subject:(DSB)

1. 川谷, 洋右; カワタニ, ヨウスケ. 抗体遺伝子のV領域におけるDNA二重鎖切断は抗体の親和性成熟に障害をもつGANP欠損マウスで低下している : コウタイ　イデンシ　ノ　V　リョウイキ　ニオケル　DNA　ニジュウサ　セツダン　ワ　コウタイ　ノ　シンワセイ　セイジュク　ニ　ショウガイ　オ　モツ　GANP　ケッソン　マウス　デ　テイカシテイル; Double-stranded DNA breaks in the igV region gene were detected at lower frequency in affinity-maturation impeded GANP-/-mice.

Degree: Kumamoto University / 熊本大学

URL: http://hdl.handle.net/2298/3112

Subjects/Keywords: DSB; AID

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

川谷, 洋右; カワタニ, �. (n.d.). 抗体遺伝子のV領域におけるDNA二重鎖切断は抗体の親和性成熟に障害をもつGANP欠損マウスで低下している : コウタイ　イデンシ　ノ　V　リョウイキ　ニオケル　DNA　ニジュウサ　セツダン　ワ　コウタイ　ノ　シンワセイ　セイジュク　ニ　ショウガイ　オ　モツ　GANP　ケッソン　マウス　デ　テイカシテイル; Double-stranded DNA breaks in the igV region gene were detected at lower frequency in affinity-maturation impeded GANP-/-mice. (Thesis). Kumamoto University / 熊本大学. Retrieved from http://hdl.handle.net/2298/3112

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

川谷, 洋右; カワタニ, ヨウスケ. “抗体遺伝子のV領域におけるDNA二重鎖切断は抗体の親和性成熟に障害をもつGANP欠損マウスで低下している : コウタイ　イデンシ　ノ　V　リョウイキ　ニオケル　DNA　ニジュウサ　セツダン　ワ　コウタイ　ノ　シンワセイ　セイジュク　ニ　ショウガイ　オ　モツ　GANP　ケッソン　マウス　デ　テイカシテイル; Double-stranded DNA breaks in the igV region gene were detected at lower frequency in affinity-maturation impeded GANP-/-mice.” Thesis, Kumamoto University / 熊本大学. Accessed April 11, 2021. http://hdl.handle.net/2298/3112.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

川谷, 洋右; カワタニ, ヨウスケ. “抗体遺伝子のV領域におけるDNA二重鎖切断は抗体の親和性成熟に障害をもつGANP欠損マウスで低下している : コウタイ　イデンシ　ノ　V　リョウイキ　ニオケル　DNA　ニジュウサ　セツダン　ワ　コウタイ　ノ　シンワセイ　セイジュク　ニ　ショウガイ　オ　モツ　GANP　ケッソン　マウス　デ　テイカシテイル; Double-stranded DNA breaks in the igV region gene were detected at lower frequency in affinity-maturation impeded GANP-/-mice.” Web. 11 Apr 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

川谷, 洋右; カワタニ �. 抗体遺伝子のV領域におけるDNA二重鎖切断は抗体の親和性成熟に障害をもつGANP欠損マウスで低下している : コウタイ　イデンシ　ノ　V　リョウイキ　ニオケル　DNA　ニジュウサ　セツダン　ワ　コウタイ　ノ　シンワセイ　セイジュク　ニ　ショウガイ　オ　モツ　GANP　ケッソン　マウス　デ　テイカシテイル; Double-stranded DNA breaks in the igV region gene were detected at lower frequency in affinity-maturation impeded GANP-/-mice. [Internet] [Thesis]. Kumamoto University / 熊本大学; [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2298/3112.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

川谷, 洋右; カワタニ �. 抗体遺伝子のV領域におけるDNA二重鎖切断は抗体の親和性成熟に障害をもつGANP欠損マウスで低下している : コウタイ　イデンシ　ノ　V　リョウイキ　ニオケル　DNA　ニジュウサ　セツダン　ワ　コウタイ　ノ　シンワセイ　セイジュク　ニ　ショウガイ　オ　モツ　GANP　ケッソン　マウス　デ　テイカシテイル; Double-stranded DNA breaks in the igV region gene were detected at lower frequency in affinity-maturation impeded GANP-/-mice. [Thesis]. Kumamoto University / 熊本大学; Available from: http://hdl.handle.net/2298/3112

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

2. giakoumakis, nickolaos nikiforos. Μελέτη μηχανισμών αντιγραφής και επιδιόρθωσης του γενετικοί υλικού με τεχνικές λειτουργικής μικροσκοπίας και χρήση αλγορίθμων επεξεργασίας-ανάλυσης εικόνας.

Degree: 2017, University of Patras; Πανεπιστήμιο Πατρών

URL: http://hdl.handle.net/10442/hedi/41177

► The spatiotemporal regulation of DNA replication is safeguarded via a process called licensing of DNA replication. In metazoan, a functionally conserved protein -Cdt1- is the… (more)

▼ The spatiotemporal regulation of DNA replication is safeguarded via a process called licensing of DNA replication. In metazoan, a functionally conserved protein -Cdt1- is the key factor that ensures the regulation of licensing and it is tightly regulated through various biological pathways. In case that the regulation of Cdt1 is disturbed, genomic instability, uncontrolled replication and apoptosis may occur.Genomic instability may also occur in an organism after DNA damage, either due to environmental factors, or due to random mutations occurring during metabolism. Evolution has provided cells with various DNA damage response mechanisms for specific kinds of damages. The cell cycle regulatory protein Cdt1 has been postulated to interlink cell cycle and DNA damage responses, therefore Cdt1 is a very interesting protein for further studying.Despite the fact that the exact role of Cdt1 at the sites of damage remains a puzzle, the current regulation model of Cdt1 is based on in vitro experiments in Xenopus egg extracts. This model postulates that upon DNA damage, PCNA is loaded onto chromatin and then Cdt1 associates with PCNA through its N-terminal PCNA interacting motif (PIP-box). Cdt1 then interacts with Cdt2 WD regions. Cdt2 is therefore recruited to the chromatin via direct interactions with Cdt1 and targets Cdt1 for ubiquitilation. At the first part of this study we aim to unravel the protein-protein interaction cascade regulating Cdt1 proteolysis after ultraviolet (UVC) induced DNA damage in human cancer cells by employing functional microscopy techniques. Initially once localised UVC radiation is inflicted upon cells, PCNA is recruited rapidly at the sites of damage and binds onto the chromatin robustly, serving as a scaffold for repairing complexes. In contrast with the current notion, Cdt2 is shown to be recruited at sites of damage independently from its substrates and maintains long-term interactions, regulating proteins that participate in the DNA damage response. It is recruited by direct interactions onto PCNA through a newly found C-terminal PiP box. Moreover, it is shown that binding of Cdt1 to sites of damage is stabilised by interactions with Cdt2. Lastly, ATR-dependent phosphorylation of Cdt2 inhibits stabilisation of Cdt1 onto damage chromatin, thereby fine-tuning Cdt1 regulation. On the second part of this study, we try to shed light on the exact role of Cdt1 at the sites of DNA damage and its implications in the choice of DNA damage repair pathways, in particular between Non-Homologous end Joining (NHEJ) and Homologous Recombination (HR). DNA double strand breaks (DSBs) were induced either with the use of X-ray irradiation or with a UVA pulsed laser (355nm) nanosurgery system in human breast (MCF7) and cervical (HeLa kyoto) cancer cells. The current study showed that the absence of Cdt1 enhances the recruitment kinetics of TLS polymerases (polκ and polη) onto PCNA and damaged sites. In addition, it is presented that the Cdt1 absence impairs the formation of 53BP1 and RIF1 irradiation induced foci…

Subjects/Keywords: Γενετικό Υλικό; Cdt1; DSB; FRAP; BRCA1; 53BP1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

giakoumakis, n. n. (2017). Μελέτη μηχανισμών αντιγραφής και επιδιόρθωσης του γενετικοί υλικού με τεχνικές λειτουργικής μικροσκοπίας και χρήση αλγορίθμων επεξεργασίας-ανάλυσης εικόνας. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/41177

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

giakoumakis, nickolaos nikiforos. “Μελέτη μηχανισμών αντιγραφής και επιδιόρθωσης του γενετικοί υλικού με τεχνικές λειτουργικής μικροσκοπίας και χρήση αλγορίθμων επεξεργασίας-ανάλυσης εικόνας.” 2017. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed April 11, 2021. http://hdl.handle.net/10442/hedi/41177.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

giakoumakis, nickolaos nikiforos. “Μελέτη μηχανισμών αντιγραφής και επιδιόρθωσης του γενετικοί υλικού με τεχνικές λειτουργικής μικροσκοπίας και χρήση αλγορίθμων επεξεργασίας-ανάλυσης εικόνας.” 2017. Web. 11 Apr 2021.

Vancouver:

giakoumakis nn. Μελέτη μηχανισμών αντιγραφής και επιδιόρθωσης του γενετικοί υλικού με τεχνικές λειτουργικής μικροσκοπίας και χρήση αλγορίθμων επεξεργασίας-ανάλυσης εικόνας. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2017. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10442/hedi/41177.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

giakoumakis nn. Μελέτη μηχανισμών αντιγραφής και επιδιόρθωσης του γενετικοί υλικού με τεχνικές λειτουργικής μικροσκοπίας και χρήση αλγορίθμων επεξεργασίας-ανάλυσης εικόνας. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2017. Available from: http://hdl.handle.net/10442/hedi/41177

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Edinburgh

3. Vasianovich, Yuliya. Investigating the roles of the Srs2 and Pif1 helicases in DNA double-strand break repair in Saccharomyces cerevisiae.

Degree: PhD, 2015, University of Edinburgh

URL: http://hdl.handle.net/1842/17984

► DNA double strand breaks (DSBs), which may occur during DNA replication or due to the action of genotoxic agents, are extremely dangerous DNA lesions as… (more)

▼ DNA double strand breaks (DSBs), which may occur during DNA replication or due to the action of genotoxic agents, are extremely dangerous DNA lesions as they can cause chromosomal rearrangements and cell death. Therefore, accurate DSB repair is vital for genome stability and cell survival. Two main mechanisms serve to repair DNA DSBs: non-homologous end joining, which re-ligates DNA ends together, and homologous recombination (HR), which restores broken DNA using homologous sequence as a template for repair. One-ended DSBs are a subject for the specialised HR-dependent repair pathway known as break-induced replication (BIR). At low frequency, DNA breaks can also be healed by telomerase, which normally extends telomeres at natural chromosome ends, but may also add de novo telomeres to DSBs due to their similarity to chromosome ends. De novo telomere addition is a deleterious event, which is effectively inhibited by the nuclear Pif1 (nPif1) helicase phosphorylated at the TLSSAES motif in response to DNA damage. In this study, it is reported that the same regulatory motif of nPif1 is also required for DSB repair via BIR. The requirement of the nPif1 TLSSAES sequence in BIR is dependent on the functional DNA damage response (DDR). Thus, nPif1 phosphorylation by the DDR machinery might mediate the role of nPif1 in BIR. In contrast, the nPif1 regulatory motif is not essential for BIR at telomeres in cells lacking telomerase. These observations indicate that the mechanism of nPif1 function in DSB repair via BIR and in BIR at telomeres might be different. In this work, a protocol for nPif1 pull-down was optimized to reveal the mechanism of the phosphorylation-dependent nPif1 functions in cells undergoing DNA repair, i. e. the mechanism of nPif1-mediated inhibition of de novo telomere addition and promoting DSB repair via BIR. In future, this protocol can be used to dissect the role of nPif1 in DNA repair through the identification of its potential interacting partners. The Srs2 helicase negatively regulates HR via dismantling Rad51 filaments. According to preliminary data from the laboratory of Sveta Makovets, Srs2 also promotes de novo telomere addition at DSBs in a Rad51-dependent manner. The work presented here establishes that Srs2 is dispensable for telomerase-mediated addition of TG1-3 repeats to DSBs. Instead, Srs2 is required for the reconstitution of the complementary DNA strand after telomerase action, thus ensuring the completion of de novo telomere addition. Overall, this study demonstrates that recombination-dependent DSB repair and de novo telomere addition share common regulatory components, i. e. the nPif1 helicase phosphorylated in response to DNA damage and the Srs2 helicase. Phosphorylated nPif1 promotes DSB repair via BIR in addition to its known role in inhibition of telomerase at DSBs, whereas Srs2 uses its well established ability to remove Rad51 from ssDNA to promote the restoration of dsDNA and thus to complete de novo telomere addition.

Subjects/Keywords: 572.8; DNA; DNA double-stranded breaks; DSB; DSB repair; homologous recombination; de novo telomere addition; break-induced replication

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vasianovich, Y. (2015). Investigating the roles of the Srs2 and Pif1 helicases in DNA double-strand break repair in Saccharomyces cerevisiae. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/17984

Chicago Manual of Style (16^th Edition):

Vasianovich, Yuliya. “Investigating the roles of the Srs2 and Pif1 helicases in DNA double-strand break repair in Saccharomyces cerevisiae.” 2015. Doctoral Dissertation, University of Edinburgh. Accessed April 11, 2021. http://hdl.handle.net/1842/17984.

MLA Handbook (7^th Edition):

Vasianovich, Yuliya. “Investigating the roles of the Srs2 and Pif1 helicases in DNA double-strand break repair in Saccharomyces cerevisiae.” 2015. Web. 11 Apr 2021.

Vancouver:

Vasianovich Y. Investigating the roles of the Srs2 and Pif1 helicases in DNA double-strand break repair in Saccharomyces cerevisiae. [Internet] [Doctoral dissertation]. University of Edinburgh; 2015. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1842/17984.

Council of Science Editors:

Vasianovich Y. Investigating the roles of the Srs2 and Pif1 helicases in DNA double-strand break repair in Saccharomyces cerevisiae. [Doctoral Dissertation]. University of Edinburgh; 2015. Available from: http://hdl.handle.net/1842/17984

Brno University of Technology

4. Vedra, Lukáš. Dekódování RDS zpráv obvodem FPGA: The RDS decoder on the FPGA.

Degree: 2019, Brno University of Technology

URL: http://hdl.handle.net/11012/31638

► This thesis deals with demodulation, decoding RDS messages and an FM receiver in FPGA. It is the processing of data after A/D conversion of radio… (more)

Subjects/Keywords: RDS; FPGA; DSB; Softwarové rádio; FM přijímač; číslicová filtrace; RDS; FPGA; DSB; software radio; FM receiver; digital filtering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vedra, L. (2019). Dekódování RDS zpráv obvodem FPGA: The RDS decoder on the FPGA. (Thesis). Brno University of Technology. Retrieved from http://hdl.handle.net/11012/31638

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Vedra, Lukáš. “Dekódování RDS zpráv obvodem FPGA: The RDS decoder on the FPGA.” 2019. Thesis, Brno University of Technology. Accessed April 11, 2021. http://hdl.handle.net/11012/31638.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Vedra, Lukáš. “Dekódování RDS zpráv obvodem FPGA: The RDS decoder on the FPGA.” 2019. Web. 11 Apr 2021.

Vancouver:

Vedra L. Dekódování RDS zpráv obvodem FPGA: The RDS decoder on the FPGA. [Internet] [Thesis]. Brno University of Technology; 2019. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/11012/31638.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Vedra L. Dekódování RDS zpráv obvodem FPGA: The RDS decoder on the FPGA. [Thesis]. Brno University of Technology; 2019. Available from: http://hdl.handle.net/11012/31638

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Irvine

5. Tat, Connie. Rad52 competes with Ku70/Ku86 for binding to switch region DSB ends to modulate immunoglobulin class switch DNA recombination.

Degree: Biomedical Sciences, 2015, University of California – Irvine

URL: http://www.escholarship.org/uc/item/03f400k9

► Class switch DNA recombination (CSR) diversifies the biological effector functions of antibodies and is critical for the maturation of the antibody response. This process is… (more)

Subjects/Keywords: Medicine; Microbiology; Immunology; CSR; DSB; HR; Ku70/Ku86; NHEJ; Rad52

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APA (6^th Edition):

Tat, C. (2015). Rad52 competes with Ku70/Ku86 for binding to switch region DSB ends to modulate immunoglobulin class switch DNA recombination. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/03f400k9

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tat, Connie. “Rad52 competes with Ku70/Ku86 for binding to switch region DSB ends to modulate immunoglobulin class switch DNA recombination.” 2015. Thesis, University of California – Irvine. Accessed April 11, 2021. http://www.escholarship.org/uc/item/03f400k9.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tat, Connie. “Rad52 competes with Ku70/Ku86 for binding to switch region DSB ends to modulate immunoglobulin class switch DNA recombination.” 2015. Web. 11 Apr 2021.

Vancouver:

Tat C. Rad52 competes with Ku70/Ku86 for binding to switch region DSB ends to modulate immunoglobulin class switch DNA recombination. [Internet] [Thesis]. University of California – Irvine; 2015. [cited 2021 Apr 11]. Available from: http://www.escholarship.org/uc/item/03f400k9.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tat C. Rad52 competes with Ku70/Ku86 for binding to switch region DSB ends to modulate immunoglobulin class switch DNA recombination. [Thesis]. University of California – Irvine; 2015. Available from: http://www.escholarship.org/uc/item/03f400k9

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas Medical Center

6. Chen, Haoyi. RMI1 is Essential for Early Embryonic Development and Attenuation of Tumor Development.

Degree: PhD, 2010, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/94

► RMI1 (BLM-Associated Protein 75 or Blap75) is highly conserved from yeast to human. Previous studies have shown that hRMI1 is required for BLM/TopoIIIα/RMI1 complex stability… (more)

Subjects/Keywords: RMI1; HR; DSB.; Molecular Genetics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chen, H. (2010). RMI1 is Essential for Early Embryonic Development and Attenuation of Tumor Development. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/94

Chicago Manual of Style (16^th Edition):

Chen, Haoyi. “RMI1 is Essential for Early Embryonic Development and Attenuation of Tumor Development.” 2010. Doctoral Dissertation, Texas Medical Center. Accessed April 11, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/94.

MLA Handbook (7^th Edition):

Chen, Haoyi. “RMI1 is Essential for Early Embryonic Development and Attenuation of Tumor Development.” 2010. Web. 11 Apr 2021.

Vancouver:

Chen H. RMI1 is Essential for Early Embryonic Development and Attenuation of Tumor Development. [Internet] [Doctoral dissertation]. Texas Medical Center; 2010. [cited 2021 Apr 11]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/94.

Council of Science Editors:

Chen H. RMI1 is Essential for Early Embryonic Development and Attenuation of Tumor Development. [Doctoral Dissertation]. Texas Medical Center; 2010. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/94

Wesleyan University

7. Zhang, Shu. Masking DNA Single-Strand Break (SSB): a New Approach to Cancer Treatment.

Degree: Chemistry, 2014, Wesleyan University

URL: https://wesscholar.wesleyan.edu/etd_mas_theses/78

► Certain types of cancer have defective repair mechanisms, which can cause the accumulation of damaged DNA. The persistent DNA damage can stall replication process… (more)

Subjects/Keywords: DNA damage; DNA damage repair; Synthetic Lethality; SSB; DSB

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APA (6^th Edition):

Zhang, S. (2014). Masking DNA Single-Strand Break (SSB): a New Approach to Cancer Treatment. (Masters Thesis). Wesleyan University. Retrieved from https://wesscholar.wesleyan.edu/etd_mas_theses/78

Chicago Manual of Style (16^th Edition):

Zhang, Shu. “Masking DNA Single-Strand Break (SSB): a New Approach to Cancer Treatment.” 2014. Masters Thesis, Wesleyan University. Accessed April 11, 2021. https://wesscholar.wesleyan.edu/etd_mas_theses/78.

MLA Handbook (7^th Edition):

Zhang, Shu. “Masking DNA Single-Strand Break (SSB): a New Approach to Cancer Treatment.” 2014. Web. 11 Apr 2021.

Vancouver:

Zhang S. Masking DNA Single-Strand Break (SSB): a New Approach to Cancer Treatment. [Internet] [Masters thesis]. Wesleyan University; 2014. [cited 2021 Apr 11]. Available from: https://wesscholar.wesleyan.edu/etd_mas_theses/78.

Council of Science Editors:

Zhang S. Masking DNA Single-Strand Break (SSB): a New Approach to Cancer Treatment. [Masters Thesis]. Wesleyan University; 2014. Available from: https://wesscholar.wesleyan.edu/etd_mas_theses/78

University of Toronto

8. Zak, Jan. Studies of DNA Double Strand Break Repair in Hypoxic S-phase Tumour Cells.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/71710

►

All solid tumours contain sub-regions of hypoxia. Increased hypoxia correlates with poor clinical prognosis. Two main DSB repair pathways are homologous recombination (HR) and non-homologous… (more)

Subjects/Keywords: cancer; dna; dsb; hypoxia; repair; s-phase; 0307

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APA (6^th Edition):

Zak, J. (2016). Studies of DNA Double Strand Break Repair in Hypoxic S-phase Tumour Cells. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/71710

Chicago Manual of Style (16^th Edition):

Zak, Jan. “Studies of DNA Double Strand Break Repair in Hypoxic S-phase Tumour Cells.” 2016. Masters Thesis, University of Toronto. Accessed April 11, 2021. http://hdl.handle.net/1807/71710.

MLA Handbook (7^th Edition):

Zak, Jan. “Studies of DNA Double Strand Break Repair in Hypoxic S-phase Tumour Cells.” 2016. Web. 11 Apr 2021.

Vancouver:

Zak J. Studies of DNA Double Strand Break Repair in Hypoxic S-phase Tumour Cells. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1807/71710.

Council of Science Editors:

Zak J. Studies of DNA Double Strand Break Repair in Hypoxic S-phase Tumour Cells. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/71710

University of Toronto

9. Wei, Chun Hua. Exploring the Role of HOP2 in the Double Strand Break Repair Pathway beyond Meiosis in Arabidopsis thaliana.

Degree: 2018, University of Toronto

URL: http://hdl.handle.net/1807/91476

►

The purpose of this study was to investigate the role of HOP2 protein in non-meiotic cells in Arabidopsis. HOP2 is known to be important to… (more)

Subjects/Keywords: Arabidopsis thaliana; DSB repair; Homologous Recombination; HOP2; Meiosis; Mitosis; 0369

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wei, C. H. (2018). Exploring the Role of HOP2 in the Double Strand Break Repair Pathway beyond Meiosis in Arabidopsis thaliana. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/91476

Chicago Manual of Style (16^th Edition):

Wei, Chun Hua. “Exploring the Role of HOP2 in the Double Strand Break Repair Pathway beyond Meiosis in Arabidopsis thaliana.” 2018. Masters Thesis, University of Toronto. Accessed April 11, 2021. http://hdl.handle.net/1807/91476.

MLA Handbook (7^th Edition):

Wei, Chun Hua. “Exploring the Role of HOP2 in the Double Strand Break Repair Pathway beyond Meiosis in Arabidopsis thaliana.” 2018. Web. 11 Apr 2021.

Vancouver:

Wei CH. Exploring the Role of HOP2 in the Double Strand Break Repair Pathway beyond Meiosis in Arabidopsis thaliana. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1807/91476.

Council of Science Editors:

Wei CH. Exploring the Role of HOP2 in the Double Strand Break Repair Pathway beyond Meiosis in Arabidopsis thaliana. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/91476

10. Layer, Jacob. POLD2 Promotes Chromosomal Rearrangements and Inaccurate End-Joining in Human Cells.

Degree: PhD, 2019, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41121277

►

Chromosomal translocations are recurrent genetic rearrangements with the potential to initiate carcinogenesis. While, the clinical etiology of chromosomal translocations is well established, the mechanisms responsible… (more)

Subjects/Keywords: DSB repair; Genome Editing

…translocation can be initiated by two simultaneous double strand breaks (DSB) on… …DSB repair joins the ends of heterologous chromosome fragments and a translocation is 2… …directed repair (HDR) (Ciccia & Elledge, 2010). C-NHEJ is the predominant DSB… …x28;Chiruvella, Liang, & Wilson, 2013). Following the formation of a DSB, the Ku70/86… …kinase and synapsis and stabilization of the DSB (Ciccia & Elledge, 2010). Accessory…

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Layer, J. (2019). POLD2 Promotes Chromosomal Rearrangements and Inaccurate End-Joining in Human Cells. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:41121277

Chicago Manual of Style (16^th Edition):

Layer, Jacob. “POLD2 Promotes Chromosomal Rearrangements and Inaccurate End-Joining in Human Cells.” 2019. Doctoral Dissertation, Harvard University. Accessed April 11, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:41121277.

MLA Handbook (7^th Edition):

Layer, Jacob. “POLD2 Promotes Chromosomal Rearrangements and Inaccurate End-Joining in Human Cells.” 2019. Web. 11 Apr 2021.

Vancouver:

Layer J. POLD2 Promotes Chromosomal Rearrangements and Inaccurate End-Joining in Human Cells. [Internet] [Doctoral dissertation]. Harvard University; 2019. [cited 2021 Apr 11]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41121277.

Council of Science Editors:

Layer J. POLD2 Promotes Chromosomal Rearrangements and Inaccurate End-Joining in Human Cells. [Doctoral Dissertation]. Harvard University; 2019. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41121277

11. So, Ayeong. RAD51 Protects Against RAD52-Dependent Non-Conservative Double-Strand Break Repair Processes, by Impeding the Annealing Step : RAD51 protège contre les processus de réparation des cassures double brin de l'ADN non-conservatifs dépendants de RAD52 en empêchant l'étape d'appariement.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2018, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2018SACLS171

►

Les cellules utilisent deux stratégies principales pour réparer les cassures double-brin (CDB) de l’ADN : la recombinaison homologue (RH) et la ligature d’extrémités non homologues… (more)

▼

Les cellules utilisent deux stratégies principales pour réparer les cassures double-brin (CDB) de l’ADN : la recombinaison homologue (RH) et la ligature d’extrémités non homologues (NHEJ). D’autres voies de réparation plus minoritaires existent qui mènent nécessairement à des altérations génétiques : Single Strand Annealing (SSA) et Alternative End Joining (A-EJ). Nous avons proposé que le choix entre les mécanismes de réparation des CDB nécessite deux étapes : 1) la compétition entre C-NHEJ et la résection, 2) sur les extrémités d’ADN résectées, la compétition entre RH, A-EJ et SSA. Ici, nous avons étudié la régulation de la deuxième étape de ce choix. En outre, la létalité synthétique a été décrite entre RAD52 et BRCA2/PALB2. Étant donné que BRCA2 et PALB2 sont nécessaires pour le chargement de RAD51 sur l’ADN simple brin, cela suggère que la formation d’un nucléofilament RAD51/ADNsb ordonné et RAD52 sont des acteurs essentiels dans le choix de la réparation à la deuxième étape. Nous avons trouvé que l’extinction de RAD51 ou BRCA2 stimule à la fois le SSA et EJ, d’une manière épistatique et que RAD52 contrôle la stimulation de SSA et A-EJ, en absence de RAD51. De plus, par séquençage haut débit, nous montrons que l’inhibition de RAD51 induit une instabilité génomique médiée par la microhomologie au niveau du génome. Cependant l’inhibition de RH n’est pas la réparation directe suffisante vers SSA et A-EJ. En effet, en utilisant des mutants dominants négatifs de RAD51, nous avons trouvé que les mutants du site de fixation/hydrolyse de l’ATP inhibent la RH et stimulent le SSA et que la chimère SMRAD51, qui inhibe la RH, inhibe également le SSA et EJ. Par TEM, nous avons observé que SMRAD51 perturbe spécifiquement la structure de l’ADNsb/SMRAD51. De l’autre côté, deux mutants d’hydrolyse de l’ATP de RAD51 ont montré que la liaison à l’ATP et l’hydrolyse d’ATP sont nécessaires pour une charge efficace de RAD51 sur l’ADN endommagé, dans les cellules vivantes. Ces deux mutants d’ATP ne se fixent pas à l’ADN en opposition à SMRAD51. Enfin, nous montrons que RAD51 n’empêche pas la résection étendue, mais que, in vitro, la protéine RAD51 empêche l’annealing de l’ADNsb complémentaire. Au total, les données montrent que RAD51 joue effectivement un rôle crucial dans la deuxième étape du choix de la voie de réparation des CDB à travers deux mécanismes distincts : 1- il déclenche la RH par son activité catalytique, 2- mail il empêche également les mécanismes non conservateurs dépendants de RAD52, SSA et A-EJ, en altérant l’étape de l’annealing. Par conséquent, le choix en deuxième étape entre la RH et les mécanismes mutagènes, SSA et A-EJ, est orchestré par un antagonisme entre RAD51 et RAD52.

Cells use two primary strategies to repair DNA double-strand break (DSB): Homologous Recombination (HR) and Non-homologous end joining (NHEJ). Beside other mechanisms exist that necessarily lead to genetic alterations: Single Strand Annealing (SSA) and Alternative End Joining (A-EJ). We have proposed that the choice between DSB repair…

Advisors/Committee Members: Guirouilh-Barbat, Josée (thesis director).

Subjects/Keywords: Réparation des CDBs; Rad51; Rad52; DSB repair; Rad51; Rad52

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

So, A. (2018). RAD51 Protects Against RAD52-Dependent Non-Conservative Double-Strand Break Repair Processes, by Impeding the Annealing Step : RAD51 protège contre les processus de réparation des cassures double brin de l'ADN non-conservatifs dépendants de RAD52 en empêchant l'étape d'appariement. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLS171

Chicago Manual of Style (16^th Edition):

So, Ayeong. “RAD51 Protects Against RAD52-Dependent Non-Conservative Double-Strand Break Repair Processes, by Impeding the Annealing Step : RAD51 protège contre les processus de réparation des cassures double brin de l'ADN non-conservatifs dépendants de RAD52 en empêchant l'étape d'appariement.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed April 11, 2021. http://www.theses.fr/2018SACLS171.

MLA Handbook (7^th Edition):

So, Ayeong. “RAD51 Protects Against RAD52-Dependent Non-Conservative Double-Strand Break Repair Processes, by Impeding the Annealing Step : RAD51 protège contre les processus de réparation des cassures double brin de l'ADN non-conservatifs dépendants de RAD52 en empêchant l'étape d'appariement.” 2018. Web. 11 Apr 2021.

Vancouver:

So A. RAD51 Protects Against RAD52-Dependent Non-Conservative Double-Strand Break Repair Processes, by Impeding the Annealing Step : RAD51 protège contre les processus de réparation des cassures double brin de l'ADN non-conservatifs dépendants de RAD52 en empêchant l'étape d'appariement. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Apr 11]. Available from: http://www.theses.fr/2018SACLS171.

Council of Science Editors:

So A. RAD51 Protects Against RAD52-Dependent Non-Conservative Double-Strand Break Repair Processes, by Impeding the Annealing Step : RAD51 protège contre les processus de réparation des cassures double brin de l'ADN non-conservatifs dépendants de RAD52 en empêchant l'étape d'appariement. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLS171

University of Gothenburg / Göteborgs Universitet

12. Zhang, Jingjing. Identification of novel BRCA2-binding proteins that are essential for meiotic homologous recombination.

Degree: 2021, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/67213

► Meiotic recombination is a molecular process in which the induction and repair of programmed DNA double-strand breaks (DSBs) creates genetic exchange between homologous chromosomes and… (more)

▼ Meiotic recombination is a molecular process in which the induction and repair of programmed DNA double-strand breaks (DSBs) creates genetic exchange between homologous chromosomes and thus increases genetic diversity and ensures chromosome segregation. Breast cancer susceptibility gene 2 (BRCA2) is a potent cancer suppressor and is required for DSB repair by homologous recombination (HR) in mitosis. However, due to the embryonic lethality of the Brca2 knockout (KO) mice, the role of BRCA2 in meiotic HR is less well defined. In our work, we have identified two novel meiosis-specific proteins, MEILB2 (meiotic localizer of BRCA2) and BRME1 (BRCA2 and MEILB2-associating protein 1) that form a ternary complex with BRCA2 and shed light on BRCA2 and its co-factors' roles during meiotic HR. In Meilb2 KO male mice, the localization of the recombinases RAD51 and DMC1, which catalyze the homology-directed repair of DSBs, is almost totally abolished, leading to errors in meiotic DSB repair and subsequent sterility. Moreover, MEILB2 binds directly to BRCA2 and is responsible for BRCA2 localization at the meiotic DSBs. BRME1 functions as a stabilizer of MEILB2 by binding to the α-helical N-terminus of MEILB2 and preventing MEILB2 self-association. In Brme1 KO mice, the BRCA2-MEILB2 complex is destabilized, leading to defects in DSB repair, homolog synapsis, and crossover formation. Persistent DSBs in Brme1 KO spermatocytes reactivate the somatic-like DNA-damage response (DDR), which repairs DSBs but cannot complement the crossover formation defects. Further, MEILB2-BRME1 is activated in many human cancers, and somatically expressed MEILB2-BRME1 impairs mitotic HR. Finally, we solved the crystal structure of the MEILB2-BRCA2 complex and showed that disruption of the MEILB2-BRCA2 interface compromises the recruitment of both MEILB2 and BRCA2 to recombination sites in mouse spermatocytes, thus demonstrating their inter-dependent localization mechanism in meiosis. Taken together, our results show that the meiotic BRCA2 complex plays a central role during meiotic HR, and its misregulation is implicated in human infertility, miscarriage, and cancer development.

Subjects/Keywords: meiosis; DSB; cancer; BRCA2; MEILB2; BRME1; HR; RAD51; DMC1; DDR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, J. (2021). Identification of novel BRCA2-binding proteins that are essential for meiotic homologous recombination. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/67213

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhang, Jingjing. “Identification of novel BRCA2-binding proteins that are essential for meiotic homologous recombination.” 2021. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed April 11, 2021. http://hdl.handle.net/2077/67213.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhang, Jingjing. “Identification of novel BRCA2-binding proteins that are essential for meiotic homologous recombination.” 2021. Web. 11 Apr 2021.

Vancouver:

Zhang J. Identification of novel BRCA2-binding proteins that are essential for meiotic homologous recombination. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2021. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2077/67213.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhang J. Identification of novel BRCA2-binding proteins that are essential for meiotic homologous recombination. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2021. Available from: http://hdl.handle.net/2077/67213

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

13. Maryna Aguilar Tannous. O papel da proteína SET no perfil de metilação do miR-9 e no reparo de DNA em células humanas de carcinoma espinocelular oral.

Degree: 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/60/60135/tde-27112014-092603/

► O início e a progressão do carcinoma espinocelular oral (CEO) são caracterizados pela aquisição de alterações genéticas e epigenéticas. A proteína SET é descrita como… (more)

▼ O início e a progressão do carcinoma espinocelular oral (CEO) são caracterizados pela aquisição de alterações genéticas e epigenéticas. A proteína SET é descrita como uma oncoproteína e, recentemente, o seu acúmulo foi mostrado em CEO. Diversas funções têm sido atribuídas à SET, tais como controle do ciclo celular, sobrevivência celular, migração celular, acetilação de histonas, e resposta ao estresse oxidativo. Este contexto sugere a SET como alvo terapêutico, mas primeiramente, é essencial entender a sua ação na tumorigênese e progressão em CEO. A hipótese central no presente estudo refere-se ao papel da SET na instabilidade genômica e reparo de DNA, bem como na regulação epigenética da expressão de miRNA, com impacto no desenvolvimento e progressão de CEO. O silenciamento estável de RNA foi realizado usando plasmídeo contendo short hairpin RNA contra SET (shSET) em linhagens de CEO in vitro (HN12 e Cal27) e in vivo (tumores xenoenxerto de HN12). Efeitos da redução da SET em CEO, in vitro e in vivo, foram avaliados no perfil de metilação (MSP, methylation specific PCR), expressão de miR-9 (qRT-PCR) e reparo de DNA (reparo mismatch e de quebra de fita dupla - DSB). A instabilidade genômica foi abordada por meio de cinco microssatélites (PCR convencional) para avaliar a instabilidade de microssatélites (MSI), e ensaio cometa para avaliar danos ao DNA (SSB, DSB, cross-link, etc.). O status de proteínas envolvidas em reparo de DSB (ATM, BRCA1 e MLH1) foi avaliado por imunofluorescência e Western blotting (WB). A resposta aos danos no DNA (DDR) induzidos por radioterapia (raios-X) foram analisados nas células HN12 por meio de ensaios clonogênico e de ciclo celular; proteínas associadas à apoptose, autofagia, ciclo celular e reparo foram avaliadas por WB. A redução da SET nas células HN12 modificou a transcrição dos loci codificantes do miR-9 por meio da reversão parcial de hipermetilação, tanto in vitro quanto in vivo, para o locus miR-9-1, e in vitro para o miR-9-3, com aumento nos níveis de miR-9 e miR-9*. A análise de 5 microssatélites mostrou alteração no perfil alélico de dois marcadores, D5S346 e D2S123, nas células HN12 shSET e nos tumores xenoenxerto da HN12 shSET (in vivo) em relação aos respectivos controles, o que sugere a presença de MSI e é um indício do papel da SET no reparo de DNA tipo mismatch. A linhagem HN12 shSET apresentou diminuição de danos no DNA e aumento das proteínas de reparo de DSB, MLH1, ATM, p-ATM e BRCA1 em relação a células HN12 shCTRL. Na DDR induzida por raios-X as células HN12 shSET apresentaram nas primeiras 48 horas uma menor perda de viabilidade (menor % em sub G0/G1), com parada em G2/M, maior nível de ATM ativa, aumento dos níveis de p21 e LC3B-II, além de menor clivagem de PARP e caspase-8 em relação as células HN12 shCTRL; isto sugere uma melhor resposta a danos de DSB e ativação de vias de sobrevivência nas células HN12 shSET. Entretanto, após 12 dias de radioterapia as células HN12 shSET mostraram uma tendência a menor sobrevivência. Portanto, os nossos resultados indicam o… Advisors/Committee Members: Andréia Machado Leopoldino, Maria Sol Brassesco Annichini, Luiz Carlos Conti de Freitas.

Subjects/Keywords: ATM; DDR; DSB; Metilação de miRNA; Reparo de DNA; SET/I2PP2A/TAF-IB; ATM; DDR; DNA repair; DSB; miRNA methylation; SET/I2PP2A/TAF-IB

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tannous, M. A. (2014). O papel da proteína SET no perfil de metilação do miR-9 e no reparo de DNA em células humanas de carcinoma espinocelular oral. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/60/60135/tde-27112014-092603/

Chicago Manual of Style (16^th Edition):

Tannous, Maryna Aguilar. “O papel da proteína SET no perfil de metilação do miR-9 e no reparo de DNA em células humanas de carcinoma espinocelular oral.” 2014. Masters Thesis, University of São Paulo. Accessed April 11, 2021. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-27112014-092603/.

MLA Handbook (7^th Edition):

Tannous, Maryna Aguilar. “O papel da proteína SET no perfil de metilação do miR-9 e no reparo de DNA em células humanas de carcinoma espinocelular oral.” 2014. Web. 11 Apr 2021.

Vancouver:

Tannous MA. O papel da proteína SET no perfil de metilação do miR-9 e no reparo de DNA em células humanas de carcinoma espinocelular oral. [Internet] [Masters thesis]. University of São Paulo; 2014. [cited 2021 Apr 11]. Available from: http://www.teses.usp.br/teses/disponiveis/60/60135/tde-27112014-092603/.

Council of Science Editors:

Tannous MA. O papel da proteína SET no perfil de metilação do miR-9 e no reparo de DNA em células humanas de carcinoma espinocelular oral. [Masters Thesis]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/60/60135/tde-27112014-092603/

14. Witter, Rute. Prevalência de Candidatus Mycoplasma haemobos e Ehrlichia sp. em bovinos leiteiros de agricultura familiar de Ji-Paraná, Rondônia.

Degree: 2016, Universidade Federal de Mato Grosso; Programa de Pós-Graduação em Ciências Veterinárias; UFMT CUC – Cuiabá; Brasil; Faculdade de Agronomia, Medicina Veterinária e Zootecnia (FAMEVZ)

URL: http://ri.ufmt.br/handle/1/1162

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Made available in DSpace on 2019-06-27T15:27:48Z (GMT). No. of bitstreams: 1 DISS_2016_Rute Witter.pdf: 2770927 bytes, checksum: 8c109288ae5ddd5f5d68fdad9ec26709 (MD5) Previous issue date: 2016-01-29

CAPES

A pecuária leiteira é diretamente influenciada pela presença de doenças no rebanho. Dessa forma, realizou-se a pesquisa de duas bactérias até então pouco estudadas em bovinos leiteiros no Brasil. Durante os meses de setembro de 2012 a novembro de 2013 foram coletadas 320 amostras de sangue e 320 amostras de soro de 64 propriedades do município de Ji-Paraná. Por meio da Reação em Cadeia pela Polimerase (PCR) para o gene 16S rRNA específico para ‘Ca. M. haemobos’ e uma heminested PCR para o gene dsb de Ehrlichia sp., determinou-se a prevalência destes dois agentes. A análise sorológica foi realizada por meio da Reação de Imunofluorescencia Indireta (RIFI), sendo utilizado a cepa Cuiabá 16 de Ehrlichia canis como antígeno. Presença de anticorpos foi observado em 178/320 (53,96%) bovinos, onde os títulos ficaram entre 40 a 5.120. Apenas 4 propriedades não tiveram pelo menos um bovino positivo. Na análise molecular, 15/320 (4,69%) bovinos estavam positivos para E. minasensis, e estas amostras formaram uma sequência (295 pares de bases - pb) que foi depositada no GenBank com número de acesso KT314243. Para ‘Ca. M. haemobos’, 207/320 (64,2%) bovinos se mostraram positivos, sendo que apenas 3 propriedades não tinham pelo menos um bovino positivo. Destas, sete amostras positivas foram selecionadas e sequenciadas, onde formaram duas sequências (460pb) com diferença em um nucleotídeo. Essas sequências foram depositadas no GenBank com números de acesso KT314241 e KT314242. Na análise do questionário a variável ‘Quantidade de fêmeas com mais de 24 meses’ se mostrou significativa para a infecção por ‘Ca. M. haemobos’ (p = 0,0372) e na presença de anticorpos para Ehrlichia sp. (p = 0,0103). Esses dados fornecem evidências de infecção natural de ambos os agentes para os bovinos da região. Implicações na saúde do rebanho foram discutidas

The dairy cattle is directly influenced by the presence of disease in the herd. Thus, we conducted a search of two bacteria hitherto little studied in dairy cattle in Brazil. During the months of September 2012 to November 2013 were collected 320 blood samples and 320 serum samples from 64 properties in the city of Ji-Paraná. Through the Polymerase Chain Reaction (PCR) for the specific 16S rRNA gene for ‘Ca. M. haemobos’ and a PCR heminested for dsb gene of Ehrlichia sp., we determined the prevalence of these two agents. Serologic analysis was performed by…

Advisors/Committee Members: Pacheco, Richard de Campos, Dutra, Valéria, Pacheco, Richard de Campos, Aguiar, Daniel Moura de, Watanabe, Michelle Igarashi, Santos, Thaís Rabelo dos.

Subjects/Keywords: CNPQ::CIENCIAS AGRARIAS::MEDICINA VETERINARIA; Agricultura familiar; Bovino; Erliquiose; Gene 16S rRNA; Gene dsb; Hemoplasma; Family farming; Cattle; Ehrlichiosis; 16S rRNA gene; Dsb gene; Hemoplasma

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Witter, R. (2016). Prevalência de Candidatus Mycoplasma haemobos e Ehrlichia sp. em bovinos leiteiros de agricultura familiar de Ji-Paraná, Rondônia. (Masters Thesis). Universidade Federal de Mato Grosso; Programa de Pós-Graduação em Ciências Veterinárias; UFMT CUC – Cuiabá; Brasil; Faculdade de Agronomia, Medicina Veterinária e Zootecnia (FAMEVZ). Retrieved from http://ri.ufmt.br/handle/1/1162

Chicago Manual of Style (16^th Edition):

Witter, Rute. “Prevalência de Candidatus Mycoplasma haemobos e Ehrlichia sp. em bovinos leiteiros de agricultura familiar de Ji-Paraná, Rondônia.” 2016. Masters Thesis, Universidade Federal de Mato Grosso; Programa de Pós-Graduação em Ciências Veterinárias; UFMT CUC – Cuiabá; Brasil; Faculdade de Agronomia, Medicina Veterinária e Zootecnia (FAMEVZ). Accessed April 11, 2021. http://ri.ufmt.br/handle/1/1162.

MLA Handbook (7^th Edition):

Witter, Rute. “Prevalência de Candidatus Mycoplasma haemobos e Ehrlichia sp. em bovinos leiteiros de agricultura familiar de Ji-Paraná, Rondônia.” 2016. Web. 11 Apr 2021.

Vancouver:

Witter R. Prevalência de Candidatus Mycoplasma haemobos e Ehrlichia sp. em bovinos leiteiros de agricultura familiar de Ji-Paraná, Rondônia. [Internet] [Masters thesis]. Universidade Federal de Mato Grosso; Programa de Pós-Graduação em Ciências Veterinárias; UFMT CUC – Cuiabá; Brasil; Faculdade de Agronomia, Medicina Veterinária e Zootecnia (FAMEVZ); 2016. [cited 2021 Apr 11]. Available from: http://ri.ufmt.br/handle/1/1162.

Council of Science Editors:

Witter R. Prevalência de Candidatus Mycoplasma haemobos e Ehrlichia sp. em bovinos leiteiros de agricultura familiar de Ji-Paraná, Rondônia. [Masters Thesis]. Universidade Federal de Mato Grosso; Programa de Pós-Graduação em Ciências Veterinárias; UFMT CUC – Cuiabá; Brasil; Faculdade de Agronomia, Medicina Veterinária e Zootecnia (FAMEVZ); 2016. Available from: http://ri.ufmt.br/handle/1/1162

Vanderbilt University

15. EPUM, ESTHER AKUNNA. Understanding the regulation of telomere healing in S. cerevisiae: a Rad51 perspective.

Degree: PhD, Biological Sciences, 2019, Vanderbilt University

URL: http://hdl.handle.net/1803/14152

► DNA double-strand breaks (DSBs) are toxic forms of DNA damage that must be repaired to maintain genome integrity. In addition to maintaining telomeres, telomerase can… (more)

▼ DNA double-strand breaks (DSBs) are toxic forms of DNA damage that must be repaired to maintain genome integrity. In addition to maintaining telomeres, telomerase can act on DSBs creating de novo telomeres, a mutagenic process associated with terminal deletions. We previously identified sequences in Saccharomyces cerevisiae (SIRTAs; Sites of Repair-associated Telomere Addition) that undergo unusually high frequencies of de novo telomere addition, even when the original chromosome break is several kilobases distal to the eventual site of telomerase action. Association of the telomere-binding protein Cdc13 with a SiRTA is required to stimulate de novo telomere addition. Here, my work shows that telomere addition is reduced significantly in the absence of RAD51 but not RAD52 at two SiRTAs. RAD52 deletion completely suppresses the telomere addition defect associated with RAD51 deletion, suggesting that Rad51 counteracts the inhibitory activity of Rad52. This work showed that a Rad51 mutant, impaired in nucleofilament formation and single-strand DNA binding, is nevertheless competent for telomere formation. In contrast, a Rad51 mutant, defective in interaction with Rad52, is deficient in telomere formation similar to a C-terminal truncation mutant of Rad52, impaired in its interaction with Rad51. Remarkably, Rad51 mutations decreasing telomere formation at SiRTAs also lead to an increase in Rad52-dependent microhomology-mediated repair(MHMR) internal to the SiRTA on chromosome IX. Finally, my work shows that a Rfa1 mutant, rfa1-44, reduced in its ability to interact with Rad52, also suppresses the telomere addition defect of RAD51 deletion. This work suggests that in the absence of Rad51, Rad52 interacts with RFA1 in a manner that inhibits telomere formation at SiRTAs and result in increased MHMR events. Advisors/Committee Members: Antonis Rokas (committee member), David Cortez (committee member), Todd Graham (committee member), Katherine Friedman (committee member), Brandt Eichman (Committee Chair).

Subjects/Keywords: Rad51 and Rad52 oppose; DNA damage; DSB repair; Cdc13 DNA repair; MHMR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

EPUM, E. A. (2019). Understanding the regulation of telomere healing in S. cerevisiae: a Rad51 perspective. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14152

Chicago Manual of Style (16^th Edition):

EPUM, ESTHER AKUNNA. “Understanding the regulation of telomere healing in S. cerevisiae: a Rad51 perspective.” 2019. Doctoral Dissertation, Vanderbilt University. Accessed April 11, 2021. http://hdl.handle.net/1803/14152.

MLA Handbook (7^th Edition):

EPUM, ESTHER AKUNNA. “Understanding the regulation of telomere healing in S. cerevisiae: a Rad51 perspective.” 2019. Web. 11 Apr 2021.

Vancouver:

EPUM EA. Understanding the regulation of telomere healing in S. cerevisiae: a Rad51 perspective. [Internet] [Doctoral dissertation]. Vanderbilt University; 2019. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1803/14152.

Council of Science Editors:

EPUM EA. Understanding the regulation of telomere healing in S. cerevisiae: a Rad51 perspective. [Doctoral Dissertation]. Vanderbilt University; 2019. Available from: http://hdl.handle.net/1803/14152

University of Toronto

16. Lee, Eva I-Hua. Distinctive Roles for FANCD2 and FANCJ in the Resection of Radiation-induced DNA Double-strand Breaks in Human Cells.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/72732

►

Fanconi anemia (FA) patients are hypersensitive to ionizing radiation and other agents that generate DNA double-strand breaks (DSBs). The major error-free DSB repair pathway in… (more)

Subjects/Keywords: DNA repair; Double strand breaks; DSB resection; FANCD2; FANCJ; Fanconi Anemia; 0369

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lee, E. I. (2016). Distinctive Roles for FANCD2 and FANCJ in the Resection of Radiation-induced DNA Double-strand Breaks in Human Cells. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/72732

Chicago Manual of Style (16^th Edition):

Lee, Eva I-Hua. “Distinctive Roles for FANCD2 and FANCJ in the Resection of Radiation-induced DNA Double-strand Breaks in Human Cells.” 2016. Masters Thesis, University of Toronto. Accessed April 11, 2021. http://hdl.handle.net/1807/72732.

MLA Handbook (7^th Edition):

Lee, Eva I-Hua. “Distinctive Roles for FANCD2 and FANCJ in the Resection of Radiation-induced DNA Double-strand Breaks in Human Cells.” 2016. Web. 11 Apr 2021.

Vancouver:

Lee EI. Distinctive Roles for FANCD2 and FANCJ in the Resection of Radiation-induced DNA Double-strand Breaks in Human Cells. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1807/72732.

Council of Science Editors:

Lee EI. Distinctive Roles for FANCD2 and FANCJ in the Resection of Radiation-induced DNA Double-strand Breaks in Human Cells. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/72732

Virginia Commonwealth University

17. Zhou, Tong. ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS.

Degree: MS, Pharmacology & Toxicology, 2012, Virginia Commonwealth University

URL: https://doi.org/10.25772/6KMG-K239 ; https://scholarscompass.vcu.edu/etd/2933

► DNA DSBs are most toxic to cells because they can lead to genomic rearrangements and even cell death. Most DSBs induced by ionizing radiation or… (more)

▼ DNA DSBs are most toxic to cells because they can lead to genomic rearrangements and even cell death. Most DSBs induced by ionizing radiation or radiomimetic drugs such as calicheamicin and bleomycin, bear 3′-phosphate or 3′- PG moieties that must be removed to allow subsequent gap filling and ligation. DSBs can be repaired by two main pathways: the homologous recombination (HR) pathway and the non-homologous end-joining (NHEJ) pathway, NHEJ is the primary repair pathway in mammalian cells. While HR repairs single strand breaks (SSBs) or DSBs accurately by using an undamaged copy of the sequence mostly at late S phase and G2 phase, the NHEJ pathway repairs DSBs without the requirement for sequence homology in a processing that may be error-free or error- prone and is most active at G1 phase. TDP1 is a DNA repair enzyme in both pathways, It associates with DNA SSB repair proteins XRCC1 and DNA ligase III and plays a role in processing of topoisomerase I- mediated SSBs. Our early results suggested that TDP1 also can remove protruding 3’- PG and other 3’ blocks from DSBs ends in vitro. A homozygous H493R mutation in the active site of TDP1 causes spinocerebellar ataxia with axonal neuropathy (SCAN1), a rare autosomal recessive genetic disease with neurological symptoms including peripheral neuropathy. DNA damage and misrepair can be determined by measuring the incidence of chromosomal aberrations such as rings, breaks, dicentrics, acentric fragments, and translocations in metaphase cells, and micronuclei in interphase cells. To assess the possible role of TDP1 in DSB repair in intact cells, the radiosensitivity of SCAN1 cells was determined by using a dose-fractionation method of irradiation. The data indicated that, when exposed to fractionated radiation doses, the SCAN1 cells were more sensitive than normal cells. Moreover, following treatment of cells with calicheamicin, SCAN1 cells showed a significantly higher incidence of dicentric chromosomes, acentric fragments, and micronuclei compared to normal cells, indicating that calicheamicin-induced DSBs were repaired less accurately and less efficiently, or more slowly in SCAN1 cells than in normal cells. All these results are consistent with a role for TDP1 in repair of 3’-PG DSBs in vivo. Oxidative stress is thought to induce replicative senescence and DNA damage in mouse embryo fibroblasts (MEFs). To determine the possible roles of oxidative stress on Tdp1-deficient MEFs, Tdp1-knockout MEFs and normal MEFs were cultured in 20% oxygen (atmospheric) and 3% (physiological) oxygen. The data from growth assays indicated that normal MEFs showed replicative senescence in 20% oxygen but not in 3% oxygen. Tdp1-knockout MEFs showed very poor growth compared to Tdp1 normal MEFs in both oxygen conditions, clearly suggesting an influence of repair of Tdp1 on oxidative stress induced DNA-DSBs in MEFs. Taken together, our results indicated that TDP1 is capable of removing protruding 3’-PG from DSB ends in intact cells. Moreover, DSBs induced by oxidative stress were repaired more… Advisors/Committee Members: Lawrence Povirk.

Subjects/Keywords: TDP1; SCAN1; NHEJ; DSB; IR; MEFs.; Medical Pharmacology; Medical Sciences; Medicine and Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhou, T. (2012). ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/6KMG-K239 ; https://scholarscompass.vcu.edu/etd/2933

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhou, Tong. “ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS.” 2012. Thesis, Virginia Commonwealth University. Accessed April 11, 2021. https://doi.org/10.25772/6KMG-K239 ; https://scholarscompass.vcu.edu/etd/2933.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhou, Tong. “ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS.” 2012. Web. 11 Apr 2021.

Vancouver:

Zhou T. ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS. [Internet] [Thesis]. Virginia Commonwealth University; 2012. [cited 2021 Apr 11]. Available from: https://doi.org/10.25772/6KMG-K239 ; https://scholarscompass.vcu.edu/etd/2933.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhou T. ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS. [Thesis]. Virginia Commonwealth University; 2012. Available from: https://doi.org/10.25772/6KMG-K239 ; https://scholarscompass.vcu.edu/etd/2933

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Benferhat, Karima. Etude structurale et fonctionnelle de complexes multi-protéiques impliqués dans la voie NHEJ humaine : Structural and Functional Study of Multi Protein Complexes Involved in Human non Homologous End Joining Pathway.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2018, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2018SACLS271

►

Chez les mammifères, la réparation des CDBs par la voie NHEJ (Non Homologous End Joining) implique plusieurs complexes multi-protéines : (i) de reconnaissance (ADN-Ku70/Ku80), (ii)… (more)

▼

Chez les mammifères, la réparation des CDBs par la voie NHEJ (Non Homologous End Joining) implique plusieurs complexes multi-protéines : (i) de reconnaissance (ADN-Ku70/Ku80), (ii) de maturation et (iii) de ligation comprenant XRCC4, XLF et ligase IV. Si les protéines impliquées dans le NHEJ sont connues, leurs propriétés structurales et fonctionnelles le sont moins. Au cours de ma thèse, j’ai combiné des approches biochimiques, de Microscopies Electronique et à Force Atomique, pour caractériser les propriétés de XRCC4, de XLF et leurs interactions avec le complexe de reconnaissance en particulier Ku. J’ai montré que la protéine complète XRCC4 est capable de polymériser et former des filaments alors qu’elle ne peut pas en faire en absence de la région C-terminale. Par Microscopies Electronique et à Force Atomique; nous avons montré que le filament XRCC4 forme une structure hélicoidale de chiralité gauche. XLF seule ne forme pas de filament mais peut être incorporé dans le filament XRCC4, ce que nous avons montré par immunomarquage. L’analyse d’images réalisé en collaboration et avec l’algorithme d’Edward Egelman (Université de Virginie-USA) a permis d’obtenir une reconstruction 3 D du filament XRCC4. Il est composé de 2 filaments enroulés l’un autour de l'autre avec un pas de 54 nm. Des Etudes sont en cours afin d’obtenir une structure 3D en CryoEM à haute résolution. L’étude des propriétés physicochimiques de l’assemblage du filament en fonction de la concentration, la température et le temps d’incubation a permis de montrer la dynamique du filament avec une stabilisation à basse température, et une concentration située entre 50 et 250 nM. L’ADN avec ou sans extrémités interagit avec les filaments. Cette interaction stabilise et promeut l’extension du filament. L’incorporation de XLF stabilise aussi le filament XRCC4. L’analyse des complexes formés entre l’ADN et XRCC4 ou XLF à l’état oligomérique montre des événements de pontage intra ou intermoléculaires. Parallèlement, nous avons étudié les propriétés de reconnaissance de l’ADN par l’hétérodimère Ku70/Ku80 et avons montré que le domaine KBM de XLF interagit avec Ku80 au sein de l’hétérodimère. En conclusion, nous montrons que le filament XRCC4 pourrait jouer un rôle d’architecture en maintenant les extrémités physiquement proches. Le recrutement de XLF dans le filament XRCC4 permettrait d’assembler le complexe de ligation avec le complexe de reconnaissance grâce aux interactions entre Ku et XLF.

In mammals, DSBs repair by the Non Homologous End Joining (NHEJ) pathway involves several multi-protein complexes : (i) the recognition complex (the Ku70 / Ku80 heterodimer), (ii) the maturation complex and (iii) the ligation complex comprising XRCC4, XLF, PAXX and ligase IV. If the proteins involved in NHEJ are identified and characterized, their structural and functional properties are often poorly understood. During my thesis I combined biochemical approaches, and molecular microscopies (Electron Microscopy and Atomic Force Microscopy), to characterize the…

Advisors/Committee Members: Le Cam, Eric (thesis director), Charbonnier, Jean-Baptiste (thesis director).

Subjects/Keywords: Réparation des CDBs d'ADN; NHEJ; Complexe de ligation; DSB repair; NHEJ; Ligation complex

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Benferhat, K. (2018). Etude structurale et fonctionnelle de complexes multi-protéiques impliqués dans la voie NHEJ humaine : Structural and Functional Study of Multi Protein Complexes Involved in Human non Homologous End Joining Pathway. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLS271

Chicago Manual of Style (16^th Edition):

Benferhat, Karima. “Etude structurale et fonctionnelle de complexes multi-protéiques impliqués dans la voie NHEJ humaine : Structural and Functional Study of Multi Protein Complexes Involved in Human non Homologous End Joining Pathway.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed April 11, 2021. http://www.theses.fr/2018SACLS271.

MLA Handbook (7^th Edition):

Benferhat, Karima. “Etude structurale et fonctionnelle de complexes multi-protéiques impliqués dans la voie NHEJ humaine : Structural and Functional Study of Multi Protein Complexes Involved in Human non Homologous End Joining Pathway.” 2018. Web. 11 Apr 2021.

Vancouver:

Benferhat K. Etude structurale et fonctionnelle de complexes multi-protéiques impliqués dans la voie NHEJ humaine : Structural and Functional Study of Multi Protein Complexes Involved in Human non Homologous End Joining Pathway. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Apr 11]. Available from: http://www.theses.fr/2018SACLS271.

Council of Science Editors:

Benferhat K. Etude structurale et fonctionnelle de complexes multi-protéiques impliqués dans la voie NHEJ humaine : Structural and Functional Study of Multi Protein Complexes Involved in Human non Homologous End Joining Pathway. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLS271

19. 민, 선우. The role of RSF1 in DNA damage signaling pathway and DSB-induced transcriptional regulation.

Degree: 2018, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/16567 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027270

► Chromatin remodeling factors are known as a key determinant of chromatin modification in DNA replication, transcription, and double strand break (DSB) repair. As a member… (more)

▼ Chromatin remodeling factors are known as a key determinant of chromatin modification in DNA replication, transcription, and double strand break (DSB) repair. As a member of imitation switch (ISWI) family in ATP-dependent chromatin remodeling factors, the remodeling and spacing factor (RSF) complex consists of two subunits, SNF2h ATPase and RSF1. Recent studies suggest that the function of chromatin remodeling factor is to temporally regulate the chromatin modification in the crosstalk between DSB signaling pathway and transcriptional regulation for the efficient DSB repair. Although it has been reported that SNF2h ATPase is recruited to DSB sites in poly(ADP-ribosyl) polymerase 1 (PARP1)-dependent manner, the function of RSF1 is still elusive. Here various cellular analyses confirmed that RSF1 is recruited and accumulated at DSBs in ATM-dependent manner, and the putative pSQ motifs of RSF1 by ATM are required for its accumulation at DSBs. In addition, depletion of RSF1 attenuates the activation of DNA damage checkpoint signals upon DNA damage. This defect is rescued by Trichostatin (TSA) treatment via chromatin relaxation. Thus, chromatin relaxation by RSF1 as chromatin remodeling factor is required for the propagation of ɣH2AX signaling pathway. As a result, RSF1 promotes homologous recombination repair (HRR) by recruiting HR factors. Although RSF1 propagates ɣH2AX signal pathway for the efficient repair as one of chromatin remodeling factors, the function of RSF1 in crosstalk between transcription and DDR is still elusive. Here inducible transcription system at DSB sites showed that RSF1 promotes DSB-induced transcriptional silencing, while SNF2h is dispensable for transcriptional silencing at DSB sites. The major determinant of DSB-induced transcriptional silencing, ATM signaling, is also impaired in RSF1 depleted cells. To determine the molecular mechanism of DSB-induced transcriptional silencing regulated by RSF1, the proteins in RSF1 mass spectrometry were screened by microirradiation. On the basis of the screening results from mass spectrometry analysis, the recruitment of transcriptional repressors at DSB sites in RSF1-dependent manner promotes DSB-induced transcriptional silencing. In addition, RSF1 interacts with polycomb repressive complex (PRC) at transcriptionally active site, and Swi3, Ada2, N-Cor, and TFIIIB (SANT) domain of enhancer of zeste homolog 2 (EZH2) is required for its recruitment and its interaction with RSF1. The impaired recruitment of EZH2 at DSB sites also leads to the defects in recruitment of RING1B and its substrate, H2AK119 ubiquitination at DSB sites. In addition, the defect in deacetylation of H2AK118 at DSB sites by HDAC1 in RSF1 depleted cells reduces the level of H2AK119 ubiquitination at DSB sites and eventually leads to the failure in DSB-induced transcriptional silencing. Finally, transcriptome analysis by RNA-sequencing reveals that transcriptome in cells upon DNA damage is changed in RSF1 depleted cells, and as a result, in RSF1 depleted cells, cell death is remarkably… Advisors/Committee Members: 대학원 의생명과학과, 201124445, 민, 선우.

Subjects/Keywords: DNA damage response; DNA repair; Chromatin remodeling factor; DSB-induced transcriptional silencing

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

민, �. (2018). The role of RSF1 in DNA damage signaling pathway and DSB-induced transcriptional regulation. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/16567 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027270

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

민, 선우. “The role of RSF1 in DNA damage signaling pathway and DSB-induced transcriptional regulation.” 2018. Thesis, Ajou University. Accessed April 11, 2021. http://repository.ajou.ac.kr/handle/201003/16567 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027270.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

민, 선우. “The role of RSF1 in DNA damage signaling pathway and DSB-induced transcriptional regulation.” 2018. Web. 11 Apr 2021.

Vancouver:

민 �. The role of RSF1 in DNA damage signaling pathway and DSB-induced transcriptional regulation. [Internet] [Thesis]. Ajou University; 2018. [cited 2021 Apr 11]. Available from: http://repository.ajou.ac.kr/handle/201003/16567 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027270.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

민 �. The role of RSF1 in DNA damage signaling pathway and DSB-induced transcriptional regulation. [Thesis]. Ajou University; 2018. Available from: http://repository.ajou.ac.kr/handle/201003/16567 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027270

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. 張, 添翼. メダカの培養細胞を用いたp53遺伝子の機能解析(要旨).

Degree: 修士(生命科学), 2017, The University of Tokyo / 東京大学

URL: http://hdl.handle.net/2261/52291

Subjects/Keywords: メダカ; p53; アポトーシス; DSB修復

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

張, �. (2017). メダカの培養細胞を用いたp53遺伝子の機能解析(要旨). (Thesis). The University of Tokyo / 東京大学. Retrieved from http://hdl.handle.net/2261/52291

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

張, 添翼. “メダカの培養細胞を用いたp53遺伝子の機能解析(要旨).” 2017. Thesis, The University of Tokyo / 東京大学. Accessed April 11, 2021. http://hdl.handle.net/2261/52291.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

張, 添翼. “メダカの培養細胞を用いたp53遺伝子の機能解析(要旨).” 2017. Web. 11 Apr 2021.

Vancouver:

張 �. メダカの培養細胞を用いたp53遺伝子の機能解析(要旨). [Internet] [Thesis]. The University of Tokyo / 東京大学; 2017. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2261/52291.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

張 �. メダカの培養細胞を用いたp53遺伝子の機能解析(要旨). [Thesis]. The University of Tokyo / 東京大学; 2017. Available from: http://hdl.handle.net/2261/52291

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

21. Diaz, Patrick Loyola. Genetic strategies to manipulate meiotic recombination in Arabidopsis thaliana.

Degree: PhD, 2018, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/271685

► During meiosis eukaryotes produce four haploid gametes from a single diploid parental cell. In meiotic S-phase homologous chromosomes, which were inherited from maternal and paternal… (more)

▼ During meiosis eukaryotes produce four haploid gametes from a single diploid parental cell. In meiotic S-phase homologous chromosomes, which were inherited from maternal and paternal parents, are replicated. Homologous chromosomes then pair and undergo reciprocal crossover, which generates new mosaics of maternal and paternal sequences. Meiosis also involves two rounds of chromosome segregation, meaning that only one copy of each chromosome is finally packaged into the resulting haploid gametes. In this work I sought to genetically engineer two elements of meiosis, in order to generate tools which may be useful for plant breeding. The first project sought to generate a second division restitution (SDR) population, where the second meiotic division is skipped. This is created by crossing an SDR mutant, omission of second division1, which produces diploid pollen due to a defective meiosis-II, to a haploid inducer line, whose chromosomes are lost from the zygote post-fertilisation. This was intended to give rise to diploid plants possessing chromosomes from just the SDR parent. Importantly, the SDR parent used was heterozygous, meaning that SDR progeny should show mostly homozygous chromosomes, but with regions of residual heterozygosity, determined by crossover locations. This project succeeded in creating a small number of plants with the predicted SDR genotype, although a range of aberrant genotypes were also observed. I present several hypotheses that could account for the observed progeny genotypes. In a second project I attempted to direct meiotic recombination using DNA double strand breaks targeted to specific sites. This project used a spo11-1 mutant, which is unable to produce the endogenous meiotic DNA DSBs that normally mature into crossovers. Instead, TALFokI nucleases (TALENs) were expressed from meiotic promoters in order to generate exogenous DSBs at sites determined by the DNA binding specificity of the TAL repeat domains. The project succeeded in transforming TALENs into spo11-1 mutants and confirming their expression. However, this was not sufficient to recover the spo11-1 mutant infertility or direct crossovers. Potential reasons for this non-complementation are discussed, as well as their implications for control of meiotic recombination in plant genomes.

Subjects/Keywords: Arabidopsis thaliana; meiosis; crossover; TALENs; FokI; DNA DSB; SDR; Second meiotic division restitution; OSD1; SPO11

2 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Diaz, P. L. (2018). Genetic strategies to manipulate meiotic recombination in Arabidopsis thaliana. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/271685

Chicago Manual of Style (16^th Edition):

Diaz, Patrick Loyola. “Genetic strategies to manipulate meiotic recombination in Arabidopsis thaliana.” 2018. Doctoral Dissertation, University of Cambridge. Accessed April 11, 2021. https://www.repository.cam.ac.uk/handle/1810/271685.

MLA Handbook (7^th Edition):

Diaz, Patrick Loyola. “Genetic strategies to manipulate meiotic recombination in Arabidopsis thaliana.” 2018. Web. 11 Apr 2021.

Vancouver:

Diaz PL. Genetic strategies to manipulate meiotic recombination in Arabidopsis thaliana. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2021 Apr 11]. Available from: https://www.repository.cam.ac.uk/handle/1810/271685.

Council of Science Editors:

Diaz PL. Genetic strategies to manipulate meiotic recombination in Arabidopsis thaliana. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://www.repository.cam.ac.uk/handle/1810/271685

University of Illinois – Chicago

22. Li, Jing. Investigating Role of Tyrosyl-DNA Phosphodiesterase 1 (TDP1) In Non-Homologous End Joining (NHEJ).

Degree: 2017, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/22078

► The repair of DNA double-strand breaks (DSB) is central to the maintenance of genomic integrity. Major DSB repair pathways in mammalian cells include homologous recombination… (more)

▼ The repair of DNA double-strand breaks (DSB) is central to the maintenance of genomic integrity. Major DSB repair pathways in mammalian cells include homologous recombination and non-homologous end joining (NHEJ). NHEJ is a template-independent mechanism, yet many NHEJ repair products carry limited genetic changes, which suggest that NHEJ includes mechanisms to minimize error. In yeast, mutations of tyrosyl-DNA phosphodiesterase 1 (TDP1) reduced NHEJ fidelity. We are investigating the role of TDP1 in NHEJ in human cells. Using affinity capture chromatography, we found human TDP1 physically interacted with the required NHEJ protein -XLF. This interaction also stimulated DNA binding for both TDP1 and XLF, and formation of TDP1:XLF:DNA complexes. TDP1 can remove adducts from DNA 3’ ends, and TDP1:XLF interactions stimulated this activity on double-stranded, but not on single-stranded DNA. To investigate role of TDP1 in NHEJ in human cells, we used CRISPR/Cas9-mediated genome editing to generate TDP1-knockout HEK 293 cells, which showed an expected increase sensitivity to Topoisomerase 1 poisoning and ionizing radiation. Using a chromosomally- integrated end-joining reporter substrate, we observed an average 4-fold reduction in repair of I-SceI-induced DSBs in TDP1-KO cells as compared to wild type cells. These data indicate that, in human cells, TDP1 contributes to repair of DSBs that lack 3’ end damage. NextGen sequencing of end-joining junctions generated in this reporter system showed that TDP1 deficiency resulted in increased use of microhomology in joining. Within the N-terminal domain of TDP1, phosphorylation at serine 81 (S81) has been reported to regulate interaction with DNA repair factors, including DNA ligase III, XRCC4 and PARP1. We observed that the TDP1-S81 phosphomimetic, TDP1-S81E, had 10-fold reduced XLF binding, and ectopic expression of TDP1-S81E in TDP1-knockout cells failed to restore NHEJ activity. These data suggest that phosphorylation of TDP1-S81 regulates TDP1 participation in NHEJ, and may also direct TDP1 towards DNA ligase III-related pathways. Our observations support the hypothesis that TDP1 participates in mammalian NHEJ, and contribute important details to our understanding of DNA repair. Advisors/Committee Members: Hanakahi, Les (advisor), Nitiss, John (committee member), Mankin, Alexander (committee member), Burdette, Joanna (committee member), Thomas, Douglas (committee member), Hanakahi, Les (chair).

Subjects/Keywords: tyrosyl-DNA phosphodiesterase 1 (TDP1); non-homologous end joining (NHEJ); DNA double-strand breaks (DSB)

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APA (6^th Edition):

Li, J. (2017). Investigating Role of Tyrosyl-DNA Phosphodiesterase 1 (TDP1) In Non-Homologous End Joining (NHEJ). (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/22078

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Li, Jing. “Investigating Role of Tyrosyl-DNA Phosphodiesterase 1 (TDP1) In Non-Homologous End Joining (NHEJ).” 2017. Thesis, University of Illinois – Chicago. Accessed April 11, 2021. http://hdl.handle.net/10027/22078.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Li, Jing. “Investigating Role of Tyrosyl-DNA Phosphodiesterase 1 (TDP1) In Non-Homologous End Joining (NHEJ).” 2017. Web. 11 Apr 2021.

Vancouver:

Li J. Investigating Role of Tyrosyl-DNA Phosphodiesterase 1 (TDP1) In Non-Homologous End Joining (NHEJ). [Internet] [Thesis]. University of Illinois – Chicago; 2017. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10027/22078.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Li J. Investigating Role of Tyrosyl-DNA Phosphodiesterase 1 (TDP1) In Non-Homologous End Joining (NHEJ). [Thesis]. University of Illinois – Chicago; 2017. Available from: http://hdl.handle.net/10027/22078

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Iowa

23. Yin, Yizhi. Resection of DNA double strand breaks in the germline of Caenorhabditis elegans.

Degree: PhD, Biology, 2015, University of Iowa

URL: https://ir.uiowa.edu/etd/5883

► Repair of double-strand DNA breaks (DSBs) by the homologous recombination (HR) pathway results in crossovers (COs) required for a successful first meiotic division. DSB… (more)

▼ Repair of double-strand DNA breaks (DSBs) by the homologous recombination (HR) pathway results in crossovers (COs) required for a successful first meiotic division. DSB resection is the nucleic degradation of DSB ends to expose 3’ single strand DNA (ssDNA), an intermediate required for HR. To investigate genes involved in meiosis, a forward genetic screen was performed to search for novel genes or informative new mutant alleles of known genes. Mre11 is one member of the MRX/N (Mre11-Rad50-Xrs2/Nbs1) complex required for meiotic DSB formation and for resection in budding yeast. In Caenorhabditis elegans, evidence for the MRX/N’s role in DSB resection is limited. We isolated the first separation of function allele in C. elegans , mre 11(iow1), isolated from our forward genetic screen. The mre-11(iow1) mutants are specifically defective in meiotic DSB resection but not in DSB formation. The mre 11(iow1) mutants display chromosomal fragmentation and aggregation in late prophase I. Recombination intermediates and crossover formation is greatly reduced in mre 11(iow1) mutants. Irradiation induced DSBs during meiosis fail to be repaired from the early to middle prophase I in mre 11(iow1) mutants. Our data suggest that some DSBs in mre 11(iow1) mutants are repaired by the non homologous end joining (NHEJ) pathway because removing NHEJ partially suppresses some meiotic defects conferred by mre 11(iow1). In the absence of NHEJ and a functional MRX/N, meiotic DSBs are channeled to an EXO 1 dependent form of recombination repair. Overall, our analysis supports a role for MRE-11 in the resection of DSBs in early to middle meiotic prophase I and in blocking NHEJ. A reverse genetic screen and a yeast two hybrid screen were performed to search for genes with genetic and/or physical interactions with mre-11. The reverse genetic screen isolated a novel meiotic gene, nhr-2, as a partial suppressor of the meiotic defects conferred by mre-11(iow1). The yeast two hybrid screen identified kin-18 interacting with mre-11. KIN-18 is the C. elegans homolog of mammalian Thousand And One kinase (TAO) kinase. KIN-18/TAO is MAPK kinase kinase whose meiotic role was unknown. We have found that KIN-18 is essential for normal meiotic progression as kin-18 mutants exhibit accelerated meiotic recombination, ectopic germ cell differentiation, and enhanced levels of germline apoptosis. In C.elegans MPK-1 activation in late pachytene is required for physiological apoptosis (nuclei removed by apoptosis serve as nursing cells for oocytes) and oocyte differentiation. The kin-18 mutants also showed absence of MPK-1 activation and aberrant MPK-1 activation that includes ectopic activation in the wrong regions in the germline or more than one time of activation. The progression defects in kin-18 mutants are suppressed by inhibiting an upstream activator, KSR-2, of the canonical MPK-1 signaling. Our data suggest KIN-18 affects meiotic progression by modulating the timing of MPK-1 activation. This regulation ensures the proper timing of… Advisors/Committee Members: Smolikove, Sarit (supervisor).

Subjects/Keywords: C. elegans; DSB repair; Meiotic recombination; MRX/N; Resection; TAO kinases; Biology

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APA (6^th Edition):

Yin, Y. (2015). Resection of DNA double strand breaks in the germline of Caenorhabditis elegans. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/5883

Chicago Manual of Style (16^th Edition):

Yin, Yizhi. “Resection of DNA double strand breaks in the germline of Caenorhabditis elegans.” 2015. Doctoral Dissertation, University of Iowa. Accessed April 11, 2021. https://ir.uiowa.edu/etd/5883.

MLA Handbook (7^th Edition):

Yin, Yizhi. “Resection of DNA double strand breaks in the germline of Caenorhabditis elegans.” 2015. Web. 11 Apr 2021.

Vancouver:

Yin Y. Resection of DNA double strand breaks in the germline of Caenorhabditis elegans. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2021 Apr 11]. Available from: https://ir.uiowa.edu/etd/5883.

Council of Science Editors:

Yin Y. Resection of DNA double strand breaks in the germline of Caenorhabditis elegans. [Doctoral Dissertation]. University of Iowa; 2015. Available from: https://ir.uiowa.edu/etd/5883

University of Edinburgh

24. Ku, Chuan-Chih. TCP6, a regulator in Arabidopsis gametophyte development and DNA damage response.

Degree: PhD, 2014, University of Edinburgh

URL: http://hdl.handle.net/1842/17892

► Plants have developed intricate mechanisms to control growth in response to a variety of environmental cues, to compensate its immobility and to survive in both… (more)

Subjects/Keywords: 572; TCP; gametophyte; pollen; embryo sac; cell cycle; DNA double-stranded breaks; DSB

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APA (6^th Edition):

Ku, C. (2014). TCP6, a regulator in Arabidopsis gametophyte development and DNA damage response. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/17892

Chicago Manual of Style (16^th Edition):

Ku, Chuan-Chih. “TCP6, a regulator in Arabidopsis gametophyte development and DNA damage response.” 2014. Doctoral Dissertation, University of Edinburgh. Accessed April 11, 2021. http://hdl.handle.net/1842/17892.

MLA Handbook (7^th Edition):

Ku, Chuan-Chih. “TCP6, a regulator in Arabidopsis gametophyte development and DNA damage response.” 2014. Web. 11 Apr 2021.

Vancouver:

Ku C. TCP6, a regulator in Arabidopsis gametophyte development and DNA damage response. [Internet] [Doctoral dissertation]. University of Edinburgh; 2014. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1842/17892.

Council of Science Editors:

Ku C. TCP6, a regulator in Arabidopsis gametophyte development and DNA damage response. [Doctoral Dissertation]. University of Edinburgh; 2014. Available from: http://hdl.handle.net/1842/17892

Cleveland State University

25. Nanavaty, Vishal P. Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei.

Degree: PhD, College of Sciences and Health Professions, 2016, Cleveland State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=csu1485424039406009

► Trypanosoma brucei is a parasite that causes fatal African sleeping sickness. Antigenic variation is an obligatory mechanism for long-term survival of T. brucei inside its… (more)

▼ Trypanosoma brucei is a parasite that causes fatal African sleeping sickness. Antigenic variation is an obligatory mechanism for long-term survival of T. brucei inside its mammalian host. T. brucei expresses VSG as its major surface antigen and regularly switches its VSG coat to evade the host immune response. Although T. brucei genome has more than 2,500 VSG genes and pseudogenes, it only expresses one VSG from one of 15 subtelomeric VSG expression sites (ESs) at any time. VSG switching can be transcriptional (in situ switching) or be mediated by DNA homologous recombination (such as gene conversion and reciprocal DNA crossover/telomere exchange). However, regulation of VSG switching is poorly understood. We previously found that T. brucei RAP1, a telomere protein, is essential for silencing subtelomeric VSG genes. Here we found that transient depletion of TbRAP1 increases the VSG switching frequency, and most switchers in TbRAP1-depleted cells arose thorough VSG-associated gene conversion events. Also, we detected increased amount of DSBs in the active and silent ESs upon TbRAP1 depletion. However, the underlying mechanisms of how TbRAP1 suppresses DSBs at telomeres/subtelomere remained unknown. T. brucei telomeres are transcribed, generating long, non-coding RNA called TERRA (Telomeric repeat-containing RNA). Now, we found that depletion of TbRAP1 not only leads to derepression of telomeric silent VSGs, but also results in increased TERRA levels. In addition, we observed a sixteen-fold increase in telomeric RNA:DNA hybrids (R-loops) in TbRAP1-depleted cells. R-loop has been shown to induce DSBs in yeast, mouse, and human cells and are sensitive to RNaseH, a ribonuclease that cleaves the RNA strand of the RNA:DNA hybrid. Ectopic expression of TbRNaseH1 in TbRAP1 RNAi cells resulted in reduction of the telomeric R-loop levels and reduced the DSB amount back to the WT level and suppressed the elevated VSG switching frequency phenotype. Therefore, we propose that increased TERRA and R-loop levels in TbRAP1-depleted cells mediate DSB-induced VSG gene conversion, resulting in increases VSG switching frequency. We have also identified that transcription read-through into the telomere repeats from the adjacent active ES (but not from silent ESs) contributes to TERRA synthesis. Advisors/Committee Members: Li, Bibo (Advisor).

Subjects/Keywords: Biology; Genetics; Molecular Biology; Trypanosoma brucei; VSG switching; TERRA; R-loop; telomeric recombination; RAP1; DSB

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APA (6^th Edition):

Nanavaty, V. P. (2016). Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei. (Doctoral Dissertation). Cleveland State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=csu1485424039406009

Chicago Manual of Style (16^th Edition):

Nanavaty, Vishal P. “Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei.” 2016. Doctoral Dissertation, Cleveland State University. Accessed April 11, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=csu1485424039406009.

MLA Handbook (7^th Edition):

Nanavaty, Vishal P. “Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei.” 2016. Web. 11 Apr 2021.

Vancouver:

Nanavaty VP. Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei. [Internet] [Doctoral dissertation]. Cleveland State University; 2016. [cited 2021 Apr 11]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu1485424039406009.

Council of Science Editors:

Nanavaty VP. Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei. [Doctoral Dissertation]. Cleveland State University; 2016. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu1485424039406009

26. Inagaki, Akiko. Meiotic and mitotic functions of mammalian RAD 18 in DNA double-strand break repair.

Degree: 2010, Erasmus University Medical Center

URL: http://hdl.handle.net/1765/21138

► This thesis focuses on the role of RAD 18 in DNA double-strand break (DSB ) repair. Much is known about the role of RAD 18,… (more)

Subjects/Keywords: DNA repair; DSB repair; RAD18

…meiosis-specific DNA double-strand breaks (DSB) is required for homologous chromosome… …pairing. In this chapter, we describe DSB repair mechanisms that operate in mitotic and meiotic… …double-strand break (DSB). During S phase, DSBs can arise when the replication fork… …Proteins involved in DSB repair, Checkpoint, and RDB pathways mammals S. pombe S. cerevisiae… …DNA repair in mitotic cells 13 1 DSB repair, in which the two ends of the broken DNA are…

11 more images…

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APA (6^th Edition):

Inagaki, A. (2010). Meiotic and mitotic functions of mammalian RAD 18 in DNA double-strand break repair. (Doctoral Dissertation). Erasmus University Medical Center. Retrieved from http://hdl.handle.net/1765/21138

Chicago Manual of Style (16^th Edition):

Inagaki, Akiko. “Meiotic and mitotic functions of mammalian RAD 18 in DNA double-strand break repair.” 2010. Doctoral Dissertation, Erasmus University Medical Center. Accessed April 11, 2021. http://hdl.handle.net/1765/21138.

MLA Handbook (7^th Edition):

Inagaki, Akiko. “Meiotic and mitotic functions of mammalian RAD 18 in DNA double-strand break repair.” 2010. Web. 11 Apr 2021.

Vancouver:

Inagaki A. Meiotic and mitotic functions of mammalian RAD 18 in DNA double-strand break repair. [Internet] [Doctoral dissertation]. Erasmus University Medical Center; 2010. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1765/21138.

Council of Science Editors:

Inagaki A. Meiotic and mitotic functions of mammalian RAD 18 in DNA double-strand break repair. [Doctoral Dissertation]. Erasmus University Medical Center; 2010. Available from: http://hdl.handle.net/1765/21138

University of California – Berkeley

27. Stamper, Ericca Lyn. Meiotic Double-Strand Break Formation in C. elegans.

Degree: Molecular & Cell Biology, 2014, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/3hn058dz

► For most eukaryotes, recombination between homologous chromosomes during meiosis is an essential aspect of sexual reproduction. Meiotic recombination is initiated by programmed double-strand breaks (DSBs)… (more)

▼ For most eukaryotes, recombination between homologous chromosomes during meiosis is an essential aspect of sexual reproduction. Meiotic recombination is initiated by programmed double-strand breaks (DSBs) in the DNA, which have the potential to induce mutations if not efficiently repaired. The focus of the work presented here is to better understand the mechanisms that govern the initiation of recombination and regulate the formation of DSBs. The nematode Caenorhabditis elegans was used as a model system for these studies. Here I describe the identification of a novel gene, dsb-1, that is required for DSB formation in C. elegans. Through analysis of DSB-1 I illuminate two important regulatory pathways that control the initiation of meiotic recombination and regulate DSB number. The first regulatory pathway presented in this work is the crossover assurance checkpoint, which promotes crossover recombination events on all chromosome pairs to ensure successful meiosis. Under the crossover assurance checkpoint, DSB formation is prolonged when one or more homologous chromosome pair fails to form a crossover precursor. This increase in meiotic recombination initiation events gives cells additional opportunities to produce the crossovers necessary for proper chromosome segregation. I also present evidence for a separate regulatory pathway that functions to limit the number of DSBs. I describe a negative feedback loop that is mediated by DNA-damage response kinases ATM and ATR and acts though DSB-1 to down-regulate DSB formation. This regulatory pathway permits the formation of a limited number of meiotic DSBs, while preventing excess DSB levels. Furthermore, my results demonstrate the resilience of meiotic cells in tolerating excess levels of meiotic DSBs without negative consequences for genomic integrity or crossover regulation.The work presented here provides important insights into the regulation of meiotic recombination initiation. Although the regulatory pathways described here were identified in C. elegans, recent studies suggest that similar regulatory pathways are likely to be conserved in other organisms. Therefore this work is important not only for understanding DSB regulation in C. elegans, but may also shed light on the regulation of meiotic DSBs in other eukaryotic organisms.

Subjects/Keywords: Cellular biology; Genetics; Molecular biology; C. elegans; crossover assurance; double-strand breaks; DSB-1; Meiosis; meiotic recombination

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APA (6^th Edition):

Stamper, E. L. (2014). Meiotic Double-Strand Break Formation in C. elegans. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/3hn058dz

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Stamper, Ericca Lyn. “Meiotic Double-Strand Break Formation in C. elegans.” 2014. Thesis, University of California – Berkeley. Accessed April 11, 2021. http://www.escholarship.org/uc/item/3hn058dz.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Stamper, Ericca Lyn. “Meiotic Double-Strand Break Formation in C. elegans.” 2014. Web. 11 Apr 2021.

Vancouver:

Stamper EL. Meiotic Double-Strand Break Formation in C. elegans. [Internet] [Thesis]. University of California – Berkeley; 2014. [cited 2021 Apr 11]. Available from: http://www.escholarship.org/uc/item/3hn058dz.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Stamper EL. Meiotic Double-Strand Break Formation in C. elegans. [Thesis]. University of California – Berkeley; 2014. Available from: http://www.escholarship.org/uc/item/3hn058dz

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Waterloo

28. Kaleem, Muhammad Khizer. Physical Layer Approach for Securing RFID Systems.

Degree: 2013, University of Waterloo

URL: http://hdl.handle.net/10012/7702

► Radio Frequency IDentification (RFID) is a contactless, automatic identification wireless technology primarily used for identifying and tracking of objects, goods and humans. RFID is not… (more)

▼ Radio Frequency IDentification (RFID) is a contactless, automatic identification wireless technology primarily used for identifying and tracking of objects, goods and humans. RFID is not only limited to identification and tracking applications. This proliferating wireless technology has been deployed in numerous securities sensitive applications e.g. access control, e-passports, contactless payments, driver license, transport ticking and health cards. RFID inherits all the security and privacy problems that are related to wireless technology and in addition to those that are specific to RFID systems. The security and privacy protection schemes proposed in literature for wireless devices are mostly secured through symmetric/asymmetric keys encryption/decryption and hash functions. The security of all these cryptographic algorithms depends on computationally complex problems that are hard to compute using available resources. However, these algorithms require cryptographic operations on RFID tags which contradict the low cost demand of RFID tags. Due to limited number of logic gates in tags, i.e., 5K-10K, these methods are not practical. Much research effort has done in attempt to solve consumer's privacy and security problem. Solutions that prevent clandestine inventory are mostly application layer techniques. To solve this problem, a new RFID physical layer scheme has been proposed namely Direct Sequence Backscatter Encryption (DSB Enc). The proposed scheme uses level generator to produce different levels before transmitting the signal to the tag. The tag response to the signal sent by the reader using backscatter communications on the same signal which looks random to the eavesdropper. Therefore eavesdropper cannot extract the information from reader to tag and tag to reader communication using passive eavesdropping. As reader knows the different generated levels added to the carrier signal, it can remove the levels and retrieve the tag's messages. We proposed a lightweight, low-cost and practically secure physical layer security to the RFID system, for a supply chain processing application, without increasing the computational power and tag's cost. The proposed scheme was validated by simulations on GNU Radio and experimentation using SDR and a WISP tag. Our implementation and experimental results validate that DSB Enc is secure against passive eavesdropping, replay and relay attacks. It provides better results in the presence of AWGN channel.

Subjects/Keywords: DSB Enc; RFID; USRP; SDR; GNU Radio; Level generator; Physical layer encryption; Software Defined Radio; Intel WISP tag; GRC; Security

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APA (6^th Edition):

Kaleem, M. K. (2013). Physical Layer Approach for Securing RFID Systems. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/7702

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kaleem, Muhammad Khizer. “Physical Layer Approach for Securing RFID Systems.” 2013. Thesis, University of Waterloo. Accessed April 11, 2021. http://hdl.handle.net/10012/7702.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kaleem, Muhammad Khizer. “Physical Layer Approach for Securing RFID Systems.” 2013. Web. 11 Apr 2021.

Vancouver:

Kaleem MK. Physical Layer Approach for Securing RFID Systems. [Internet] [Thesis]. University of Waterloo; 2013. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10012/7702.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kaleem MK. Physical Layer Approach for Securing RFID Systems. [Thesis]. University of Waterloo; 2013. Available from: http://hdl.handle.net/10012/7702

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

29. Moussa, Angela. Altering the level of lamin B1 leads to double-strand break repair defects and replicative stress : L'altération du niveau de la lamine B1 induit des défauts de réparation de cassures double-brin et un stress réplicatif.

Degree: Docteur es, Sciences de la vie et de la santé, 2018, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2018SACLS011

► La surexpression de la lamine B1, un composant majeur de l'enveloppe nucléaire, a été rapportée dans diverses tumeurs. Cependant, les causes et les conséquences de… (more)

▼ La surexpression de la lamine B1, un composant majeur de l'enveloppe nucléaire, a été rapportée dans diverses tumeurs. Cependant, les causes et les conséquences de cette augmentation sur la stabilité du génome n'ont pas été étudiées à ce jour. En effet, l'instabilité du génome est considérée comme une caractéristique majeure des cellules cancéreuses. Pour assurer le maintien de la stabilité du génome, les cellules ont développé de multiples et complexes mécanismes parmi lesquels les voies de réparation de l'ADN et la gestion du stress réplicatif sont essentielles. Au cours de ma thèse, l'impact de l'augmentation de niveau de lamine B1 sur la stabilité du génome, en particulier sur la réparation de cassure double-brin (CDB) et sur le contrôle du stress réplicatif a été étudié. En effet, nous montrons qu'une augmentation de la lamine B1 entraîne une accumulation de CDB et leur persistance en réponse à l'irradiation (foyers γH2AX), en plus d'une sensibilité accrue à l'irradiation (formation de colonies et cassures chromosomiques). Les cellules surexprimant la lamine B1 montrent également des défauts de recrutement de 53BP1 aux sites de dommages d’ADN, couplés à une diminution de l'efficacité de la réparation de CDB par NHEJ (Non-Homologous End-Joining). De plus, nous avons identifié une interaction directe entre la lamine B1 et 53BP1 régulant le recrutement de ce dernier aux CDB. Nos résultats supportent un modèle dans lequel l'augmentation de la lamine B1 conduit à la séquestration de 53BP1, modifiant ainsi son recrutement aux CDBs. En parallèle, nous montrons que les cellules surexprimant la lamine B1 présentent des signes accrus de stress réplicatif tels que l'accumulation de foyers spontanés de p-RPA, l'augmentation des figures radiales lors du traitement par mitomycine C, et une sensibilité accrue au traitement par camptothécine. Nous avons en outre cherché à identifier les causes de l'augmentation du stress réplicatif dans ces cellules, et les conséquences potentielles, en particulier sur l'induction de phénotypes inflammatoires. En fait, nous montrons que la surexpression de la lamine B1 conduit à une diminution de l'efficacité de la réparation de CDB par la recombinaison homologue, couplée à un défaut de formation de foyers BRCA1 après irradiation. De plus, nous avons obtenu des données préliminaires suggérant une induction de l'inflammation lors de la surexpression de la lamine B1. En résumé, ce travail de Thèse a permis d’identifier un nouveau mécanisme régulant le recrutement de 53BP1 aux CDB par son interaction avec la lamine B1, et souligne le rôle de l'augmentation de la lamine B1 dans la promotion de l'instabilité génomique au moins partiellement par des défauts de réparation de CDB et une augmentation de stress réplicatif. Après confirmation de l'induction de phénotypes inflammatoires, nous aurions identifié des rôles de l'augmentation de la lamine B1 dans la promotion de deux caractéristiques majeures du cancer - l'instabilité génomique et l'inflammation - favorisant ainsi le rôle de la lamine B1 dans… Advisors/Committee Members: Bertrand, Pascale (thesis director).

Subjects/Keywords: Lamine B1; 53BP1; Instabilité du génome; Réparation CDB; Stress Réplicatif; Inflammation; Lamin B1; 53BP1; Genome Instability; DSB repair; Replicative Stress; Inflammation

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APA (6^th Edition):

Moussa, A. (2018). Altering the level of lamin B1 leads to double-strand break repair defects and replicative stress : L'altération du niveau de la lamine B1 induit des défauts de réparation de cassures double-brin et un stress réplicatif. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLS011

Chicago Manual of Style (16^th Edition):

Moussa, Angela. “Altering the level of lamin B1 leads to double-strand break repair defects and replicative stress : L'altération du niveau de la lamine B1 induit des défauts de réparation de cassures double-brin et un stress réplicatif.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed April 11, 2021. http://www.theses.fr/2018SACLS011.

MLA Handbook (7^th Edition):

Moussa, Angela. “Altering the level of lamin B1 leads to double-strand break repair defects and replicative stress : L'altération du niveau de la lamine B1 induit des défauts de réparation de cassures double-brin et un stress réplicatif.” 2018. Web. 11 Apr 2021.

Vancouver:

Moussa A. Altering the level of lamin B1 leads to double-strand break repair defects and replicative stress : L'altération du niveau de la lamine B1 induit des défauts de réparation de cassures double-brin et un stress réplicatif. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Apr 11]. Available from: http://www.theses.fr/2018SACLS011.

Council of Science Editors:

Moussa A. Altering the level of lamin B1 leads to double-strand break repair defects and replicative stress : L'altération du niveau de la lamine B1 induit des défauts de réparation de cassures double-brin et un stress réplicatif. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLS011

Université de Lorraine

30. Zhang, Lingli. Vers la compréhension des mécanismes de réparation de l'ADN chez Streptomyces : identification d'acteurs de la recombinaison : Towards the understanding of DNA repair in streptomyces : identification of DNA recombination players.

Degree: Docteur es, Écotoxicologie, biodiversité et écosystèmes, 2014, Université de Lorraine

URL: http://www.theses.fr/2014LORR0104

► Les cassures double brin de l’ADN sont des dommages pouvant engendrer la mort cellulaire. Deux mécanismes majeurs sont impliqués dans leur réparation chez les bactéries… (more)

▼ Les cassures double brin de l’ADN sont des dommages pouvant engendrer la mort cellulaire. Deux mécanismes majeurs sont impliqués dans leur réparation chez les bactéries : la recombinaison homologue et le Non-Homologous End Joining (NHEJ). Streptomyces est une bactérie modèle pour étudier l'impact relatif des mécanismes de recombinaison sur la structure du génome et son évolution ; le chromosome est en effet caractérisé par sa linéarité, son organisation génétique compartimentée et sa plasticité génomique remarquable. L'objectif de cette recherche est d'identifier les acteurs impliqués dans les mécanismes de réparation des cassures double brin qui restent inconnus chez Streptomyces à ce jour. Concernant la recombinaison homologue, la première étape consiste en une maturation des extrémités d’ADN générées par la cassure. Cette première étape est assurée par un complexe à activité hélicase-nuclease : RecBCD (chez Escherichia coli), AddAB (chez Bacillus subtilis) ou AdnAB (chez les mycobactéries). Une analyse in silico des génomes disponibles de Streptomyces a permis d’identifier chez ces organismes, deux gènes conservés et adjacents, nommés adnA et adnB en raison de leur homologie avec les gènes adnAB récemment identifiés chez les mycobactéries. Les tentatives visant à déléter ces gènes chez Streptomyces ambofaciens et Streptomyces coelicolor ont été infructueuses. Cependant, le fait que leur délétion soit rendue possible par l’ajout d’une copie ectopique du locus sauvage nous a amené à conclure au caractère essentiel d’adnA et adnB chez Streptomyces. La trans-complémentation d’un mutant [delta]recB d’E. coli par le locus adnAB de S. ambofaciens restaure l’activité nucléase cellulaire et la survie en présence ou non d’agent génotoxique, suggérant qu’adnAB code l’homologue fonctionnel de RecBCD d’E. coli. Le rôle central d’adnAB dans la recombinaison homologue et la réplication est discuté. Le mécanisme NHEJ montre une distribution sporadique chez les bactéries et implique les deux protéines Ku et LigD. La protéine Ku se fixe sur les extrémités de l’ADN et recrute la ligase LigD. Cette dernière est une protéine multifonctionnelle présentant, outre une activité ligase, une activité polymérase et parfois une activité nucléase. L’analyse des génomes de Streptomyces a révélé un nombre variable d’homologues de ku (1-3) et d’homologues codant pour l’une ou l’autre des trois activités de LigD. Ces différents gènes définissent deux loci conservés entre espèces de Streptomyces. Chez S. ambofaciens, trois homologues de ku (nommés kuA, kuB et kuC) et deux ligases ATP-dépendantes (nommés ligC et ligD) ont été identifiés. L’exposition de souches déficientes pour ces différents gènes aux agents endommageant l’ADN (la mitomycine C, l’irradiation par faisceau d’électrons) a démontré l’implication de kuA et ligC, deux acteurs conservés, mais aussi des gènes variables kuC et ligD, dans la réparation de l’ADN. Ces résultats ouvrent de nouvelles perspectives pour comprendre le rôle du NHEJ dans l'évolution du génome et la biologie… Advisors/Committee Members: Leblond, Pierre (thesis director), Thibessard, Annabelle (thesis director).

Subjects/Keywords: Streptomyces; Réparation de DSB; Recombinaison homologue; NHEJ; Streptomyces; DNA repair; Homologous recombination; NHEJ; 572.864 59; 572.877

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, L. (2014). Vers la compréhension des mécanismes de réparation de l'ADN chez Streptomyces : identification d'acteurs de la recombinaison : Towards the understanding of DNA repair in streptomyces : identification of DNA recombination players. (Doctoral Dissertation). Université de Lorraine. Retrieved from http://www.theses.fr/2014LORR0104

Chicago Manual of Style (16^th Edition):

Zhang, Lingli. “Vers la compréhension des mécanismes de réparation de l'ADN chez Streptomyces : identification d'acteurs de la recombinaison : Towards the understanding of DNA repair in streptomyces : identification of DNA recombination players.” 2014. Doctoral Dissertation, Université de Lorraine. Accessed April 11, 2021. http://www.theses.fr/2014LORR0104.

MLA Handbook (7^th Edition):

Zhang, Lingli. “Vers la compréhension des mécanismes de réparation de l'ADN chez Streptomyces : identification d'acteurs de la recombinaison : Towards the understanding of DNA repair in streptomyces : identification of DNA recombination players.” 2014. Web. 11 Apr 2021.

Vancouver:

Zhang L. Vers la compréhension des mécanismes de réparation de l'ADN chez Streptomyces : identification d'acteurs de la recombinaison : Towards the understanding of DNA repair in streptomyces : identification of DNA recombination players. [Internet] [Doctoral dissertation]. Université de Lorraine; 2014. [cited 2021 Apr 11]. Available from: http://www.theses.fr/2014LORR0104.

Council of Science Editors:

Zhang L. Vers la compréhension des mécanismes de réparation de l'ADN chez Streptomyces : identification d'acteurs de la recombinaison : Towards the understanding of DNA repair in streptomyces : identification of DNA recombination players. [Doctoral Dissertation]. Université de Lorraine; 2014. Available from: http://www.theses.fr/2014LORR0104

Open Access Theses and Dissertations