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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/83822完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 陳美如(Mei-Ru Chen) | |
| dc.contributor.author | Dan-fang Wei | en |
| dc.contributor.author | 魏丹芳 | zh_TW |
| dc.date.accessioned | 2023-03-19T21:19:24Z | - |
| dc.date.copyright | 2022-10-03 | |
| dc.date.issued | 2022 | |
| dc.date.submitted | 2022-07-28 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/83822 | - |
| dc.description.abstract | EB病毒（EBV）是人類第四型皰疹病毒，感染後會引起傳染性單核細胞增多癥，並與各種惡性腫瘤高度相關。EBV的生命周期分為潛伏期和溶裂期，分別具有不同的基因表現。病毒從潛伏期被激活後，病毒DNA聚合?輔助因子BMRF1會穩定DNA聚合?BALF5與DNA的結合，以促進EBV的DNA復製。此外，BMRF1作為一個轉錄調節因子，會激活幾個病毒溶裂期早期和晚期基因的表達。在我們以前的研究中，通過免疫沈澱法結合質譜分析，染色質重塑復合物NuRD的成員CHD4和RBBP4被確定與BMRF1間存在相互作用。本實驗中我們會進一步探討CHD4在EBV從潛伏期到溶裂期轉變中的調控作用。在此，我們發現利用shRNA降低CHD4的表基因現，減少了TW01-EBV和AGS-BX1細胞中EBV溶裂期蛋白質表現量。用shRNA抗性的CHD4（rCHD4）進行回補實驗，可以拯救Rta誘導的TW01-EBV中CHD4的表達水平。此外，熒光素?報導基因檢測實驗顯示，CHD4以ATP?活性依賴的方式促進了Rta介導的Zta啟動子的反式激活和Zta，Rta介導的BMRF1啟動子的反式激活。此外，CHD4以劑量依賴的方式影響Zta介導的BMRF1啟動子的轉活性。最後，Rta、Zta和BMRF1分別與CHD4免疫共沈澱。總之，這些結果表明，CHD4通過促進Zta和BMRF1的啟動子活性來支持EB病毒溶裂期的基因表現。其他NuRD成員是否參與在其中則需要進一步研究。 | zh_TW |
| dc.description.abstract | Epstein-Barr virus (EBV) is a gamma-herpesvirus that causes infectious mononucleosis and is highly associated with various malignancies. The life cycle of EBV is divided into latent and lytic stages with different gene expression profiles. Upon lytic reactivation, BMRF1, the viral DNA polymerase processivity factor, stabilizes the DNA binding ability of DNA polymerase BALF5 to facilitate EBV DNA replication. In addition, BMRF1 functions as a transcriptional regulator to activate the expression of several viral early and late genes. In our previous study, CHD4 and RBBP4, the components of the chromatin remodeling complex NuRD, were identified as BMRF1-interacting proteins by IP-mass spectrometry analysis. We are interested in further exploring the regulatory role of CHD4 in the EBV lytic cycle switch. Here we found knockdown of CHD4 reduced the lytic protein expression in both EBV-reactivated TW01-EBV and AGS-BX1cells. Complementation with shRNA-resistant form of CHD4 (rCHD4) rescue the expression level of CHD4 in Rta-induced TW01-EBV. Furthermore, luciferase reporter assays reveal that CHD4 contributes to Rta-mediated transactivation of Zta promoter and Zta- and Rta-mediated transactivation on BMRF1 promoter in an ATPase activity dependent manner. In addition, CHD4 affect Zta-mediated transactivation on BMRF1 in a dose-dependent manner. Moreover, Rta, Zta and BMRF1 are co-immunoprecipitated with CHD4 respectively. Taken together, the results suggest that CHD4 supports EBV lytic cycle by promoting the promoter activity of Zta and BMRF1. The role of other NuRD components in EBV lytic cycle needs further investigation. | en |
| dc.description.provenance | Made available in DSpace on 2023-03-19T21:19:24Z (GMT). No. of bitstreams: 1 U0001-2707202214042000.pdf: 11515078 bytes, checksum: 37b856223e726d3483096cc92e58602e (MD5) Previous issue date: 2022 | en |
| dc.description.tableofcontents | 致謝 2 中文摘要 3 ABSTRACT 4 1. Introduction 9 1.1. Epstein-Barr Virus 9 1.1.1. Latent stage 10 1.1.2. Lytic switch 10 1.1.3. Reactivation of EBV 11 1.1.4. EBV associated diseases 12 1.2. ATP-dependent chromatin remodeling 13 1.2.1. The CHD (Chromatin-Helicase-DNA binding) family 13 1.3. Nucleosome remodeling and deacetylase (NuRD) complex 14 1.3.1. CHD4/ NuRD 15 1.3.2. Herpesvirus and NuRD 15 1.4. Aims of this study 16 2. MATERIALS AND METHODS 18 2.1. Antibodies 18 2.2. Primers 18 2.3. Plasmids 19 2.4. Cell lines and induction into lytic cycle 21 2.5. Lentivirus shRNA knockdown 21 2.6. Lytic cycle induction 22 2.7. Cell transfection 22 2.8. Co-immunoprecipitation 23 2.9. Luciferase reporter assay 23 2.10. Preparation of whole cell extracts for western blot 24 2.11. SDS-PAGE and Western blot analysis 24 2.12. Intracellular EBV DNA extraction and quantitative real-time PCR (q-PCR) analysis 25 3. Results 27 3.1. shRNA-mediated knockdown of CHD4 affects EBV lytic replication in both TW01-EBV and AGS-BX1 cells 27 3.2. shRNA-mediated knockdown of CHD4 in Akata cells did not affect lytic protein expression after anti-human IgG treatment 28 3.3. Complementation of rCHD4 rescues EBV lytic replication in CHD4-KD TWO1-EBV cells 29 3.4. The role of CHD4 in Zta and Rta mediated transactivation on BMRF1 promoter 31 3.5. Zta, Rta and BMRF1 were co-immunoprecipitated with CHD4 in 293T cells respectively 34 4. Discussion 36 5. Figures 41 41 Figure 1. shRNA-mediated knockdown of CHD4 attenuates Rta transfection-mediated EBV reactivation and mildly affects EBV lytic replication in TSA-induced TW01-EBV cells. 41 Figure 2. shRNA-mediated knockdown of CHD4 significantly reduced EBV lytic replication in DFO and pSIN-Zta transduced but not in TSA treated AGS-BX1 cells. 43 Figure 3. shRNA-mediated knockdown of CHD4 does not affect anti-human IgG reactivated lytic gene expression in Akata cells. 45 Figure 4. The design of shRNA-resistant CHD4 and ATPase-dead CHD4. 46 Figure 5. Complementation of rCHD4 rescues EBV lytic replication in CHD4-KD TWO1-EBV cells. 48 Figure 6. The shRNA-mediated knockdown of CHD4 significantly reduces the transactivation activity of Rta on the Zta promoter. 49 Figure 7. shRNA-mediated knockdown of CHD4 did not significantly affect the transactivation activity of Rta on ZII element in reporter assay. 51 Figure 8. Transactivation activities of Rta and Zta on BMRF1 promoter showed different results in shCHD4 knockdown and rescue experiments. 53 Figure 9. The pattern of Zta and Rta co-transactivation on pBMRF1 is similar to that of Rta on pBMRF1. 55 Figure 10. shRNA-mediated knockdown of CHD4 significantly decreased the transactivation activities of Zta on Zta responsive elements and Rta on Rta responsive element of BMRF1 promoter. 57 Figure 11. Rta, Zta, and BMRF1 was co-immunoprecipitated with CHD4 respectively in transiently transfected 293T cells. 58 Figure 12. Rta was co-immunoprecipitated with CHD4 in 293T cells. 60 Figure 13. The hypothetic model for the regulation of CHD4 on pBMRF1 promoters. 61 Reference 62 | |
| dc.language.iso | en | |
| dc.title | 染色質重塑蛋白CHD4在EB病毒溶裂期的調控 | zh_TW |
| dc.title | The role of chromatin remodeler CHD4 in EBV lytic cycle | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 110-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 陳紀如(Chi-Ju Chen),張麗冠(Li-Kwan Chang),李建國(Chien-Kuo Li) | |
| dc.subject.keyword | EB病毒,染色質重塑,CHD4,Zta,BMRF1輔助聚合?因子, | zh_TW |
| dc.subject.keyword | EBV,chromatin remodeling,CHD4,Zta,BMRF1, | en |
| dc.relation.page | 66 | |
| dc.identifier.doi | 10.6342/NTU202201773 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2022-07-28 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| 顯示於系所單位： | 微生物學科所 | |
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