The Drosophila disembodied gene controls late embryonic morphogenesis and codes for a cytochrome P450 enzyme that regulates embryonic ecdysone levels.
The Drosophila disembodied gene controls late embryonic morphogenesis and codes for a cytochrome P450 enzyme that regulates embryonic ecdysone levels.
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发表时间：
2000-10
期刊：
影响因子：
4.6
通讯作者：
V. M. Chávez;G. Marqués;J. Delbecque;Koichi Kobayashi;M. Hollingsworth;J. Burr;J. Natzle;M. O’Connor
中科院分区：
文献类型：
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作者：
V. M. Chávez;G. Marqués;J. Delbecque;Koichi Kobayashi;M. Hollingsworth;J. Burr;J. Natzle;M. O’Connor
蜕皮激素在节肢动物发育过程中调节着多种细胞过程，但对参与这些激素生物合成的基因知之甚少。以往的研究表明，在果蝇和其他节肢动物中，20-羟基蜕皮激素的产生涉及一系列细胞色素P450催化的胆固醇羟基化。在这份报告中，我们表明，无实体（dib）基因座的果蝇编码的P450样序列。此外，我们发现dib突变胚胎具有非常低的蜕皮激素和20-羟基蜕皮激素（20 E）滴度，并且在胚胎的某些组织中不能表达IMP-E1和L1这两个20 E诱导基因。原位杂交研究表明，dib在早期胚胎中以复杂的模式表达，最终在环腺的前胸部分中被限制性表达。在幼虫和成虫组织中，分别在前胸腺和卵巢滤泡细胞中观察到dib表达，这两种组织已知合成蜕皮类固醇。表型分析表明，dib突变胚胎产生很少或没有角质层，并表现出严重的缺陷，在许多后期形态发生过程，如头部退化，背部关闭和肠道发育。此外，我们还研究了其他几种产生缺陷性胚胎细胞的突变体的表型。与dib一样，spook（spo）基因座的突变会导致胚胎蜕皮类固醇滴度较低、严重的晚期胚胎形态缺陷以及未能诱导IMP-E1。从这些数据中，我们得出结论，dib和spo可能编码蜕皮激素生物合成途径中的重要成分，蜕皮激素调节许多晚期胚胎形态发生过程，如细胞运动和角质层沉积。
Ecdysteroids regulate a wide variety of cellular processes during arthropod development, yet little is known about the genes involved in the biosynthesis of these hormones. Previous studies have suggested that production of 20-hydroxyecdysone in Drosophila and other arthropods involves a series of cytochrome P450 catalyzed hydroxylations of cholesterol. In this report, we show that the disembodied (dib) locus of Drosophila codes for a P450-like sequence. In addition, we find that dib mutant embryos have very low titers of ecdysone and 20-hydroxyecdysone (20E) and fail to express IMP-E1 and L1, two 20E-inducible genes, in certain tissues of the embryo. In situ hybridization studies reveal that dib is expressed in a complex pattern in the early embryo, which eventually gives way to restricted expression in the prothoracic portion of the ring gland. In larval and adult tissues, dib expression is observed in the prothoracic gland and follicle cells of the ovaries respectively, two tissues known to synthesize ecdysteroids. Phenotypic analysis reveals that dib mutant embryos produce little or no cuticle and exhibit severe defects in many late morphogenetic processes such as head involution, dorsal closure and gut development. In addition, we examined the phenotypes of several other mutants that produce defective embryonic cuticles. Like dib, mutations in the spook (spo) locus result in low embryonic ecdysteroid titers, severe late embryonic morphological defects, and a failure to induce IMP-E1. From these data, we conclude that dib and spo likely code for essential components in the ecdysone biosynthetic pathway and that ecdysteroids regulate many late embryonic morphogenetic processes such as cell movement and cuticle deposition.