Steiner A M
Botanisches Institut der Universität Freiburg i. Br., Freiburg i. Br., Deutschland.
Planta. 1968 Sep;83(3):282-94. doi: 10.1007/BF00385338.
The effect of actinomycin D, hydroxyproline, cycloheximide, and chloramphenicol on the soluble sugar and cell-wall carbohydrate content was studied in an effort to look for the primary action of these antimetabolites on the cell-wall in connection with cell elongation during inhibition of endogenous hypocotyl growth in mustard seedlings (Sinapis alba L.). The experiments have been done under steady state conditions as far as the parameters under examination are concerned. During the experimental period hypocotyl elongation is due almost exclusively to cell elongation (GEISER, 1964). Antimetabolite concentrations in an 1 hr feeding period have been chosen to effect about 70% relative inhibition 12 hrs after feeding.All antimetabolites confermably caused hypocotyl inhibition already about 1 hr after the beginning of their application. Cycloheximide and chloramphenicol inhibited or impaired fructose and glucose accumulation 1-2 hrs, and cell-wall carbohydrate synthesis about 3 hrs after the onset of hypocotyl inhibition. In contrast, actinomycin D and hydroxyproline leave fructose and glucose accumulation unchanged up to 9 hrs, but they do inhibit cell-wall carbohydrate synthesis approximately as fast as they inhibit hypocotyl elongation. However, the relative inhibition of cell-wall carbohydrate synthesis is only 1/3 of the relative inhibition of hypocotyl elongation.A comparison of the lag-phases and the courses of the kinetics reveals that the changes in the soluble sugar and cell-wall carbohydrate content starting 3-4 hrs after antimetabolite application are only secondary changes not directly concerned with the primary processes leading to hypocotyl inhibition. From the far reaching independence of hypocotyl inhibition and cell-wall carbohydrate synthesis during the first hours after feeding, the conclusion can be drawn that in the case of cycloheximide and chloramphenicol the primary inhibition of hypocotyl elongation must be due to changes in the structural arrangement of cell-wall elements and not to any kind of inhibition of the synthesis of cell-wall carbohydrates. In the case of actinomycin D and hydroxyproline also at least the greatest part of the inhibition, if not all of it, must also be mediated by the same process. Though secondary changes observed in soluble sugar and cell-wall carbohydrate content point to rather different patterns of antimetabolite action, the primary action on the cell-wall in connection with cell growth inhibition, according to the present data, seems to be generally the same regardless of which inhibitor is used.
研究了放线菌素D、羟脯氨酸、环己酰亚胺和氯霉素对可溶性糖及细胞壁碳水化合物含量的影响，旨在探寻这些抗代谢物在芥菜幼苗（白芥）内源下胚轴生长受抑制期间，与细胞伸长相关的对细胞壁的主要作用。就所检测的参数而言，实验是在稳态条件下进行的。在实验期间，下胚轴伸长几乎完全归因于细胞伸长（盖泽尔，1964）。已选定在1小时投喂期内的抗代谢物浓度，以使投喂后12小时的相对抑制率达到约70%。所有抗代谢物在施用开始后约1小时即确实导致下胚轴受到抑制。环己酰亚胺和氯霉素在抑制下胚轴开始后1 - 2小时抑制或损害果糖和葡萄糖积累，约3小时后抑制细胞壁碳水化合物合成。相比之下，放线菌素D和羟脯氨酸在长达9小时内使果糖和葡萄糖积累保持不变，但它们抑制细胞壁碳水化合物合成的速度与抑制下胚轴伸长的速度大致相同。然而，细胞壁碳水化合物合成的相对抑制率仅为下胚轴伸长相对抑制率的1/3。对延迟期和动力学过程的比较表明抗代谢物施用3 - 4小时后开始的可溶性糖和细胞壁碳水化合物含量变化只是次要变化，与导致下胚轴抑制的主要过程并无直接关联。从投喂后最初几小时内下胚轴抑制与细胞壁碳水化合物合成的极大独立性可以得出结论，对于环己酰亚胺和氯霉素而言，下胚轴伸长的主要抑制必定归因于细胞壁成分结构排列的变化，而非对细胞壁碳水化合物合成的任何形式的抑制。对于放线菌素D和羟脯氨酸而言，至少其大部分抑制作用（如果不是全部的话）也必定由相同过程介导。尽管在可溶性糖和细胞壁碳水化合物含量中观察到的次要变化表明抗代谢物作用模式相当不同，但根据目前的数据，与细胞生长抑制相关的对细胞壁的主要作用，无论使用哪种抑制剂，似乎总体上是相同的。
