Max-Planck-Institut für Züchtungsforschung, D-5000, Köln 30, Federal Republic of Germany.
Planta. 1984 Jul;161(5):475-80. doi: 10.1007/BF00394581.
The biosynthesis of ethylene was examined in suspension-cultured cells of parsley (Petroselinum hortense) treated with an elicitor from cell walls of Phytophthora megasperma. Untreated cells contained 50 nmol g(-1) of the ethylene precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), and produced ethylene at a rate of about 0.5 nmol g(-1) h(-1). Within 2 h after addition of elicitor to the culture medium, the cells started to produce more ethylene and accumulated more ACC. Exogenously added ACC did not increase the rate of ethylene production in control or elicitor-treated cells, indicating that the enzyme converting ACC to ethylene was limiting in both cases. The first enzyme in ethylene biosynthesis, ACC synthase, was very rapidly and transiently induced by the elicitor treatment. Its activity increased more than tenfold within 60 min. Density labelling with (2)H2O showed that this increase was caused by the denovo synthesis of the enzyme protein. Cordycepin and actinomycin D did not affect the induction of ACC synthase, indicating that the synthesis of new mRNA was not required. The peak of ACC-synthase activity preceded the maximal phenylalanine ammonia-lyase (PAL) activity by several hours. Exogenously supplied ethylene or ACC did not induce PAL. However, aminoethoxyvinylglycine, an inhibitor of ACC synthase, suppressed the rise in ethylene production in elicitor-treated cells and partially inhibited the induction of PAL. Exogenously supplied ACC reversed this inhibition. It is concluded that induction of the ethylene biosynthetic pathway is a very early symptom of elicitor action. Although ethylene alone is not a sufficient signal for PAL induction, the enhanced activity of ACC synthase and the ethylene biosynthetic pathway may be important for the subsequent induction of PAL.
在经卵菌细胞壁激发子处理的欧芹（Petroselinum hortense）悬浮培养细胞中研究了乙烯的生物合成。未经处理的细胞含有 50 nmol g(-1) 的乙烯前体 1-氨基环丙烷-1-羧酸（ACC），并以约 0.5 nmol g(-1) h(-1)的速率产生乙烯。在将激发子添加到培养基中后 2 小时内，细胞开始产生更多的乙烯并积累更多的 ACC。在对照或激发子处理的细胞中外源添加 ACC 不会增加乙烯的产生速率，表明在这两种情况下，将 ACC 转化为乙烯的酶是有限的。乙烯生物合成的第一酶，ACC 合酶，被激发子处理非常迅速和短暂地诱导。其活性在 60 分钟内增加了十倍以上。用（2）H2O 进行密度标记表明，这种增加是由酶蛋白的从头合成引起的。cordycepin 和放线菌素 D 不影响 ACC 合酶的诱导，表明不需要新的 mRNA 合成。ACC 合酶活性的峰值早于苯丙氨酸氨解酶（PAL）活性的峰值几个小时。外源乙烯或 ACC 不能诱导 PAL。然而，ACC 合酶抑制剂氨基乙氧乙烯基甘氨酸抑制了激发子处理细胞中乙烯产生的增加，并部分抑制了 PAL 的诱导。外源供应的 ACC 逆转了这种抑制。因此，可以得出结论，诱导乙烯生物合成途径是激发子作用的一个非常早期的症状。尽管单独的乙烯不是 PAL 诱导的充分信号，但 ACC 合酶和乙烯生物合成途径的增强活性可能对随后 PAL 的诱导很重要。
