JUVENILE HORMONE-III BIOSYNTHESIS - STOICHIOMETRIC INCORPORATION OF [2-C-14] ACETATE AND EFFECTS OF EXOGENOUS FARNESOL AND FARNESOIC ACID
JUVENILE HORMONE-III BIOSYNTHESIS - STOICHIOMETRIC INCORPORATION OF [2-C-14] ACETATE AND EFFECTS OF EXOGENOUS FARNESOL AND FARNESOIC ACID
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DOI：
10.1016/0020-1790(84)90043-x
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发表时间：
1984-01-01
期刊：
影响因子：
--
通讯作者：
TOBE, SS
中科院分区：
文献类型：
--
作者：
FEYEREISEN, R;RUEGG, RP;TOBE, SS
使用放射化学测定在体外研究了成年雌性蟑螂双翅目蟑螂的分离体对倍半萜保幼激素 III（JH-III、C16JH、甲基-10,11-环氧-3,7,11-三甲基-2E,6E-十二碳二烯酸酯）的从头生物合成。甲酯部分中的 L-[甲基-3H]甲硫氨酸的标记用于定量生物合成的 JH-III。当将阿拉塔体在缺乏乙酸盐但含有[1-14C]葡萄糖的培养基中孵育时，来自葡萄糖的C标记至倍半萜类化合物C链的30%。当腺体在缺乏葡萄糖但含有[2-14C]乙酸盐的培养基中孵育时，在保幼激素及其直接前体法尼索酸盐的生物合成中观察到标记乙酸盐的剂量依赖性利用，在化学计量处达到平台，即当每摩尔合成的JH-III掺入9摩尔乙酸盐时。这是将外源标记乙酸盐掺入类异戊二烯中而无需显着稀释的独特案例。利用外源性[2-14C]乙酸盐的化学计量掺入来测量金合欢醇和金合欢酸（JH-III 的 2 种倍半萜类前体）对通过该生物合成途径的 C 流的影响。两种化合物均刺激 JH-III 生物合成，并以剂量依赖性方式抑制 [2-14C] 乙酸盐掺入保幼激素和法尼索酸甲酯，从而几乎完全抑制从头 JH-III 生物合成。
De novo biosynthesis of the sesquiterpenoid juvenile hormone III (JH-III, C16JH, methyl-10,11-epoxy-3,7,11-trimethyl-2E,6E-dodecadienoate) by isolated corpora allata of the adult female cockroach Diploptera punctata was studied in vitro using a radiochemical assay. Labeling from L-[methyl-3H]methionine in the methyl ester moiety was used to quantify biosynthesized JH-III. When corpora allata were incubated in a medium lacking acetate but containing [1-14C]glucose, C from glucose labeled up to 30% of the sesquiterpenoid C chain. When the glands were incubated in a medium lacking glucose but containing [2-14C]acetate, dose-dependent utilization of labeled acetate was observed for the biosynthesis of juvenile hormone and its immediate precursor farnesoate, reaching a plateau at stoichiometry, i.e., when 9 mol of acetate were incorporated for each mole of JH-III synthesized. This is a unique case of incorporation of exogenous, labeled acetate into an isoprenoid without significant dilution. The stoichiometric incorporation of exogenous [2-14C]acetate was utilized to measure the influence of farnesol and farnesoic acid (2 sesquiterpenoid precursors of JH-III) on the C flow through this biosynthetic pathway. Both compounds stimulated JH-III biosynthesis and inhibited [2-14C]acetate incorporation into juvenile hormone and methyl farnesoate in a dose-dependent fashion, resulting in a nearly total suppression of de novo JH-III biosynthesis.