Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, Princeton, New Jersey, United States.
Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, Princeton, New Jersey, United States.
Dev Biol. 2014 Feb 15;386(2):408-18. doi: 10.1016/j.ydbio.2013.12.013. Epub 2013 Dec 27.
The border cells of Drosophila are a model system for coordinated cell migration. Ecdysone signaling has been shown to act as the timing signal to initiate the migration process. Here we find that mutations in phantom (phm), encoding an enzyme in the ecdysone biosynthesis pathway, block border cell migration when the entire follicular epithelium of an egg chamber is mutant, even when the associated germline cells (nurse cells and oocyte) are wild-type. Conversely, mutant germline cells survive and do not affect border cell migration, as long as the surrounding follicle cells are wild-type. Interestingly, even small patches of wild-type follicle cells in a mosaic epithelium are sufficient to allow the production of above-threshold levels of ecdysone to promote border cell migration. The same phenotype is observed with mutations in shade (shd), encoding the last enzyme in the pathway that converts ecdysone to the active 20-hydroxyecdysone. Administration of high 20-hydroxyecdysone titers in the medium can also rescue the border cell migration phenotype in cultured egg chambers with an entirely phm mutant follicular epithelium. These results indicate that in normal oogenesis, the follicle cell epithelium of each individual egg chamber must supply sufficient ecdysone precursors, leading ultimately to high enough levels of mature 20-hydroxyecdysone to the border cells to initiate their migration. Neither the germline, nor the neighboring egg chambers, nor the surrounding hemolymph appear to provide threshold amounts of 20-hydroxyecdysone to do so. This "egg chamber autonomous" ecdysone synthesis constitutes a useful way to regulate the individual maturation of the asynchronous egg chambers present in the Drosophila ovary.
果蝇的边缘细胞是协调细胞迁移的模型系统。蜕皮激素信号已被证明是作为启动迁移过程的定时信号。在这里，我们发现 phm（编码蜕皮激素生物合成途径中的一种酶）的突变，即使卵室的整个滤泡上皮都是突变体，也会阻止边缘细胞迁移，即使相关的生殖细胞（滋养细胞和卵母细胞）是野生型。相反，只要周围的滤泡细胞是野生型，突变的生殖细胞就会存活下来，并且不会影响边缘细胞的迁移。有趣的是，即使在马赛克上皮中只有一小部分野生型滤泡细胞，也足以产生超过阈值水平的蜕皮激素来促进边缘细胞迁移。在 shade（编码该途径将蜕皮激素转化为活性 20-羟基蜕皮激素的最后一种酶）的突变中也观察到相同的表型。在培养基中添加高浓度的 20-羟基蜕皮激素也可以挽救 phm 突变滤泡上皮的培养卵室中的边缘细胞迁移表型。这些结果表明，在正常的卵子发生中，每个卵室的滤泡细胞上皮必须提供足够的蜕皮激素前体，最终导致成熟的 20-羟基蜕皮激素水平足够高，以启动边缘细胞的迁移。生殖细胞、相邻的卵室或周围的血淋巴似乎都不能提供足够的 20-羟基蜕皮激素来实现这一点。这种“卵室自主”蜕皮激素合成构成了一种调节果蝇卵巢中存在的异步卵室个体成熟的有用方法。
