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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/49566完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 潘俊良 | |
| dc.contributor.author | Kwei-Yan Liu | en |
| dc.contributor.author | 劉奎延 | zh_TW |
| dc.date.accessioned | 2021-06-15T11:35:06Z | - |
| dc.date.available | 2021-08-26 | |
| dc.date.copyright | 2016-08-26 | |
| dc.date.issued | 2016 | |
| dc.date.submitted | 2016-08-16 | |
| dc.identifier.citation | Arata, Y., Kouike, H., Zhang, Y., Herman, M.A., Okano, H., Sawa, H., 2006. Wnt signaling and a Hox protein cooperatively regulate psa-3/Meis to determine daughter cell fate after asymmetric cell division in C. elegans. Dev Cell 11, 105-115.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/49566 | - |
| dc.description.abstract | 不對稱細胞分裂可以增加細胞的多樣性，對擁有許多不同種類細胞的神經系統來說至關重要。Wnt-Frizzled 訊息路徑是調控不對稱細胞分裂的重要因子。在線蟲中，V5 側縫細胞系會產生，身體兩側各一個PVD痛覺神經細胞，而lin-17/Frizzled 突變造成PVD數目異常增加。我們的研究顯示，lin-17 和Wnt基因的突變導致V5.pa母細胞產生對稱而非不對稱的分裂，進而使神經膠質母細胞被轉化成神經母細胞。我們發現許多 Wnt 訊息傳遞路徑的基因都影響PVD的分化，而Wnt 訊號的分布方向能引導細胞不對稱分裂的極性。我們發現控制真皮細胞和神經膠細胞分化的C2H2轉錄因子LIN-26，其在神經膠母細胞中的表現量在lin-17突變株中明顯減少。利用RNA干擾技術，我們發現 lin-26和同屬於lin-26操縱子的另一類似基因lir-1在決定V5.pa細胞系性狀分化上的重要性，尤其lin-17突變的狀態下，失去lin-26或lir-1都會產生更多PVD神經細胞。除此之外，lin-17與mom-5/Frizzled同時突變時，側縫細胞大量消失且造成極度異常的PVD數目。這個結果表示Frizzled在調控不對稱細胞分裂中的重要性，並證明其透過影響lin-26/lir-1操縱子的表現而引導神經膠細胞與外皮層細胞的分化，以防止神經細胞異常的產生。 | zh_TW |
| dc.description.abstract | Wnt-Frizzled signaling is an important regulator of asymmetric cell division that increases cellular diversity. In the nematode Caenorhabditis elegans, mutations in lin-17/Frizzled resulted in supernumerary PVDs, one of the two postdeirid neurons generated by the V5 seam cell lineage. The asymmetric division of the V5.pa, which generated the neuroblast and the glioblast of the postdeirid, was often disrupted in the lin-17 and Wnt mutants. We identified multiple Wnt pathway genes that controlled PVD specification, and showed that Wnts instructed the asymmetry of cell division. Interestingly, expression of lin-26, a C2H2 transcription factor critical for hypodermal and glial cell specification, was significantly diminished in the postdeirid glial lineage of the lin-17 mutant. Reduced activity of lin-26 or lir-1, a lin-26-like gene encoded by the lir-1/lin-26 operon, resulted in supernumerary PVDs and enhanced lin-17 mutant phenotypes. Moreover, combining mutations of lin-17 and another Frizzled, mom-5, resulted in substantial loss of seam cells and extremely aberrant PVD numbers. These results support a model in which Frizzled couples asymmetric cell division to a switch in lin-26/lir-1 transcriptional activity to promote glial or epidermal fates against an otherwise differentiation program towards neurons. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T11:35:06Z (GMT). No. of bitstreams: 1 ntu-105-D98448010-1.pdf: 9639313 bytes, checksum: e6d52a7b7c48cef57c247a9311cbf7b7 (MD5) Previous issue date: 2016 | en |
| dc.description.tableofcontents | 口試委員會審定書 #
ACKNOWLEDGEMENT i IMPORTANT NOTICE iii 中文摘要 iv ABSTRACT v CONTENTS vi Chapter 1 INTRODUCTION 1 1.1 Asymmetric Cell Division 1 1.1.1 Asymmetric Cell Division Coupled with Cell Fate Determination 1 1.1.2 Asymmetric Cell Division in C. elegans 2 1.1.3 Asymmetric Cell Division in the Drosophila Nervous System 4 1.2 Wnt Signals in Asymmetric Cell Division and Cell Fate Determination 6 1.2.1 Overview of Wnt Signaling Pathways 6 1.2.2 Wnt Pathways in C. elegans 7 1.2.3 Wnt Signaling Regulates Asymmetric Cell Divisions in C. elegans 8 1.3 Cell Fate Diversification by Reiterative β-Catenin Asymmetry 11 Chapter 2 MATERIALS and METHODS 15 2.1 C. elegans Mutants and Transgenes 15 2.2 Quantification of PVD and PDE Neurons 16 2.3 Confocal Microscopy of the PVD Neuron 16 2.4 Temperature-Shift Experiments 17 2.5 Molecular Biology and Plasmid Construction 17 2.6 RNA Interference by Feeding 17 2.7 Imaging and Quantification of V5 Division and Expression of POP-1 or lin-26 18 2.8 Immunofluorescence Microscopy 19 2.9 RNA Isolation 19 2.10 Reverse Transcription 20 2.11 Quantitative Real-Time PCR（qRT-PCR） 20 2.12 Chromatin Immunoprecipitation 20 Chapter 3 RESULTS 21 3.1 Mutations in lin-17/Frizzled Caused PVD Duplication 21 3.2 Mutations in the Wnt/β-catenin Asymmetry Pathway Produced Extra PVD Neurons 22 3.3 Defects in Neuroblast Division Occurred at Multiple Levels of the V5 Lineage in the lin-17 Mutant 23 3.4 lin-17 Controls Cell Fate, Rather than Apoptosis, of V5.paapp 24 3.5 Wnt-Frizzled Signaling Regulates Asymmetric V5.pa and V5.paap Divisions 25 3.6 lin-17 was Expressed and Acted in the V5 lineage to Control Asymmetric Cell Divisions 26 3.7 Directional Wnt Signals are Required for Asymmetric Divisions of the V5 Lineage 26 3.8 Wnt-Frizzled Signaling Regulates Nuclear POP-1 Asymmetry between the Daughter Cells of V5.pa or V5.paap 27 3.9 Loss of lin-26 and lir-1 C2H2 Transcription Factors Resulted in Extra PVDs 27 3.10 Wnt-Frizzled Signaling Controls lir-1/lin-26 Expression 29 3.11 Extremely Aberrant Numbers of Postdeirid Neurons in the Double Frizzled Mutants Associated with Extensive Seam Cell Loss 30 Chapter 4 DISCUSSION 33 4.1 POP-1 Asymmetry and Cell Fate Specification 33 4.2 lin-26 and lir-1 Are Potential Targets of Wnt/ Frizzled Signaling 34 4.3 Concluding Remarks 36 Chapter 5 FIGURES 37 Chapter 6 SUPPLEMENTARY TABLE 93 Chapter 7 REFERENCE 95 | |
| dc.language.iso | en | |
| dc.subject | Wnt訊息 | zh_TW |
| dc.subject | 線蟲 | zh_TW |
| dc.subject | 不對稱細胞分裂 | zh_TW |
| dc.subject | 細胞分化 | zh_TW |
| dc.subject | 神經 | zh_TW |
| dc.subject | cell fate determination | en |
| dc.subject | Wnt signaling | en |
| dc.subject | neuron | en |
| dc.subject | C. elegant | en |
| dc.subject | asymmetric cell division | en |
| dc.title | 線蟲Wnt Signaling調控不對稱分裂與細胞分化 | zh_TW |
| dc.title | Regulation of Asymmetric Division and Cell Fate Determination by C. elegans Wnt-Frizzled Signaling | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 104-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 簡正鼎,皮海薇,吳益群,李秀香 | |
| dc.subject.keyword | 線蟲,不對稱細胞分裂,細胞分化,神經,Wnt訊息, | zh_TW |
| dc.subject.keyword | C. elegant,asymmetric cell division,cell fate determination,neuron,Wnt signaling, | en |
| dc.relation.page | 99 | |
| dc.identifier.doi | 10.6342/NTU201602876 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2016-08-17 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 分子醫學研究所 | zh_TW |
| 顯示於系所單位： | 分子醫學研究所 | |
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