Schwartzbach S D, Schiff J A, Goldstein N H
Department of Biology, Brandeis University, Waltham, Massachusetts 02154.
Plant Physiol. 1975 Aug;56(2):313-7. doi: 10.1104/pp.56.2.313.
The degradation of the storage carbohydrate, paramylum, is induced by light in wild-type Euglena gracilis Klebs var. bacillaris Pringsheim and in a mutant, W(3)BUL, 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 W(3)BUL with levulinic acid in darkness produces a larger paramylum degradation than light, with values similar to wild type in the light. Treatment of W(3)BUL 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 W(3)BUL, W(3)BUL 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.
在野生型纤细裸藻克莱布斯变种巴氏裸藻普林斯海姆以及缺乏可检测到的质体DNA的突变体W(3)BUL中，储存碳水化合物副淀粉的降解是由光诱导的。在黑暗中用环己酰亚胺处理野生型，副淀粉的分解量为光照下的60%，而在黑暗中用乙酰丙酸处理产生的反应比光照下略大。环己酰亚胺和乙酰丙酸在光照下比在黑暗中都能产生更大程度的副淀粉分解。在黑暗中用乙酰丙酸处理W(3)BUL产生的副淀粉降解比光照下更大，其值与野生型在光照下相似。在黑暗中用环己酰亚胺处理W(3)BUL可诱导副淀粉降解，与野生型一样，在同时存在环己酰亚胺或乙酰丙酸的情况下，光照有轻微的刺激作用。链霉素在黑暗中仅引起极少量的副淀粉分解，在光照下仅轻微抑制分解。因此，光诱导的副淀粉分解不需要在细胞质或质体核糖体上合成蛋白质。一个解释这些结果的模型假定存在一种抑制副淀粉分解的蛋白质。当这种蛋白质的合成被光、环己酰亚胺或作为δ-氨基乙酰丙酸调节类似物的乙酰丙酸阻止时，副淀粉就会发生分解。因为乙酰丙酸在W(3)BUL中比光更好地诱导分解，W(3)BUL在光照下可能无法像野生型那样形成那么多的δ-氨基乙酰丙酸。链霉素的少量诱导作用被视为一种次要的调节效应，归因于对质体蛋白质合成的干扰，这种干扰影响了从质体到细胞其他部分的调节信号。
