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Coupled Functions of CTCF in Transcription & Repair in Response to DNA Double-Strand Breaks
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.advisor | 이종수 | - |
| dc.contributor.author | 윤다미 | - |
| dc.date.accessioned | 2025-01-25T01:36:03Z | - |
| dc.date.available | 2025-01-25T01:36:03Z | - |
| dc.date.issued | 2023-08 | - |
| dc.identifier.other | 33009 | - |
| dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/24535 | - |
| dc.description | 학위논문(석사)--생명과학과,2023. 8 | - |
| dc.description.tableofcontents | Ⅰ. Introduction 1 <br>Ⅱ. Material and Methods 4 <br> 1. Cell culture 4 <br> 2. Plasmid construction and transfection 4 <br> 3. Live Laser micro-irradiation 4 <br> 4. Immunofluorescence 5 <br> 5. Immunoprecipitation 5 <br> 6. HR, canonical and alternative NHEJ, and single-strand annealing (SSA) DNA repair assays 5 <br>Ⅲ. Results 9 <br> 1. CTCF regulates NELF-E recruitment at DSB site 9 <br> 2. CTCF Promotes R-loop formation at DSB site via NELF-E recruitment 13 <br> 3. NELF-E regulates the recruitment of HR factors 19 <br> 4. NELF-E regulates HR in a CTCF dependent manner 27 <br>Ⅳ. Discussion 34 <br>Ⅴ. References 36 | - |
| dc.language.iso | kor | - |
| dc.publisher | The Graduate School, Ajou University | - |
| dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
| dc.title | Coupled Functions of CTCF in Transcription & Repair in Response to DNA Double-Strand Breaks | - |
| dc.type | Thesis | - |
| dc.contributor.affiliation | 아주대학교 대학원 | - |
| dc.contributor.department | 일반대학원 생명과학과 | - |
| dc.date.awarded | 2023-08 | - |
| dc.description.degree | Master | - |
| dc.identifier.localId | T000000033009 | - |
| dc.identifier.url | https://dcoll.ajou.ac.kr/dcollection/common/orgView/000000033009 | - |
| dc.subject.keyword | CTCF | - |
| dc.subject.keyword | DNA Double-Strand Breaks | - |
| dc.subject.keyword | DNA damage repair | - |
| dc.subject.keyword | NELF-E | - |
| dc.description.alternativeAbstract | A variety of factors are commonly or differentially involved in the repair of DNA damage depending on types of DNA insults. Among them, DNA double-strand breaks (DSBs) are the most severe lesions that, if left unrepaired, can lead to serious genome aberrations, potentially affecting cell survival. Two major DSB repair pathways include non-homologous end joining (NHEJ) and homologous recombination (HR). At the vicinity of DSBs occurring within transcriptional active regions of the genome, several HR proteins are preferentially recruited and DNA-RNA hybrid R loop structures are formed via the negative elongation factor NELF-dependent transient transcription suppression. Little is known about the mechanisms that ensure coupled transcription suppression and HR-mediated repair in response to DSBs. <br> In this study, I identified the multifunctional transcriptional factor CCCTC-binding factor (CTCF), which engages in the initial step in HR by recruiting the resection endonuclease CtIP, as a crucial factor that facilitates the rapid recruitment of NELF-E and its resultant R-loop formation via transcription suppression at DSBs. CTCF interacts with NELF-E. Depletion of CTCF attenuates DSB recruitment of NELF-E and resultantly impairs the DSB-induced transcriptional suppression and R-loop generation at DSBs. Either CTCF or NELF-E depletion impairs recruitment of several HR factors including BARD1, BRCA1, and RAD51, and heterochromatin protein1γ (HP1γ) at DSBs, thereby resulting in compromised DSB R-loop formation and HR. However, NELF-E depletion has little effects on the CTCF recruitment at DSB, suggesting that CTCF acts upstream of NELF-E and R-loop in the HR pathway. <br> Overall, my findings demonstrate that CTCF directs rapid and transient transcription suppression and HR-mediated repair of DSBs at transcriptionally active regions through establishing CTCF-NELF-HR factor axis. | - |
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- Graduate School of Ajou University > Department of Bioscience > 3. Theses(Master)
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