INHIBITION OF STEROL BIOSYNTHESIS DURING ELICITOR-INDUCED ACCUMULATION OF FURANOCOUMARINS IN PARSLEY CELL-SUSPENSION CULTURES
INHIBITION OF STEROL BIOSYNTHESIS DURING ELICITOR-INDUCED ACCUMULATION OF FURANOCOUMARINS IN PARSLEY CELL-SUSPENSION CULTURES
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DOI：
10.1016/0031-9422(95)00434-9
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发表时间：
1995-11-01
期刊：
影响因子：
3.8
通讯作者：
HARTMANN, MA
中科院分区：
文献类型：
--
作者：
HAUDENSCHILD, C;HARTMANN, MA
添加来自 Phytophthora megasperma f 的细胞壁提取物。 sp。通过在短时间内添加示踪量的放射性乙酸钠进行实验，发现甘氨酸和欧芹细胞悬浮培养物会引发甾醇生物合成的快速且显着的抑制。在添加激发子后 7 小时，即就在培养基中呋喃香豆素积累之前，就检测到了这种抑制。它导致主要 Delta(5)-甾醇（24-甲基胆固醇、谷甾醇和豆甾醇）及其前体角鲨烯、4,4-二甲基-和 4-α-甲基-甾醇的放射性急剧下降。在经激发子处理的细胞中，大部分残余放射性被回收到4,4-二甲基甾醇库中，表明24-亚甲基环木菠萝醇的C-4去甲基化水平被阻断，生成环桉油烯醇。还发现添加激发子可引起香蜂草细胞甾醇谱的重要变化，包括 80 小时后豆甾醇与谷甾醇的比例增加 8 倍。对对照和激发子处理的细胞培养物的微粒体级分中角鲨烯合酶活性的测量清楚地表明，该酶活性响应激发子的添加而快速下降，这可能至少部分地导致了整个甾醇途径的抑制。
Addition of a cell wall extract from Phytophthora megasperma f. sp. glycinea to parsley cell suspension cultures was found to trigger a rapid and marked inhibition of sterol biosynthesis as demonstrated by feeding experiments with tracer amounts of radioactive sodium acetate over short periods of time. Such an inhibition was detected as soon as 7 hr after elicitor addition, i.e. just before the furanocoumarin accumulation in the culture medium. It resulted in a dramatic decrease in the radioactivity incorporated into the main Delta(5)-sterols (24-methylcholesterol, sitosterol and stigmasterol) as well as into their precursors, squalene, 4,4-dimethyl- and 4 alpha-methyl-sterols. In elicitor-treated cells, the bulk of the residual radioactivity was recovered into the 4,4-dimethylsterol pool, suggesting a block at the level of the C-4 demethylation of 24-methylenecycloartanol to give cycloeucalenol. The elicitor addition was also found to induce an important change in the sterol profile of parsely cells consisting of an 8-fold increase in the ratio of stigmasterol to sitosterol after 80 hr. Measurements of the squalene synthase activity in microsomal fractions from control and elicitor-treated cell cultures clearly showed a rapid decline of this enzyme activity in response to the elicitor addition, which might be responsible, at least in part, for the inhibition of the overall sterol pathway.