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Endophilin B is required for the Drosophila oocyte to endocytose yolk downstream of Oskar

  • Yi Cheng Tsai
  • , Wei Chiang
  • , Willisa Liou
  • , Wei Hao Lee
  • , Yu Wei Chang
  • , Pei Yu Wang
  • , Yi Chen Li
  • , Tsubasa Tanaka
  • , Akira Nakamura
  • , Li Mei Pai*
  • *此作品的通信作者

研究成果: 期刊稿件文章同行評審

7 引文 斯高帕斯(Scopus)

摘要

The nutritional environment is crucial for Drosophila oogenesis in terms of controlling hormonal conditions that regulate yolk production and the progress of vitellogenesis. Here, we discovered that Drosophila Endophilin B (D-EndoB), a member of the endophilin family, is required for yolk endocytosis as it regulates membrane dynamics in developing egg chambers. Loss of D-EndoB leads to yolk content reduction, similar to that seen in yolkless mutants, and also causes poor fecundity. In addition, mutant egg chambers exhibit an arrest at the previtellogenic stage. D-EndoB displayed a crescent localization at the oocyte posterior pole in an Oskar-dependent manner; however, it did not contribute to pole plasm assembly. D-EndoB was found to partially colocalize with Long Oskar and Yolkless at the endocytic membranes in ultrastructure analysis. Using an FM4-64 dye incorporation assay, D-EndoB was also found to promote endocytosis in the oocyte. When expressing the full-length D-endoBFL or D-endoBΔSH3 mutant transgenes in oocytes, the blockage of vitellogenesis and the defect in fecundity in D-endoB mutants was restored. By contrast, a truncated N-BAR domain of the D-EndoB only partially rescued these defects. Taken together, these results allow us to conclude that D-EndoB contributes to the endocytic activity downstream of Oskar by facilitating membrane dynamics through its N-BAR domain in the yolk uptake process, thereby leading to normal progression of vitellogenesis.

原文英語
頁(從 - 到)563-573
頁數11
期刊Development (Cambridge)
141
發行號3
DOIs
出版狀態已出版 - 01 2014

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