| Summary: | 碩士 === 國立成功大學 === 生物科技研究所碩博士班 === 101 === Cell migration is a critical process for animal development. In order to study the complicated process, we focus on a cluster of epithelial cells which are migratory in Drosophila oogenesis called border cells to screen for novel genes for further exploring basic mechanism in cell migration. Of these, dysfusion (dys), which encodes a basic helix-loop-helix (bHLH)-PAS domain transcription factor, was identified to cause nearly 90% of migration defects in border cells when dys was overexpressed. To analyze the function of dys, we generated mutant clones in polar cells and found nearly 64% of border cell cluster fail to migrate. In addition, the mutant clone in border cells also showed 100% defects in motility. The expression of Dys was shown at the nuclear membrane of germline and all follicle cells including border cells but the expression of Dys was reduced once border cells start to migrate, and it was undetectable when border cells reached the oocyte. Therefore Dys is required both in border cells and polar cells during migration. Interestingly, overexpression of UAS-dys in border cells not only severely impeded migration but also made 50% of border cells fail to form a cluster. To recruit neighboring follicle cells into the migratory cluster, polar cells secrete Upd to activate JAK/STAT signaling in adjacent follicle cells. Therefore graded morphogen, Upd, determines how many follicle cells are recruited, which is 4-8 in wild type border cell cluster. Overexpression of dys, the number of recruited follicle cells was reduced to 3.2. To further validate whether the reduced number of border cells in overexpression of dys is through suppression of JAK/STAT signaling, we analyzed the STAT activity by STAT-GFP. In wild type border cells, the intensity of GFP gradually increased during migration. Consistent our hypothesis, we observed nearly 30% reduction of the expression level in STAT-GFP while dys was overexpressed. Taken together, my thesis work demonstrates that the function of Dys in border cell migration might be involved in regulation of JAK/STAT signaling.
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