The endocytic pathway acts downstream of Oskar in Drosophila germ plasm assembly
The endocytic pathway acts downstream of Oskar in Drosophila germ plasm assembly
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DOI：
10.1242/dev.017293
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发表时间：
2008-03-15
期刊：
影响因子：
4.6
通讯作者：
Nakamura, Akira
中科院分区：
文献类型：
--
作者：
Tanaka, Tsubasa;Nakamura, Akira
细胞命运通常由细胞内rna和蛋白质的定位决定。在果蝇卵母细胞中，后极的oskar (osk) RNA定位和随后的osk合成指导了极质的组装，在那里，生殖系和腹部形成的因素积累。osk RNA产生长osk和短osk两种异构体，它们在极质组装中具有不同的功能。短Osk招募下游的极质成分，其锚定到后皮层需要长Osk。极质成分的锚定也需要肌动蛋白细胞骨架，而Osk促进了f -肌动蛋白在卵母细胞后细胞质中的长投射。然而，Osk介导f -肌动蛋白重组的机制尚不清楚。此外，尽管在免疫电镜下已知长Osk与核内体相关，但尚不清楚这种关联是否具有功能意义。本研究表明rabensyn -5 （Rbsn-5）是早期内噬途径所需的Rab5效应蛋白，对极质组装至关重要。rbsn-5（-）卵母细胞不能维持微管极性，这二级破坏了风险RNA定位。然而，先前错误表达的Osk，特别是长Osk，招募包括Rbsn-5在内的内体蛋白，并刺激内吞作用。在缺乏rbsn-5的卵母细胞中，异位的Osk诱导异常的f -肌动蛋白聚集，其与极质成分一起扩散到细胞质中。我们提出Osk刺激内体循环，这反过来促进f -肌动蛋白重组，将极质成分锚定在卵母细胞皮层。
Cell fate is often determined by the intracellular localization of RNAs and proteins. In Drosophila oocytes, oskar (osk) RNA localization and the subsequent Osk synthesis at the posterior pole direct the assembly of the pole plasm, where factors for the germline and abdomen formation accumulate. osk RNA produces two isoforms, long and short Osk, which have distinct functions in pole plasm assembly. Short Osk recruits downstream components of the pole plasm, whose anchoring to the posterior cortex requires long Osk. The anchoring of pole plasm components also requires actin cytoskeleton, and Osk promotes long F-actin projections in the oocyte posterior cytoplasm. However, the mechanism by which Osk mediates F-actin reorganization remains elusive. Furthermore, although long Osk is known to associate with endosomes under immuno-electron microscopy, it was not known whether this association is functionally significant. Here we show that Rabenosyn-5 (Rbsn-5), a Rab5 effector protein required for the early endocytic pathway, is crucial for pole plasm assembly. rbsn-5(-) oocytes fail to maintain microtubule polarity, which secondarily disrupts osk RNA localization. Nevertheless, anteriorly misexpressed Osk, particularly long Osk, recruits endosomal proteins, including Rbsn-5, and stimulates endocytosis. In oocytes lacking rbsn-5, the ectopic Osk induces aberrant F-actin aggregates, which diffuse into the cytoplasm along with pole plasm components. We propose that Osk stimulates endosomal cycling, which in turn promotes F-actin reorganization to anchor the pole plasm components to the oocyte cortex.