from a dissertation submitted by S.D.S. to the Graduate Faculty of Brandeis University in partial fulfillment of the requirements for the Ph.D. degree. Present address: Biology Division, Oak Ridge National Laboratory, P.O. Box Y, Oak Ridge, Tenn. 37830. 3 Abraham and Etta Goodman Professor of Biology, to whom reprint requests should be sent. 1 This work was supported by Grant GM 14595 from the National Institutes of Health.
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