رسالة جامعية
果蠅卵子生成中核膜蛋白與dysfusion交互作用的遺傳篩選 ; Genetic screen for nuclear membrane protein that interacts with dysfusion in Drosophila oogenesis
| العنوان: | 果蠅卵子生成中核膜蛋白與dysfusion交互作用的遺傳篩選 ; Genetic screen for nuclear membrane protein that interacts with dysfusion in Drosophila oogenesis |
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| المؤلفون: | 詹煜梃, Chan, Yu-Ting |
| المساهمون: | 生物科技與產業科學系, 張純純, Jang, Anna C.-C. |
| سنة النشر: | 2021 |
| المجموعة: | National Cheng Kung University: NCKU Institutional Repository / 國立成功大學機構典藏 |
| مصطلحات موضوعية: | 邊境細胞遷移, JAK/STAT訊號傳遞鏈, 核轉運, Drosophila Border cell migration, JAK/STAT signal pathway, dysfusion, Nuclear transport |
| الوصف: | 細胞遷移在個體胚胎發育的過程不可或缺，至今其分子機制仍未完全解析，本研究以黑腹果蠅(Drosophila melanogaster)卵子生成(oogenesis)中的邊境細胞(Border cells)作為研究模型，進行遺傳篩選找出群體細胞遷移相關基因。根據先前研究， JAK / STAT信號傳導途徑強弱決定邊境細胞的數目及遷移，任一傳遞分子發生突變皆導致邊境細胞數目下降及遷移缺陷;另一核蛋白Dysf基因突變時，邊境細胞群異常增加，而過度表現Dysf時不但使邊境細胞發生遷移缺陷、細胞群生成困難，也造成STAT入核比例下降，染色結果也發現，Dysf蛋白表現在核膜上，因為核孔複合物管控大分子物質進出細胞核，可能影響STAT進核，所以本論文主要解析dysf與核孔蛋白之間是否發生交互作用，進而影響JAK/STAT訊號傳導途徑？因此，本論文測試了24種核孔蛋白、9種核轉運蛋白(Impβ)以及2種Ran Binding蛋白共68個突變株，分析過度表現Dysf的前提下，這些突變株是否影響邊境細胞遷移。其中，核孔蛋白Nup153以及Nup98-96，顯著降低遷移失敗比例;而核轉運蛋白Artemis突變，則顯著提升遷移失敗比例，因此根據結果推論dysf可能透過與核孔蛋白Nup153、Nup98-96或轉運蛋白Artemis之間的交互作用，調節STAT的進核。 ; In embryogenesis, collective cell migration plays an important role but the molecular mechanism has not been fully elucidated. We apply 6~8 migratory cells called border cells that migrate as a group in Drosophila melanogaster oogenesis as a research model to investigate the underline mechanism of group cell migration. In my thesis, I took advantage of forward genetic screen to identify genes which are related with controlling the JAK / STAT signal pathway that is essential to determine the number border cells and persistent migration. Mutations in any JAK/STAT signaling molecule result in a decrease in the number of border cells and lead to migration defect. Gain-of-function in JAK/STAT signaling induces extra migrating border cells. Thus, the level of JAK/STAT signaling should be modulated properly to ensure the correct size of migration cohort. In our lab's previous investigation, a nuclear protein mutation, dysf, extra cluster of border cells were induced. Over-expression of dysf caused not only migration defects but also led to cluster failing to form, which was due to suppression of the nuclear import of STAT. The staining of andi-Dysf found it expression on the nuclear membrane so we hypothesized that Dysf may localize on the nuclear membrane and interact with the nuclear pore complex proteins to control the nucleocytoplasmic transport of nuclear protein to affect the nuclear localization of STAT. Therefore, the main object of this ... |
| نوع الوثيقة: | thesis |
| وصف الملف: | 142 bytes; text/html |
| اللغة: | Chinese |
| العلاقة: | http://ir.lib.ncku.edu.tw/handle/987654321/205076Test; http://ir.lib.ncku.edu.tw/bitstream/987654321/205076/1/index.htmlTest |
| الإتاحة: | http://ir.lib.ncku.edu.tw/handle/987654321/205076Test http://ir.lib.ncku.edu.tw/bitstream/987654321/205076/1/index.htmlTest |
| رقم الانضمام: | edsbas.3799549 |
| قاعدة البيانات: | BASE |
| الوصف غير متاح. |