Institute for Photobiology of Cells, 02154, Waltham, MA, USA.
Planta. 1976 Jan;131(1):1-9. doi: 10.1007/BF00387337.
Levulinic acid, a competitive inhibitor of δ aminolevulinic acid dehydratase, cycloheximide, an inhibitor of translation on 89s cytoplasmic ribosomes, and chloramphenicol, an inhibitor of translation on 68s chloroplast ribosomes, are reversible inhibitors of light induced chlorophyll synthesis in resting Euglena gracilis Klebs. When dark grown resting cells are preilluminated for 2 h followed by darkness for 12 h prior to exposure to continuous light, the usual lag period in chlorophyll formation is eliminated. If cycloheximide, chloramphenicol, or levulinic acid are present during either the preillumination period or the subsequent dark period, the lag is reestablished. Only the very beginning of the dark period is sensitive to cycloheximide but the dark period is less sensitive to levulinic acid than is the light period. Exposure of preilluminated cells to cycloheximide or levulinic acid at the time of exposure to continuous illumination completely inhibits chlorophyll synthesis indicating that the potential for rapid chlorophyll synthesis generated by preillumination and a dark period does not result simply from the accumulation of porphyrin precursors. Preillumination has little effect on the development of the capacity to fix CO2 photosynthetically. These results indicate that the control of chlorophyll formation is more complex than in higher plants and a model based on the formation of certain crucial enzymes in the porphyrin pathway, rather than simply upon the accumulation of δ aminolevulinic acid is presented to explain the experimental findings.
乙酰丙酸,δ 氨基乙酰丙酸脱水酶的竞争性抑制剂,环己亚胺,89s 细胞质核糖体翻译的抑制剂,以及氯霉素,68s 叶绿体核糖体翻译的抑制剂,是光诱导休眠衣藻叶绿素合成的可逆抑制剂。当黑暗生长的休眠细胞在暴露于连续光之前先预照光 2 小时,然后黑暗 12 小时时,通常的叶绿素形成潜伏期被消除。如果环己亚胺、氯霉素或乙酰丙酸在预照光期间或随后的黑暗期间存在,则潜伏期重新建立。只有黑暗期的开始对环己亚胺敏感,但黑暗期对乙酰丙酸的敏感性低于光期。将预照光的细胞暴露于连续光照下的环己亚胺或乙酰丙酸完全抑制叶绿素合成,表明预照光和黑暗期产生的快速叶绿素合成的潜力并非仅仅来自卟啉前体的积累。预照光对光合作用固定 CO2 的能力的发展几乎没有影响。这些结果表明,叶绿素形成的控制比高等植物更为复杂,提出了一个基于卟啉途径中某些关键酶形成的模型,而不是简单地基于 δ 氨基乙酰丙酸的积累,以解释实验发现。