The plant-derived triterpenoid, cucurbitacin B, but not cucurbitacin E, inhibits the developmental transition associated with ecdysone biosynthesis in Drosophila melanogaster

The plant-derived triterpenoid, cucurbitacin B, but not cucurbitacin E, inhibits the developmental transition associated with ecdysone biosynthesis in Drosophila melanogaster
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植物来源的三萜类化合物葫芦素 B(但葫芦素 E 不受影响)会抑制与黑腹果蝇蜕皮激素生物合成相关的发育转变

DOI:
10.1016/j.jinsphys.2021.104294
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发表时间:
2021
影响因子:
2.2
通讯作者:
Hajime Ono
Hajime Ono
中科院分区:
农林科学3区
文献类型:
--
作者:
Miwako Toyofuku;Daiki Fujinaga;Kazue Inaba;Tomoki Funahashi;Yuuta Fujikawa;Hideshi Inoue;Hiroshi Kataoka;Ryusuke Niwa;Hajime Ono

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在昆虫中,一些甾醇不仅对细胞膜的稳态是必需的,而且对类固醇激素蜕皮激素的生物合成也是必需的。昆虫的发育需要膳食固醇,因为昆虫不能重新合成固醇。因此,能与必需甾醇竞争的类甾醇化合物是昆虫生长调节剂的良好候选物。在本研究中,我们研究了植物源性三萜,葫芦素B和E (CucB和CucE)对果蝇发育的影响。为了减少食物中含有过量固醇的影响,我们饲养了dd。含或不含葫芦素的低固醇食物(LSF)对黑胃幼虫的影响。在LSF不添加或添加CucE的条件下饲养的幼虫大部分在第二或第三龄(L2或L3)死亡,而在cucb中饲养的幼虫大部分在没有蜕皮的情况下死亡。由CucB引起的发育停滞可以通过补充蜕皮激素部分恢复。此外,我们通过在L2/L3蜕皮后将含有胆固醇的LSF转移到含有CucB的LSF,研究了CucB对幼虫-前蛹转变的影响。用CucB在LSF上饲养的L3幼虫不能羽化,发育迟缓。补充蜕皮激素可改善发育迟缓,但不能改善蛹期缺陷。此外,我们还对家蚕(bombyx mori)的类固醇生成器官——前胸腺(PG)进行了添加或不添加葫芦素的培养。CucB能降低PG中蜕皮激素的产生,而CucE不能。这些结果表明,CucB不仅可以作为蜕皮激素受体的拮抗剂,而且还可以作为蜕皮激素生物合成的抑制剂。
In insects, some sterols are essential not only for cell membrane homeostasis, but for biosynthesis of the steroid hormone ecdysone. Dietary sterols are required for insect development because insects cannot synthesize sterolsde novo. Therefore, sterol-like compounds that can compete with essential sterols are good candidates for insect growth regulators. In this study, we investigated the effects of the plant-derived triterpenoids, cucurbitacin B and E (CucB and CucE) on the development of the fruit fly,Drosophila melanogaster. To reduce the effects of supply with an excess of sterols contained in food, we rearedD.melanogasterlarvae on low sterol food (LSF) with or without cucurbitacins. Most larvae raised on LSF without supplementation or with CucE died at the second or third larval instar (L2 or L3) stages, whereas CucB-administered larvae mostly died without molting. The developmental arrest caused by CucB was partially rescued by ecdysone supplementation. Furthermore, we examined the effects of CucB on larval-prepupal transition by transferring larvae from LSF supplemented with cholesterol to that with CucB just after the L2/L3 molt. L3 larvae raised on LSF with CucB failed to pupariate, with a remarkable developmental delay. Ecdysone supplementation rescued the developmental delay but did not rescue the pupariation defect. Furthermore, we cultured the steroidogenic organ, the prothoracic gland (PG) of the silkwormBombyx mori, with or without cucurbitacin. Ecdysone production in the PG was reduced by incubation with CucB, but not with CucE. These results suggest that CucB acts not only as an antagonist of the ecdysone receptor as previously reported, but also acts as an inhibitor of ecdysone biosynthesis.