subject:(DNA replication)

1. Kadota, Léo. Ecdysone-Regulated DNA Amplification in Sciara coprophila.

Degree: Department of Molecular Biology, Cell Biology and Biochemistry, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:733373/

► Abstract of ‘Ecdysone-Regulated DNA Amplification in Sciara coprophila’, by Léo Kadota, Sc.M., Brown University, May 2017. The eukaryotic genome contains thousands of origins (ORIs) of… (more)

Subjects/Keywords: DNA replication

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APA (6^th Edition):

Kadota, L. (2017). Ecdysone-Regulated DNA Amplification in Sciara coprophila. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:733373/

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):

Kadota, Léo. “Ecdysone-Regulated DNA Amplification in Sciara coprophila.” 2017. Thesis, Brown University. Accessed February 24, 2020. https://repository.library.brown.edu/studio/item/bdr:733373/.

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

MLA Handbook (7^th Edition):

Kadota, Léo. “Ecdysone-Regulated DNA Amplification in Sciara coprophila.” 2017. Web. 24 Feb 2020.

Vancouver:

Kadota L. Ecdysone-Regulated DNA Amplification in Sciara coprophila. [Internet] [Thesis]. Brown University; 2017. [cited 2020 Feb 24]. Available from: https://repository.library.brown.edu/studio/item/bdr:733373/.

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

Council of Science Editors:

Kadota L. Ecdysone-Regulated DNA Amplification in Sciara coprophila. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:733373/

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

East Carolina University

2. Chmielewski, Jeffrey Patrick. Drosophila Psf2 Has a Role In Chromosome Condensation.

Degree: 2012, East Carolina University

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14010

► The condensation state of chromosomes is a critical parameter in multiple processes within the cell. Failures in the maintenance of appropriate condensation states may lead… (more)

Subjects/Keywords: DNA replication; Chromosome replication; Drosophila

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APA (6^th Edition):

Chmielewski, J. P. (2012). Drosophila Psf2 Has a Role In Chromosome Condensation. (Masters Thesis). East Carolina University. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14010

Chicago Manual of Style (16^th Edition):

Chmielewski, Jeffrey Patrick. “Drosophila Psf2 Has a Role In Chromosome Condensation.” 2012. Masters Thesis, East Carolina University. Accessed February 24, 2020. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14010.

MLA Handbook (7^th Edition):

Chmielewski, Jeffrey Patrick. “Drosophila Psf2 Has a Role In Chromosome Condensation.” 2012. Web. 24 Feb 2020.

Vancouver:

Chmielewski JP. Drosophila Psf2 Has a Role In Chromosome Condensation. [Internet] [Masters thesis]. East Carolina University; 2012. [cited 2020 Feb 24]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14010.

Council of Science Editors:

Chmielewski JP. Drosophila Psf2 Has a Role In Chromosome Condensation. [Masters Thesis]. East Carolina University; 2012. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14010

3. Chmielewski, Jeffrey Patrick. Drosophila Psf2 Has a Role In Chromosome Condensation.

Degree: 2012, NC Docks

URL: http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt

► The condensation state of chromosomes is a critical parameter in multiple processes within the cell. Failures in the maintenance of appropriate condensation states may lead… (more)

Subjects/Keywords: DNA replication; Chromosome replication; Drosophila

Record Details Similar Records Cite « Share

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APA (6^th Edition):

Chmielewski, J. P. (2012). Drosophila Psf2 Has a Role In Chromosome Condensation. (Thesis). NC Docks. Retrieved from http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt

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):

Chmielewski, Jeffrey Patrick. “Drosophila Psf2 Has a Role In Chromosome Condensation.” 2012. Thesis, NC Docks. Accessed February 24, 2020. http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt.

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

MLA Handbook (7^th Edition):

Chmielewski, Jeffrey Patrick. “Drosophila Psf2 Has a Role In Chromosome Condensation.” 2012. Web. 24 Feb 2020.

Vancouver:

Chmielewski JP. Drosophila Psf2 Has a Role In Chromosome Condensation. [Internet] [Thesis]. NC Docks; 2012. [cited 2020 Feb 24]. Available from: http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt.

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

Council of Science Editors:

Chmielewski JP. Drosophila Psf2 Has a Role In Chromosome Condensation. [Thesis]. NC Docks; 2012. Available from: http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt

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

University of Aberdeen

4. Hameister, Heike. Mathematical models for DNA replication machinery.

Degree: 2012, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=186178 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558612

► DNA replication and associated processes take place in all living organisms with the same constitutions. The knowledge of the duplication process, chromatin building and repair… (more)

▼ DNA replication and associated processes take place in all living organisms with the same constitutions. The knowledge of the duplication process, chromatin building and repair mechanisms has increased explosively over the last years, but the complex interplay of different proteins and their mechanisms are not conceived properly. During DNA replication, the DNA has to be unpacked, duplicated and finally repacked into chromatin. These steps require different proteins, e.g. new histone proteins on demand to secure an error-free and undelayed DNA replication. This thesis includes different mathematical models for DNA replication, repair and chromatin formation, which are based on experimental results. Three models of chromatin formation provide a simplified description of histone gene expression and protein synthesis during G1/S/G2 phase and include the contribution of different regulatory elements. Furthermore, all models present two different mechanisms of regulation to test possible scenarios of newly synthesised histones and free DNA binding sites. The basic model presents a single histone gene, which codes for a single histone protein. The stem-loop binding protein (SLBP) acts as a master regulator, which is only present during S phase. Different analyses of early S-phase, over- and underexpressed replication and the down-regulation of SLBP proof the model under extreme conditions. This basic model serves as a template for further scenarios with several genes and different histone families. For this, a second model is realised to simulate imbalances in the histone mRNA synthesis and translation. Additionally, a third model tests a gene knock-out and mRNA silencing. The initial histone model is able to qualitatively reproduce experimental observations and shows basic regulatory principles. The adaptation with several genes and different histone families presents qualitatively different system responses for the discussed regulatory mechanisms and illustrates the ability to compensate the effect of mRNA silencing.

Subjects/Keywords: 572.8645; DNA replication

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APA (6^th Edition):

Hameister, H. (2012). Mathematical models for DNA replication machinery. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=186178 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558612

Chicago Manual of Style (16^th Edition):

Hameister, Heike. “Mathematical models for DNA replication machinery.” 2012. Doctoral Dissertation, University of Aberdeen. Accessed February 24, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=186178 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558612.

MLA Handbook (7^th Edition):

Hameister, Heike. “Mathematical models for DNA replication machinery.” 2012. Web. 24 Feb 2020.

Vancouver:

Hameister H. Mathematical models for DNA replication machinery. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2020 Feb 24]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=186178 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558612.

Council of Science Editors:

Hameister H. Mathematical models for DNA replication machinery. [Doctoral Dissertation]. University of Aberdeen; 2012. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=186178 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558612

University of Waterloo

5. Prasad, Ajai Anand. The Roles of Conserved Dbf4 Motifs in DNA Replication and Checkpoint Responses in Saccharomyces cerevisiae.

Degree: 2010, University of Waterloo

URL: http://hdl.handle.net/10012/4933

► The Dbf4 protein is involved in the initiation of DNA replication, in complex with Cdc7 kinase, and also plays a role in the intra-S-phase checkpoint… (more)

▼ The Dbf4 protein is involved in the initiation of DNA replication, in complex with Cdc7 kinase, and also plays a role in the intra-S-phase checkpoint response via an interaction with Rad53 in Saccharomyces cerevisiae. The Dbf4 protein has three highly conserved motifs, called the N, M and C motifs. In view of the fact that a comprehensive analysis of the roles of the three motifs in the initiation of DNA replication and checkpoint response was not previously available, this study was, therefore, conducted. The objectives of the study were: (1) to assess the function of the three conserved motifs, with respect to their essentiality for cell viability, (2) to determine their roles in mediating interactions with other proteins (i.e. Cdc7, Orc2, Mcm2) involved in the initiation of DNA replication and with Rad53 in the intra-S-phase checkpoint response, and (3) to obtain the three-dimensional structure of the Dbf4 N-motif by X-ray crystallography. The Dbf4 N-motif was found to be nonessential for cell viability, mediates the interaction between Dbf4 and Rad53, and as well as the interaction with Orc2. A mutant lacking the N-motif (dbf4N), was found to have a growth defect and was hypersensitive to the genotoxic agents: hydroxyurea (HU) and methyl methane sulfonate (MMS), suggesting that a disruption in the intra-S-phase checkpoint occurred because of an abrogated Dbf4-Rad53 interaction. Double point mutation of two threonine residues of the N-motif (threonines 171 and 175) to alanines also caused an abrogated Dbf4-Rad53 FHA1 domain interaction. The Dbf4 M-motif was found to be essential for cell viability and mediates the interaction between Dbf4 and Mcm2. A single proline to leucine point mutation at amino acid residue 277 conferred resistance to HU and MMS and caused disrupted Dbf4-Mcm2 and Dbf4-Orc2 interaction, while Dbf4-Rad53 interaction was maintained. Thus, the alteration of the M-motif may facilitate the role of Dbf4 as a checkpoint target. The Dbf4-C motif was also found to be essential for cell viability. Deletion and point mutations to the C-motif affected the interactions between Dbf4 and Rad53, Orc2, Mcm2 and also with Mcm4. Attempts were also made to obtain the three-dimensional structure of Dbf4, using X-ray crystallography methods. The work presented here represents a thorough functional analysis of the three conserved domains of Dbf4 in Saccharomyces cerevisiae. These results can be used as a baseline for further research involving higher eukaryotic organisims, including humans. This is particularly of relevance in light of recent evidence demonstrating an overexpression of the human Dbf4 orthologue overexpression as a cancer phenotype in human cancer cells.

Subjects/Keywords: DBF4; DNA REPLICATION

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APA (6^th Edition):

Prasad, A. A. (2010). The Roles of Conserved Dbf4 Motifs in DNA Replication and Checkpoint Responses in Saccharomyces cerevisiae. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/4933

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):

Prasad, Ajai Anand. “The Roles of Conserved Dbf4 Motifs in DNA Replication and Checkpoint Responses in Saccharomyces cerevisiae.” 2010. Thesis, University of Waterloo. Accessed February 24, 2020. http://hdl.handle.net/10012/4933.

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

MLA Handbook (7^th Edition):

Prasad, Ajai Anand. “The Roles of Conserved Dbf4 Motifs in DNA Replication and Checkpoint Responses in Saccharomyces cerevisiae.” 2010. Web. 24 Feb 2020.

Vancouver:

Prasad AA. The Roles of Conserved Dbf4 Motifs in DNA Replication and Checkpoint Responses in Saccharomyces cerevisiae. [Internet] [Thesis]. University of Waterloo; 2010. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/10012/4933.

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

Council of Science Editors:

Prasad AA. The Roles of Conserved Dbf4 Motifs in DNA Replication and Checkpoint Responses in Saccharomyces cerevisiae. [Thesis]. University of Waterloo; 2010. Available from: http://hdl.handle.net/10012/4933

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

Hong Kong University of Science and Technology

6. Xing, Li. Structural studies of Cba3 and biochemical studies of human Orc6.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-67034 ; https://doi.org/10.14711/thesis-b1254492 ; http://repository.ust.hk/ir/bitstream/1783.1-67034/1/th_redirect.html

► In the first part of this dissertation, the structural studies of Cba3 were described. Cellulose is the main structural component of the plant cell wall,… (more)

▼ In the first part of this dissertation, the structural studies of Cba3 were described. Cellulose is the main structural component of the plant cell wall, the most abundant polysaccharide on Earth, and an important renewable resource. It consists of D-glucose residues linked by β-1,4-glycosidic bonds to form linear polymeric chains of over 10,000 glucose residues. Enzymatic conversion of cellulose to glucose is a complicated process and involves cooperative action of three enzymes: endoglucanas, exoglucanase, and cellobiase. Cba3, characterized from Cellulomonas biazotea in 2012, was a cellobiase catalyzing the breakdown reaction of one cellobiose into two glucoses. Previous sequence alignment studies reveal that Cba3 belongs to GH1 (Glycoside hydrolases 1) family and it is the first discovered GH1 β-glucosidase of C. biazotea. As the studies looking for high efficient cellobiase for industrial application are extensively increased, the structural studies of Cba3 would provide insights into the engineering of enzymes for enhanced protein stability and increased activity. On the other hand, as Cba3 presents different enzymatic activities towards cellobiose and lactose, the structural studies of Cba3 with its substrates would be greatly helpful for the elucidation of mechanism of substrate specificity. We expressed, purified and crystallized Cba3. We also resolved the three dimensional structure of Cba3. By the analysis of its structure, we found that Cba3 adopts classic (β/α)₈ barrel fold. According to the experiment result, we make some primary discussion about its biological function. The second part of this dissertation describes the biochemical and structural studies of human Orc6 involved in origins recognition and binding during DNA replication initiation process. DNA replication initiation in eukaryotes requires a series of steps raging from origin recognition by ORC (origin recognition complex) to the activation of DNA helicase. The whole process is highly regulated to ensure that DNA is replicated a single round during each cell cycle which is crucial for the maintenance of the genome integrity. Through increasing studies on eukaryotes from yeast to human, it is indicated that the fundamental mechanism of DNA replication is well conserved. Orc6 is the least conserved of all ORC subunits. Sequence alignment between budding yeast and metazoan do not show statistically significant homology. In budding yeast, Orc6 is significantly larger than in metazoan species. Various studies show that Orc6 plays different functions in different species. In budding yeast Orc6 is dispensible for DNA binding in vitro. Further studies even report that yeast Orc6 interacts with Cdt1 and is involved in the loading of MCM helicase. In Xenopus and humans, Orc6 does not seem to be tightly associated with other core ORC subunits. Nevertheless, Orc6 is an integral part of Drosophila ORC and is essential for both DNA binding and replication both in vitro and in vivo. Moreover, Orc6 is reported to be implicated in cytokinesis…

Subjects/Keywords: Cellulomonas ; DNA replication

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APA (6^th Edition):

Xing, L. (2013). Structural studies of Cba3 and biochemical studies of human Orc6. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-67034 ; https://doi.org/10.14711/thesis-b1254492 ; http://repository.ust.hk/ir/bitstream/1783.1-67034/1/th_redirect.html

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):

Xing, Li. “Structural studies of Cba3 and biochemical studies of human Orc6.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed February 24, 2020. http://repository.ust.hk/ir/Record/1783.1-67034 ; https://doi.org/10.14711/thesis-b1254492 ; http://repository.ust.hk/ir/bitstream/1783.1-67034/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Xing, Li. “Structural studies of Cba3 and biochemical studies of human Orc6.” 2013. Web. 24 Feb 2020.

Vancouver:

Xing L. Structural studies of Cba3 and biochemical studies of human Orc6. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Feb 24]. Available from: http://repository.ust.hk/ir/Record/1783.1-67034 ; https://doi.org/10.14711/thesis-b1254492 ; http://repository.ust.hk/ir/bitstream/1783.1-67034/1/th_redirect.html.

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

Council of Science Editors:

Xing L. Structural studies of Cba3 and biochemical studies of human Orc6. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-67034 ; https://doi.org/10.14711/thesis-b1254492 ; http://repository.ust.hk/ir/bitstream/1783.1-67034/1/th_redirect.html

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

Vanderbilt University

7. Badu-Nkansah, Akosua Agyeman. Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks.

Degree: PhD, Biochemistry, 2016, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;

► Genomic replication is a highly challenging task. The DNA replication machinery must precisely duplicate billions of base pairs while tolerating a multitude of obstacles including… (more)

▼ Genomic replication is a highly challenging task. The DNA replication machinery must precisely duplicate billions of base pairs while tolerating a multitude of obstacles including damaged DNA, collisions with transcriptional machineries, unusual DNA structures and other difficult to replicate sequences. Many of these obstacles stall replication forks and activate replication stress responses that stabilize and restart persistently stalled forks. These mechanisms include fork remodeling to regress replication forks into a chicken foot DNA structure. Fork regression may facilitate DNA repair or template switching to bypass the obstruction. Several members of the SNF2 family of DNA-dependent ATPases including SMARCAL1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A-like protein 1), HLTF (Helicase like transcription factor) and ZRANB3 (Zinc finger Ran-binding protein 2- type containing 3) are replication stress response proteins that catalyze fork remodeling including fork regression. The enzymatic activities of SMARCAL1 and HLTF are dependent on a SNF2 ATPase motor domain and a substrate recognition domain (SRD) that is thought to mediate binding to specific structures at stalled replication forks. The SRD of SMARCAL1 is its HARP2 domain, which is required for SMARCAL1 binding to branched DNA structures as well as its DNA-dependent ATPase and fork regression activities. The SRD in HLTF is its HIRAN domain, which is unrelated in sequence and structure to the HARP domain and interacts with the exposed 3â end of small DNA flaps. The HIRAN domain is also important for HLTF mediated fork regression activity. Interestingly, unlike SMARCAL1 and HLTF, ZRANB3 contains a highly conserved ATP-dependent, substrate specific HNH endonuclease domain and catalyzes nuclease activity to branched DNA substrates. How ZRANB3 catalyzes fork remodeling and endonuclease activities is unknown. This work identified a substrate recognition domain within ZRANB3 that is needed for it to recognize and bind forked DNA structures, hydrolyze ATP, and catalyze fork remodeling and endonuclease activities. Importantly, this work provides a mechanistic understanding of how these enzymes operate within the replication stress response to restart stalled replication forks. Advisors/Committee Members: Nicholas Reiter (committee member), Katherine Friedman (committee member), Brandt Eichman (committee member), David Cortez (chair), Scott Hiebert (committee member).

Subjects/Keywords: DNA Repair; Replication Stress; Replication Forks; DNA Replication; DNA Damage

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APA (6^th Edition):

Badu-Nkansah, A. A. (2016). Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;

Chicago Manual of Style (16^th Edition):

Badu-Nkansah, Akosua Agyeman. “Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed February 24, 2020. http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;.

MLA Handbook (7^th Edition):

Badu-Nkansah, Akosua Agyeman. “Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks.” 2016. Web. 24 Feb 2020.

Vancouver:

Badu-Nkansah AA. Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2020 Feb 24]. Available from: http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;.

Council of Science Editors:

Badu-Nkansah AA. Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;

8. Sahashi, Ritsuko. Cell biological and genetical studies on DNA replication enzyme and protein modification enzyme in Drosophila : ショウジョウバエ DNA 複製酵素及びタンパク質修飾酵素の細胞生物学・遺伝学的解析.

Degree: 博士（学術）, 2014, Kyoto Institute of Technology / 京都工芸繊維大学

URL: http://hdl.handle.net/10212/2155

DNAポリメラーゼα,δ,そしてε（polα, polδ,polε）はゲノムのDNA合成を行う酵素である。polαがRNAプライマーとそれに引き続く20〜30塩基のDNAを合成し、その後、polαと置き換わったpolδ,polεが、それぞれ、ラギング鎖、リーディング鎖の合成を行うことがわかっている。先行研究によりpolαと相互作用する因子の１つとして、ヒストンH4の20番目のリジン残基（H4-K20）をモノメチル化する酵素であるPr-Set7が同定された。第1章において、私はDNA複製とヒストンH4-K20メチル化との関係及び、polαとPr-Set7の相互作用について注目をした。翅原基特異的にショウジョウバエpolαの触媒サブユニットであるpolα180kDaサブユニット（dpolαp180）をノックダウンすると成虫翅の萎縮（atrophied wing表現型）が見られdpolαp180とdPr-Set7のダブルノックダウン系統では、atrophied wing表現型の増強が見られた。また、dpolαp180ノックダウン系統の翅原基でのDNA合成をモニターするためBrdU incorporation assayを行なった結果、BrdU ポジティブな細胞数に減少がみられ、dpolαp180とdPr-Set7のダブルノックダウン系統では、BrdU ポジティブな細胞数は、さらに減少した。これらのことより、個体レベルでも両者の機能的関連が示唆され、dPr-Set7がdpolαとの相互作用を介してDNA複製の制御に関与することが示唆された。また、dpolαp180をノックダウンした翅原基における抗H4-K20モノメチル化抗体を用いた免疫染色法の結果、H4-K20モノメチル化のシグナルが減少するこを明らかにした。このことより、Pr-Set7のメチル化活性制御にdpolαが重要な働きを担っている可能性が示された。　2章では、ショウジョウバエpolεの58 kDサブユニット（dpolεp58）の機能解析を行った。polεはヘテロ4量体タンパク質であることが報告されているが、ショウジョウバエでは、現在のところ、触媒サブユニットである255 kD (dpolεp255)サブユニットと、2番目サブユニットのdpolεp58サブユニットが同定されている。dpolεp58変異系統は、蛹で致死となり、3齢幼虫の成虫原基や唾腺が野生型と比較して小型化していた。これらのことからdpolεp58が組織の成長、細胞増殖および生存に必須であると示唆された。dpolεp58変異系統3齢幼虫の複眼原基では、形態形成溝の後極側におけるBrdUの取り込みが減少し、通常は増殖が停止し、分化している後極側の細胞でM期のシグナルが増加していた。S期の遅延が引き起こされたため、後極側の細胞におけるM期のシグナルが増加したと考えられる。これらの結果より、dpolεp58がS期の進行に関与している事が明らかとなった。また、唾腺の核が野生型と比較して小型化している事が観察され、dpolεp58のendoreplicationへの関与も示唆された。さらに、変異系統を用いて他の複製関連因子の抗体でウエスタン免疫ブロットを行った結果、複製開始因子であるdOrc2レベルの顕著な減少が見られた。このことからdpolεp58とdOrc2が細胞内で相互作用する可能性が示めされ、これらのことよりpolεが複製開始に関与することが示唆された。第3章では、ショウジョウバエの発生において、私は、ショウジョウバエトランスグルタミナーゼ B（dTG-B）の働きを理解することを目的にdTG-B過剰発現系統を用いてその表現型の解析を行った。トランスグルタミナーゼ（TG）は、タンパク質間の架橋反応を触媒するタンパク質間翻訳後酵素で、様々な生物学的プロセスに関わっている。ショウジョウバエトランスグルタミナーゼの遺伝子は1種類で、A型とB型の2種類の転写産物が作られる。dTG-B過剰発現系統では、rough eye表現型と翅脈の過形成が観察された。これらの表現型は、先行研究により報告されているトランスグルタミナーゼA（dTG-A）の過剰発現系統において観察された表現型と同様であり、これらの結果からdTG-Aだけでなく、dTG-Bも複眼の形成と翅脈の形成において、その制御に関わっていることが示唆された。

Subjects/Keywords: DNA replication; DNA polymerase; Transglutaminase

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APA (6^th Edition):

Sahashi, R. (2014). Cell biological and genetical studies on DNA replication enzyme and protein modification enzyme in Drosophila : ショウジョウバエ DNA 複製酵素及びタンパク質修飾酵素の細胞生物学・遺伝学的解析. (Thesis). Kyoto Institute of Technology / 京都工芸繊維大学. Retrieved from http://hdl.handle.net/10212/2155

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):

Sahashi, Ritsuko. “Cell biological and genetical studies on DNA replication enzyme and protein modification enzyme in Drosophila : ショウジョウバエ DNA 複製酵素及びタンパク質修飾酵素の細胞生物学・遺伝学的解析.” 2014. Thesis, Kyoto Institute of Technology / 京都工芸繊維大学. Accessed February 24, 2020. http://hdl.handle.net/10212/2155.

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

MLA Handbook (7^th Edition):

Sahashi, Ritsuko. “Cell biological and genetical studies on DNA replication enzyme and protein modification enzyme in Drosophila : ショウジョウバエ DNA 複製酵素及びタンパク質修飾酵素の細胞生物学・遺伝学的解析.” 2014. Web. 24 Feb 2020.

Vancouver:

Sahashi R. Cell biological and genetical studies on DNA replication enzyme and protein modification enzyme in Drosophila : ショウジョウバエ DNA 複製酵素及びタンパク質修飾酵素の細胞生物学・遺伝学的解析. [Internet] [Thesis]. Kyoto Institute of Technology / 京都工芸繊維大学; 2014. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/10212/2155.

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

Council of Science Editors:

Sahashi R. Cell biological and genetical studies on DNA replication enzyme and protein modification enzyme in Drosophila : ショウジョウバエ DNA 複製酵素及びタンパク質修飾酵素の細胞生物学・遺伝学的解析. [Thesis]. Kyoto Institute of Technology / 京都工芸繊維大学; 2014. Available from: http://hdl.handle.net/10212/2155

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

Cornell University

9. Hartford, Suzanne. The Role For Dna Replication And Repair Genes In Germ-Line Maintenance And Tumor Suppression .

Degree: 2012, Cornell University

URL: http://hdl.handle.net/1813/29477

► : Faithful DNA replication and repair of DNA damage is important for prevention of disease and birth defects. My thesis work utilized reverse and forward… (more)

Subjects/Keywords: DNA Replication; DNA Repair; mcm9

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APA (6^th Edition):

Hartford, S. (2012). The Role For Dna Replication And Repair Genes In Germ-Line Maintenance And Tumor Suppression . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/29477

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):

Hartford, Suzanne. “The Role For Dna Replication And Repair Genes In Germ-Line Maintenance And Tumor Suppression .” 2012. Thesis, Cornell University. Accessed February 24, 2020. http://hdl.handle.net/1813/29477.

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

MLA Handbook (7^th Edition):

Hartford, Suzanne. “The Role For Dna Replication And Repair Genes In Germ-Line Maintenance And Tumor Suppression .” 2012. Web. 24 Feb 2020.

Vancouver:

Hartford S. The Role For Dna Replication And Repair Genes In Germ-Line Maintenance And Tumor Suppression . [Internet] [Thesis]. Cornell University; 2012. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/1813/29477.

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

Council of Science Editors:

Hartford S. The Role For Dna Replication And Repair Genes In Germ-Line Maintenance And Tumor Suppression . [Thesis]. Cornell University; 2012. Available from: http://hdl.handle.net/1813/29477

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

Hong Kong University of Science and Technology

10. Huang, Yining. The role of hIpi3 in human DNA replication.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-62314 ; https://doi.org/10.14711/thesis-b1254380 ; http://repository.ust.hk/ir/bitstream/1783.1-62314/1/th_redirect.html

► Ipi3 is required for cell viability in Saccharomyces cerevisiae. Yeast Ipi3 has been reported to be an essential component of the Rix1 complex (Rix1-Ipi1-Ipi3) that… (more)

Subjects/Keywords: DNA replication ; DNA-protein interactions

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APA (6^th Edition):

Huang, Y. (2013). The role of hIpi3 in human DNA replication. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-62314 ; https://doi.org/10.14711/thesis-b1254380 ; http://repository.ust.hk/ir/bitstream/1783.1-62314/1/th_redirect.html

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):

Huang, Yining. “The role of hIpi3 in human DNA replication.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed February 24, 2020. http://repository.ust.hk/ir/Record/1783.1-62314 ; https://doi.org/10.14711/thesis-b1254380 ; http://repository.ust.hk/ir/bitstream/1783.1-62314/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Huang, Yining. “The role of hIpi3 in human DNA replication.” 2013. Web. 24 Feb 2020.

Vancouver:

Huang Y. The role of hIpi3 in human DNA replication. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Feb 24]. Available from: http://repository.ust.hk/ir/Record/1783.1-62314 ; https://doi.org/10.14711/thesis-b1254380 ; http://repository.ust.hk/ir/bitstream/1783.1-62314/1/th_redirect.html.

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

Council of Science Editors:

Huang Y. The role of hIpi3 in human DNA replication. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-62314 ; https://doi.org/10.14711/thesis-b1254380 ; http://repository.ust.hk/ir/bitstream/1783.1-62314/1/th_redirect.html

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

Portland State University

11. Hamilton, Nicklas Alexander. Use of Two-replisome Plasmids to Characterize How Chromosome Replication Completes.

Degree: MS(M.S.) in Biology, Biology, 2019, Portland State University

URL: https://pdxscholar.library.pdx.edu/open_access_etds/5064

► All living organisms need to accurately replicate their genome to survive. Genomic replication occurs in three phases; initiation, elongation, and completion. While initiation and… (more)

▼ All living organisms need to accurately replicate their genome to survive. Genomic replication occurs in three phases; initiation, elongation, and completion. While initiation and elongation have been extensively characterized, less is known about how replication completes. In Escherichia coli completion occurs at sites where two replication forks converge and is proposed to involve the transiently bypass of the forks, before the overlapping sequences are resected and joined. The reaction requires RecBCD, and involves several other gene products including RecG, ExoI, and SbcDC but can occur independent of recombination or RecA. While several proteins are known to be involved, how they promote this reaction and the intermediates that arise remain uncharacterized. In the first part of this work, I describe the construction of plasmid "mini-chromosomes" containing a bidirectional origin of replication that can be used to examine the intermediates and factors required for the completion reaction. I verify that these substrates can be used to study the completion reaction by demonstrating that these plasmids require completion enzymes to propagate in cells. The completion enzymes are required for plasmids containing two-replisomes, but not one replisome, indicating that the substrate these enzymes act upon in vivo is specifically created when two replication forks converge. Completion events in E. coli are localized to one of the six termination (ter) sequences within the 400-kb terminus region due to the autoregulated action of Tus, which binds to ter and inhibits replication fork progression in an orientation-dependent manner. In the second part of this work, I examine how the presence of ter sequences affect completion on the 2-replisome plasmid. I show that addition of ter sequences modestly decreases the stability of the two-replisome plasmid and that this correlates with higher levels of abnormal, amplified molecules. The results support the idea that ter sites are not essential to completion of DNA replication; similar to what is seen on the chromosome. Rec-B-C-D forms a helicase-nuclease complex that, in addition to completion, is also required for double-strand break repair in E. coli. RecBCD activity is altered upon encountering specific DNA sequences, termed chi, in a manner that promotes crossovers during recombinational processes. In the third part of this work, I demonstrate that the presence of chi in a bidirectional plasmid model promotes the appearance of over-replicated linear molecules and that these products correlate with a reduced stability of the plasmid. The effect appears specific to plasmids containing two replisomes, as chi on the leading or lagging strand of plasmids containing one replisome had no-effect. The observation implies chi promotes a reaction that may encourage further synthesis during the completion reaction, and that at least on the mini-chromosomes substrates, this appears to… Advisors/Committee Members: Justin Courcelle.

Subjects/Keywords: Chromosome replication; DNA replication – Research; Biology

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APA (6^th Edition):

Hamilton, N. A. (2019). Use of Two-replisome Plasmids to Characterize How Chromosome Replication Completes. (Masters Thesis). Portland State University. Retrieved from https://pdxscholar.library.pdx.edu/open_access_etds/5064

Chicago Manual of Style (16^th Edition):

Hamilton, Nicklas Alexander. “Use of Two-replisome Plasmids to Characterize How Chromosome Replication Completes.” 2019. Masters Thesis, Portland State University. Accessed February 24, 2020. https://pdxscholar.library.pdx.edu/open_access_etds/5064.

MLA Handbook (7^th Edition):

Hamilton, Nicklas Alexander. “Use of Two-replisome Plasmids to Characterize How Chromosome Replication Completes.” 2019. Web. 24 Feb 2020.

Vancouver:

Hamilton NA. Use of Two-replisome Plasmids to Characterize How Chromosome Replication Completes. [Internet] [Masters thesis]. Portland State University; 2019. [cited 2020 Feb 24]. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/5064.

Council of Science Editors:

Hamilton NA. Use of Two-replisome Plasmids to Characterize How Chromosome Replication Completes. [Masters Thesis]. Portland State University; 2019. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/5064

Vanderbilt University

12. Guler, Gulfem Dilek. Human DNA helicase B in replication fork surveillance and replication stress recovery.

Degree: PhD, Biological Sciences, 2012, Vanderbilt University

URL: http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;

► Correct and faithful genome duplication is crucial for preserving genomic integrity. Genome duplication is, therefore, highly regulated through a complex network of proteins that accomplish… (more)

▼ Correct and faithful genome duplication is crucial for preserving genomic integrity. Genome duplication is, therefore, highly regulated through a complex network of proteins that accomplish DNA replication in addition to DNA repair, as needed. Human DNA helicase B (HDHB) was previously proposed to function in DNA replication and DNA damage response. Work presented in this dissertation aimed to gain insight into the cellular pathway(s) HDHB participates in, particularly in response to replication stress. Contrary to previous studies where helicase-dead DHB inhibited DNA replication, we did not observe any cell cycle or DNA replication defect in HDHB silenced cells, suggesting that HDHB activity in DNA replication can be compensated by other proteins in the absence of HDHB. On the other hand, HDHB silencing disrupted efficient recovery from replication stress. HDHB silenced cells were capable of activating checkpoint signaling, suggesting a checkpoint-independent or downstream pathway for HDHB function. Consistent with a role in replication stress response, HDHB accumulated on chromatin upon UV, hydroxyurea and camptothecin exposure in a time- and dose-dependent manner. We found that genotoxin-induced HDHB accumulation on chromatin is RPA-dependent. Biophysical and biochemical characterization revealed a direct physical interaction between RPA70N basic cleft and a conserved acidic motif in HDHB helicase domain. The interaction interface between HDHB and RPA70N is strikingly similar to the previously reported interaction interfaces of RPA70N and p53, ATRIP, Rad9 or Mre11. Site-directed mutagenesis of the HDHB-RPA70N interaction interface demonstrated its contribution to HDHB recruitment to chromatin upon genotoxin exposure. These results altogether implicate HDHB in replication stress response. Advisors/Committee Members: Ellen Fanning (committee member), Daniel Kaplan (committee member), David Cortez (committee member), Walter J. Chazin (committee member), James G. Patton (chair).

Subjects/Keywords: Replication protein A; RPA; DNA helicase; DNA replication; DNA repair; replication stress; HelB; HDHB

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APA (6^th Edition):

Guler, G. D. (2012). Human DNA helicase B in replication fork surveillance and replication stress recovery. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;

Chicago Manual of Style (16^th Edition):

Guler, Gulfem Dilek. “Human DNA helicase B in replication fork surveillance and replication stress recovery.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed February 24, 2020. http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;.

MLA Handbook (7^th Edition):

Guler, Gulfem Dilek. “Human DNA helicase B in replication fork surveillance and replication stress recovery.” 2012. Web. 24 Feb 2020.

Vancouver:

Guler GD. Human DNA helicase B in replication fork surveillance and replication stress recovery. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2020 Feb 24]. Available from: http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;.

Council of Science Editors:

Guler GD. Human DNA helicase B in replication fork surveillance and replication stress recovery. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;

Oregon State University

13. Song, Shiwei. Precursors for mitochondrial DNA replication : metabolic sources and relations to mutagenesis and human diseases.

Degree: PhD, Molecular And Cellular Biology, 2005, Oregon State University

URL: http://hdl.handle.net/1957/28973

► It is well known that the mitochondrial genome has a much higher spontaneous mutation rate than the nuclear genome. mtDNA mutations have been identified in… (more)

▼ It is well known that the mitochondrial genome has a much higher spontaneous mutation rate than the nuclear genome. mtDNA mutations have been identified in association with many diseases and aging. mtDNA replication continues throughout the cell cycle, even in post-mitotic cells. Therefore, a constant supply of nucleotides is required for replication and maintenance of the mitochondrial genome. However, it is not clear how dNTPs arise within mitochondria nor how mitochondrial dNTP pools are regulated. Recent evidence suggests that abnormal mitochondrial nucleoside and nucleotide metabolism is associated with several human diseases. Clearly, to uncover the pathogenesis of these diseases and the mechanisms of mitochondrial mutagenesis, information is needed regarding dNTP biosynthesis and maintenance within mitochondria, and biochemical consequences of disordered mitochondrial dNTP metabolism. The studies described in this thesis provide important insight into these questions. First, we found that a distinctive form of ribonucleotide reductase is associated with mammalian liver mitochondria, indicating the presence of de novo pathway for dNTP synthesis within mitochondria. Second, we found that long term thymidine treatment could induce mtDNA deletions and the mitochondrial dNTP pool changes resulting from thymidine treatment could account for the spectrum of mtDNA point mutations found in Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) patients. These results support the proposed pathogenesis of this disease. Third, we found that normal intramitochondrial dNTP pools in rat tissues are highly asymmetric, and in vitro fidelity studies show that these imbalanced pools can stimulate base substitution and frameshift mutations, with a substitution pattern that correlates with mitochondrial substitution mutations in vivo. These findings suggest that normal intramitochondrial dNTP pool asymmetries could contribute to mitochondrial mutagenesis and mitochondrial diseases. Last, Amish lethal microcephaly (MCPHA) has been proposed to be caused by insufficient transport of dNTPs into mitochondria resulting from a loss-of-function mutation in the gene encoding a mitochondrial deoxynucleotide carrier (DNC). We found that there are no significant changes of intramitochondrial dNTP levels in both a MCPHA patient's lymphoblasts with a missense point mutation in Dnc gene and the homozygous mutant cells extracted from Dnc gene knockout mouse embryos. These results do not support the proposed pathogenesis of this disease and indicate that the DNC protein does not play a crucial role in the maintenance of intramitochondrial dNTP pools. Advisors/Committee Members: Mathews, Christopher K. (advisor), Pearson, George D. (committee member).

Subjects/Keywords: DNA replication

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APA (6^th Edition):

Song, S. (2005). Precursors for mitochondrial DNA replication : metabolic sources and relations to mutagenesis and human diseases. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/28973

Chicago Manual of Style (16^th Edition):

Song, Shiwei. “Precursors for mitochondrial DNA replication : metabolic sources and relations to mutagenesis and human diseases.” 2005. Doctoral Dissertation, Oregon State University. Accessed February 24, 2020. http://hdl.handle.net/1957/28973.

MLA Handbook (7^th Edition):

Song, Shiwei. “Precursors for mitochondrial DNA replication : metabolic sources and relations to mutagenesis and human diseases.” 2005. Web. 24 Feb 2020.

Vancouver:

Song S. Precursors for mitochondrial DNA replication : metabolic sources and relations to mutagenesis and human diseases. [Internet] [Doctoral dissertation]. Oregon State University; 2005. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/1957/28973.

Council of Science Editors:

Song S. Precursors for mitochondrial DNA replication : metabolic sources and relations to mutagenesis and human diseases. [Doctoral Dissertation]. Oregon State University; 2005. Available from: http://hdl.handle.net/1957/28973

University of Hong Kong

14. Xie, Si. Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation.

Degree: PhD, 2015, University of Hong Kong

URL: Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643

► Faithful transmission of genetic information from parent cells to daughter cells is crucial for the survival of all eukaryotic organisms. To achieve high fidelity of… (more)

▼ Faithful transmission of genetic information from parent cells to daughter cells is crucial for the survival of all eukaryotic organisms. To achieve high fidelity of inheritance, cells need to resist constant insults on genome from both environmental and endogenous sources which may lead to loss of genome integrity. Eukaryotic cells have evolved the surveillance mechanisms termed checkpoints for DNA damage detection and response. The S-phase checkpoint is activated by DNA damages during the replication process. Although the cascade of the S-phase checkpoint activation has been revealed to a great extent, the molecular basis of its intricate protein interaction network is not well understood. My studies focus on the interaction network of the replication fork protection complex (FPC) including Tipin and Timeless, which preserves the replication fork structure and facilitates the sufficient phosphorylation of Chk1 in the S-phase checkpoint activation. In Chapter 2, X-ray crystallography and biochemical binding assays were employed to define the complete RPA32 recognition mode shared by multiple RPA32-interacting proteins, which represents the molecular mechanism of Tipin recruitment by RPA32. Tipin has been considered as a constitutive binding partner of Timeless. In Chapter 3, my study focused on Timeless and has for the first time identified the physical interaction between Timeless and PARP-1. The crystal structures were determined for the Timeless PARP-1-binding domain in free form and in complex with PARP-1 catalytic domain which is the first reported PARP-1 crystal structure in complex with any of its interacting proteins. In vitro PARP-1 auto-modification assay indicates that the association of Timeless does not interfere with PARP-1 enzymatic activity. Interestingly, Timeless specifically interacts with PARP-1, but not PARP-2 or PARP-3. The PARP-1 and Timeless interaction raises the possibility that PARP-1 functions together with Timeless in the S-phase checkpoint pathway, while the preliminary data also supports that Timeless functions in homologous recombination for DSB repair which has not been demonstrated before. The second part of my work presented in Chapter 4 focuses on human UHRF1. UHRF1 has been extensively characterized for its function in histone methylation and DNA methylation maintenance, while the molecular mechanism of histone H3 recognition by UHRF1 remains elusive. The crystal structure of UHRF1 PHD finger in complex with histone H3 N-terminal tail is presented, demonstrating that PHD finger of UHRF1 recognizes the N-terminus of histone H3 containing unmodified R2 and K4. Structural analysis together with biochemical assays indicated that UHRF1 PHD finger and the adjacent dTudor domain act as one functional unit to specifically recognize the H3K9me3 mark. Based on these observations, a novel model is proposed demonstrating that histone methylation and DNA methylation reinforce each other through UHRF1, which is supported by experimental evidence from other groups in later…

Subjects/Keywords: Cell cycle; DNA replication

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APA (6^th Edition):

Xie, S. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Doctoral Dissertation). University of Hong Kong. Retrieved from Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643

Chicago Manual of Style (16^th Edition):

Xie, Si. “Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed February 24, 2020. Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643.

MLA Handbook (7^th Edition):

Xie, Si. “Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation.” 2015. Web. 24 Feb 2020.

Vancouver:

Xie S. Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Feb 24]. Available from: Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643.

Council of Science Editors:

Xie S. Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643

University of Minnesota

15. Becker, Jordan. Postreplicative repair is an integral component of lagging strand DNA replication and a suppressor of replication stress.

Degree: PhD, Biochemistry, Molecular Bio, and Biophysics, 2016, University of Minnesota

URL: http://hdl.handle.net/11299/188873

► Cell division is a basic requirement for the propagation of all organisms. This process begins with a parental cell which divides, leaving two daughter cells.… (more)

Subjects/Keywords: DNA replication; Okazaki fragment; Rad27

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APA (6^th Edition):

Becker, J. (2016). Postreplicative repair is an integral component of lagging strand DNA replication and a suppressor of replication stress. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/188873

Chicago Manual of Style (16^th Edition):

Becker, Jordan. “Postreplicative repair is an integral component of lagging strand DNA replication and a suppressor of replication stress.” 2016. Doctoral Dissertation, University of Minnesota. Accessed February 24, 2020. http://hdl.handle.net/11299/188873.

MLA Handbook (7^th Edition):

Becker, Jordan. “Postreplicative repair is an integral component of lagging strand DNA replication and a suppressor of replication stress.” 2016. Web. 24 Feb 2020.

Vancouver:

Becker J. Postreplicative repair is an integral component of lagging strand DNA replication and a suppressor of replication stress. [Internet] [Doctoral dissertation]. University of Minnesota; 2016. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/11299/188873.

Council of Science Editors:

Becker J. Postreplicative repair is an integral component of lagging strand DNA replication and a suppressor of replication stress. [Doctoral Dissertation]. University of Minnesota; 2016. Available from: http://hdl.handle.net/11299/188873

East Carolina University

16. Knuckles, Christopher. Investigating the genetic interaction between DNA replication proteins Mcm10 and RecQ4 in Drosophila melanogaster.

Degree: 2017, East Carolina University

URL: http://hdl.handle.net/10342/6533

► Necessary to the survival of cellular life is proper replication and maintenance of the genome. Replication proteins Mcm10 and RecQ4 have well-characterized essential roles in… (more)

Subjects/Keywords: DNA replication; Mcm10; RecQ4

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APA (6^th Edition):

Knuckles, C. (2017). Investigating the genetic interaction between DNA replication proteins Mcm10 and RecQ4 in Drosophila melanogaster. (Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/6533

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):

Knuckles, Christopher. “Investigating the genetic interaction between DNA replication proteins Mcm10 and RecQ4 in Drosophila melanogaster.” 2017. Thesis, East Carolina University. Accessed February 24, 2020. http://hdl.handle.net/10342/6533.

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

MLA Handbook (7^th Edition):

Knuckles, Christopher. “Investigating the genetic interaction between DNA replication proteins Mcm10 and RecQ4 in Drosophila melanogaster.” 2017. Web. 24 Feb 2020.

Vancouver:

Knuckles C. Investigating the genetic interaction between DNA replication proteins Mcm10 and RecQ4 in Drosophila melanogaster. [Internet] [Thesis]. East Carolina University; 2017. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/10342/6533.

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

Council of Science Editors:

Knuckles C. Investigating the genetic interaction between DNA replication proteins Mcm10 and RecQ4 in Drosophila melanogaster. [Thesis]. East Carolina University; 2017. Available from: http://hdl.handle.net/10342/6533

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

University of Toledo

17. Easthon, Lindsey. Conformational analysis of E. coli DnaT and the complex with PriA N-terminal domain.

Degree: MS, Chemistry, 2010, University of Toledo

URL: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1271434912

► The fidelity of DNA replication is essential to maintaining genomic integrity. Therfore, pathways to restart DNA replication upon fork arrest are essential to an organism’s… (more)

Subjects/Keywords: Biochemistry; DNA replication Restart; DnaT

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APA (6^th Edition):

Easthon, L. (2010). Conformational analysis of E. coli DnaT and the complex with PriA N-terminal domain. (Masters Thesis). University of Toledo. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=toledo1271434912

Chicago Manual of Style (16^th Edition):

Easthon, Lindsey. “Conformational analysis of E. coli DnaT and the complex with PriA N-terminal domain.” 2010. Masters Thesis, University of Toledo. Accessed February 24, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1271434912.

MLA Handbook (7^th Edition):

Easthon, Lindsey. “Conformational analysis of E. coli DnaT and the complex with PriA N-terminal domain.” 2010. Web. 24 Feb 2020.

Vancouver:

Easthon L. Conformational analysis of E. coli DnaT and the complex with PriA N-terminal domain. [Internet] [Masters thesis]. University of Toledo; 2010. [cited 2020 Feb 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1271434912.

Council of Science Editors:

Easthon L. Conformational analysis of E. coli DnaT and the complex with PriA N-terminal domain. [Masters Thesis]. University of Toledo; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1271434912

University of Aberdeen

18. Christopher, Andrea. Mathematical model of 'on-demand' histone protein synthesis during S phase in humans.

Degree: PhD, 2016, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230770 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698846

► During DNA replication the DNA has to be unpacked, duplicated and repacked into chromatin, which is comprised of DNA and histone proteins (Nicholson and Muller,… (more)

▼ During DNA replication the DNA has to be unpacked, duplicated and repacked into chromatin, which is comprised of DNA and histone proteins (Nicholson and Muller, 2008b). The coordinated replication of DNA and histone protein synthesis is vital for the correct chromatin formation (Marzluff et al., 2008). The mechanism controlling the histone gene expression is only partially understood, especially the mechanism controlling any disturbances in the coordination of DNA replication and histone protein synthesis. Previous experiments suggested that the regulation mechanism of histone balance could involve regulation by a free histone protein pool (Takami and Nakayama, 1997b; Takami and Nakayama, 1997a; Dominski et al., 2005; Kroeger et al., 1995). A mathematical model was produced by Dr Hameister (Hameister, 2012) to describe the control of histone production during S phase. The parameters used were taken from literature. Modifications were made using experimentally measured data to replace literature values (Harris et al., 1991; Clark, 2006; Strachen and Read, 2003). The aim of the project was to both optimise the model by defining parameters to reflect what occurs naturally in the cell, as well as trying to validate the model. The DNA replication rate was measured by FACS analysis and was input into the model. Histone RNA levels during S phase were measured by Northern blots and histone RNA degradation rates were analysed. To confirm that the modified DNA replication rate was producing accurate simulations, the curve produced for the mRNA levels could be compared to the experimentally measured mRNA values (Figure 4.3.1). The over expression of an H2B gene was verified using Western and Northern analysis. The validation of the model that the histone gene balance was being regulated by a free histone pool was not absolutely confirmed. However, results seen in Figure 3.6.1, showed an increase in H2B RNA degradation in the sample with the additional gene due to the additional histone proteins. Further work is required for confirmation of the regulation mechanism.

Subjects/Keywords: 572.8; DNA replication; Histones

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APA (6^th Edition):

Christopher, A. (2016). Mathematical model of 'on-demand' histone protein synthesis during S phase in humans. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230770 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698846

Chicago Manual of Style (16^th Edition):

Christopher, Andrea. “Mathematical model of 'on-demand' histone protein synthesis during S phase in humans.” 2016. Doctoral Dissertation, University of Aberdeen. Accessed February 24, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230770 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698846.

MLA Handbook (7^th Edition):

Christopher, Andrea. “Mathematical model of 'on-demand' histone protein synthesis during S phase in humans.” 2016. Web. 24 Feb 2020.

Vancouver:

Christopher A. Mathematical model of 'on-demand' histone protein synthesis during S phase in humans. [Internet] [Doctoral dissertation]. University of Aberdeen; 2016. [cited 2020 Feb 24]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230770 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698846.

Council of Science Editors:

Christopher A. Mathematical model of 'on-demand' histone protein synthesis during S phase in humans. [Doctoral Dissertation]. University of Aberdeen; 2016. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230770 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698846

University of Aberdeen

19. Hameister, Heike. Mathematical models for DNA replication machinery.

Degree: Dept. of Physics., 2012, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=186178 ; http://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=186178&custom_att_2=simple_viewer

Subjects/Keywords: DNA replication

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

APA (6^th Edition):

Hameister, H. (2012). Mathematical models for DNA replication machinery. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=186178 ; http://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=186178&custom_att_2=simple_viewer

Chicago Manual of Style (16^th Edition):

Hameister, Heike. “Mathematical models for DNA replication machinery.” 2012. Doctoral Dissertation, University of Aberdeen. Accessed February 24, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=186178 ; http://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=186178&custom_att_2=simple_viewer.

MLA Handbook (7^th Edition):

Hameister, Heike. “Mathematical models for DNA replication machinery.” 2012. Web. 24 Feb 2020.

Vancouver:

Hameister H. Mathematical models for DNA replication machinery. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2020 Feb 24]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=186178 ; http://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=186178&custom_att_2=simple_viewer.

Council of Science Editors:

Hameister H. Mathematical models for DNA replication machinery. [Doctoral Dissertation]. University of Aberdeen; 2012. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=186178 ; http://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=186178&custom_att_2=simple_viewer

University of Arizona

20. Langston, Rachel Elizabeth. DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle .

Degree: 2016, University of Arizona

URL: http://hdl.handle.net/10150/622910

► Errors in DNA replication can cause chromosome instability and gross chromosomal rearrangements (GCRs). For my thesis work I investigate how chromosome instability can originate in… (more)

Subjects/Keywords: DNA replication; telomere; Chromosome instability

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APA (6^th Edition):

Langston, R. E. (2016). DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/622910

Chicago Manual of Style (16^th Edition):

Langston, Rachel Elizabeth. “DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle .” 2016. Doctoral Dissertation, University of Arizona. Accessed February 24, 2020. http://hdl.handle.net/10150/622910.

MLA Handbook (7^th Edition):

Langston, Rachel Elizabeth. “DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle .” 2016. Web. 24 Feb 2020.

Vancouver:

Langston RE. DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/10150/622910.

Council of Science Editors:

Langston RE. DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/622910

Cornell University

21. Plys, Aaron. Analysis Of The Movement Of Saccharomyces Cerevisiae Mismatch Repair Proteins On Dna .

Degree: 2011, Cornell University

URL: http://hdl.handle.net/1813/30604

► Replication errors that escape DNA polymerase proof-reading activity are efficientl y recognized and repaired by conserved DNA mismatch repair factors. The overall result is a… (more)

▼ Replication errors that escape DNA polymerase proof-reading activity are efficientl y recognized and repaired by conserved DNA mismatch repair factors. The overall result is a drastic reduction in deletion mutations. The mechanistic details of how mismatch repair proteins execute mismatch removal have not been elucidated. The aim of my thesis is to better understand how mismatch repair factors interact with DNA in order to identify mismatch sites. My work reveals that the mismatch repair complex, MLH1-PMS1, has unique DNA diffusion characteristics facilitated by structural features of the two subunits. Through bulk assays and total internal reflectance fluorescence microscopy (TIRFM), I found that MLH1PMS1 could independently bind DNA and rapidly diffuse using the thermal energy of the system. Furthermore, MLH1-PMS1 was shown to be the first passively diffusing protein that could bypass stationary nucleosomes. In contrast, the DNA diffusion activity of the mismatch recognition complex MSH2-MSH6 was blocked by nucleosomes. The timing and nature of mismatch repair is linked with replication and is thus proposed that the differences seen for the two complexes have important implications for repair in the context of the chromatin state directly at the replication fork. Each subunit of the MLH1-PMS1 complex is composed of two defined globular domains connected by an unstructured linker arm. The linker arms of the complex are proposed to facilitate topological DNA binding and diffusion along DNA in a hopping/stepping mechanism. I found that TEV protease cleavage within the linker arms of MLH1-PMS1 disrupted DNA binding and mismatch repair in vitro and in vivo. Using a genetic mismatch repair assay I found that shortening of the linker arms in MLH1 had a drastic effect on function whereas similar changes in PMS1 had little or no effect. Purified truncated complexes were able to interact with DNA and form ternary complexes with MSH2-MSH6 at a mismatch. Future studies should focus on the diffusion characteristic for these complexes. Together, my work has important implications for understanding how mismatch repair proteins can rapidly identify their targets in a chromatin landscape. Advisors/Committee Members: Weiss, Robert S. (committeeMember).

Subjects/Keywords: DNA mismatch repair; Replication; Cancer

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APA (6^th Edition):

Plys, A. (2011). Analysis Of The Movement Of Saccharomyces Cerevisiae Mismatch Repair Proteins On Dna . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/30604

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):

Plys, Aaron. “Analysis Of The Movement Of Saccharomyces Cerevisiae Mismatch Repair Proteins On Dna .” 2011. Thesis, Cornell University. Accessed February 24, 2020. http://hdl.handle.net/1813/30604.

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

MLA Handbook (7^th Edition):

Plys, Aaron. “Analysis Of The Movement Of Saccharomyces Cerevisiae Mismatch Repair Proteins On Dna .” 2011. Web. 24 Feb 2020.

Vancouver:

Plys A. Analysis Of The Movement Of Saccharomyces Cerevisiae Mismatch Repair Proteins On Dna . [Internet] [Thesis]. Cornell University; 2011. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/1813/30604.

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

Council of Science Editors:

Plys A. Analysis Of The Movement Of Saccharomyces Cerevisiae Mismatch Repair Proteins On Dna . [Thesis]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/30604

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

Cornell University

22. Li, Xin. Aspects Of Eukaryotic Dna Replication, Repair And Recombination .

Degree: 2009, Cornell University

URL: http://hdl.handle.net/1813/13522

► The mechanism that replicates, maintains, and sometimes alters the DNA is most fundamental and important for life. Three processes (DNA Replication, Repair, and Recombination) that… (more)

▼ The mechanism that replicates, maintains, and sometimes alters the DNA is most fundamental and important for life. Three processes (DNA Replication, Repair, and Recombination) that are involved in this mechanism are closely related and well conserved in evolution. In my Ph.D. studies, I have used the cross model-organism approach to investigate the molecular mechanisms of DNA replication stress induced cancer as well as meiosis disruption caused infertility. Mcm4Chaos3, which encodes a mutant subunit of the hexameric MCM helicase, was previously reported to cause genetic instability (GIN) in mice and predispose homozygous female mice to mammary adenocarcinomas. My results show that homozygous diploid yeast carrying the equivalent mutation are defective in replicating long terminal repeat (LTR) elements. The replication stress at these interspersed repeat sequences coupled with error prone repair is the source of GIN, which is the driving force for the acquisition of an accelerated proliferation (AP) phenotype with aneuploidy as byproducts. I showed that mutations unrelated to aneuploidy are the cause of the AP phenotype. Moreover, the fragility of LTR regions is dependent on ploidy. The LTRs are not vulnerable to replication stress in haploid yeast and mcm4Chaos3 haploids use other repair pathways without generating GIN. Therefore, the dichotomy of consequences of DNA replication stress and repair pathway choice stems from cell-type specific regulation of fragile sites. In mammalian meiosis, homologous chromosome synapsis is coupled with recombination. As in most eukaryotes, mammalian meiocytes have checkpoints that monitor the fidelity of these processes. I reported that the mouse ortholog (Trip13) of pachytene checkpoint 2 (PCH2), an essential component of the synapsis checkpoint in S. cerevisiae and C. elegans, is required after strand invasion for completing a subset of recombination events, but possibly not those destined to be crossovers (Li and Schimenti 2007). TRIP13-deficient mice exhibit spermatocyte death in pachynema and loss of oocytes around birth. The chromosomes of mutant spermatocytes synapse fully, yet retain several markers of recombination intermediates. This is the first model to separate recombination defects from asynapsis in mammalian meiosis. Surprisingly, we found no evidence for checkpoint function, suggesting different pachytene checkpoint mechanisms may be involved in different species (Li et al. 2008).

Subjects/Keywords: DNA Replication

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APA (6^th Edition):

Li, X. (2009). Aspects Of Eukaryotic Dna Replication, Repair And Recombination . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/13522

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, Xin. “Aspects Of Eukaryotic Dna Replication, Repair And Recombination .” 2009. Thesis, Cornell University. Accessed February 24, 2020. http://hdl.handle.net/1813/13522.

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, Xin. “Aspects Of Eukaryotic Dna Replication, Repair And Recombination .” 2009. Web. 24 Feb 2020.

Vancouver:

Li X. Aspects Of Eukaryotic Dna Replication, Repair And Recombination . [Internet] [Thesis]. Cornell University; 2009. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/1813/13522.

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

Council of Science Editors:

Li X. Aspects Of Eukaryotic Dna Replication, Repair And Recombination . [Thesis]. Cornell University; 2009. Available from: http://hdl.handle.net/1813/13522

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

Cornell University

23. Dowicki, Michael. The Wing Helix Domain Of Orc4 Is The Primary Determinant Of Dna Binding Specificity Of The Origin Recognition Complex .

Degree: 2015, Cornell University

URL: http://hdl.handle.net/1813/40691

► The process of DNA replication is regulated to ensure that the entire genome is replicated only once during every cell division cycle. Eukaryotic DNA replication… (more)

▼ The process of DNA replication is regulated to ensure that the entire genome is replicated only once during every cell division cycle. Eukaryotic DNA replication begins with the binding of the Origin Replication Complex (ORC) to multiple replication origins or Autonomously Replicating Sequences (ARSs) on every chromosome. The ORC machinery is conserved from fungal to mammalian systems, however the ARSs to which the ORC binds have diverged significantly. In the budding yeast S. cerevisiae the ORC binds a well-defined 17bp ACS, conversely in the fission yeast S. pombe ORC binds to AT rich sequences in a stochastic manner. Previously the replication origins of the yeast K .lactis have been identified as a 50bp sequence necessary and largely sufficient for replication. Through testing of plasmids constructed to contain either S. cerevisiae or K. lactis ARSs, it was found that each species is largely unable to replicate ARSs from the other species, indicating that the replication machinery has significantly diverged to specifically recognize its own origin sequence. In this thesis, I am examining the role subunits of the ORC complex play in determining the binding specificity of the ORC complex. The ORC proteins contain a DNA binding Winged Helix Domain in their C-termini. I have constructed S. cerevisiae strains containing chimeric ORC proteins which interact with the S. cerevisiae machinery while containing the K. lactis WHD. The chimeric ORC4 and ORC5 proteins fail to substitute for their respective endogenous proteins but the ORC4 chimera results in a dominant loss of silencing at the HMR locus, which is mediated by ORC. ChIP-Seq analysis showed that the chimeric strain binds to a K. lactis ACS at this locus and at several other distinct sites in the S. cerevisiae genome including the centromeres. Additionally the chimeric ORC4 demonstrates the ability to replicate plasmids containing a K. lactis ARS, unlike the wild type S. cerevisiae strain and S. cerevisiae containing a chimeric ORC5. This study suggests that the DNA binding specificity for the S. cerevisiae ORC, K. lactis ORC and most likely ORCs in other fungi is primarily determined by the WHD of Orc4. Advisors/Committee Members: Gu,Zhenglong (committeeMember), Weiss,Robert S. (committeeMember).

Subjects/Keywords: DNA Replication; Origin Recognition Complex

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APA (6^th Edition):

Dowicki, M. (2015). The Wing Helix Domain Of Orc4 Is The Primary Determinant Of Dna Binding Specificity Of The Origin Recognition Complex . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/40691

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):

Dowicki, Michael. “The Wing Helix Domain Of Orc4 Is The Primary Determinant Of Dna Binding Specificity Of The Origin Recognition Complex .” 2015. Thesis, Cornell University. Accessed February 24, 2020. http://hdl.handle.net/1813/40691.

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

MLA Handbook (7^th Edition):

Dowicki, Michael. “The Wing Helix Domain Of Orc4 Is The Primary Determinant Of Dna Binding Specificity Of The Origin Recognition Complex .” 2015. Web. 24 Feb 2020.

Vancouver:

Dowicki M. The Wing Helix Domain Of Orc4 Is The Primary Determinant Of Dna Binding Specificity Of The Origin Recognition Complex . [Internet] [Thesis]. Cornell University; 2015. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/1813/40691.

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

Council of Science Editors:

Dowicki M. The Wing Helix Domain Of Orc4 Is The Primary Determinant Of Dna Binding Specificity Of The Origin Recognition Complex . [Thesis]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/40691

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

Cornell University

24. Lee, Chanmi. Interplay Between Mcm Helicase And Checkpoint Proteins Rescues Replication Fork Defects Of Mcm10 .

Degree: 2009, Cornell University

URL: http://hdl.handle.net/1813/14066

► Mcm10 is essential in the initiation and elongation of DNA replication. It is implicated in the activation and stable assembly of various elongation factors such… (more)

Subjects/Keywords: DNA replication

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APA (6^th Edition):

Lee, C. (2009). Interplay Between Mcm Helicase And Checkpoint Proteins Rescues Replication Fork Defects Of Mcm10 . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/14066

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):

Lee, Chanmi. “Interplay Between Mcm Helicase And Checkpoint Proteins Rescues Replication Fork Defects Of Mcm10 .” 2009. Thesis, Cornell University. Accessed February 24, 2020. http://hdl.handle.net/1813/14066.

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

MLA Handbook (7^th Edition):

Lee, Chanmi. “Interplay Between Mcm Helicase And Checkpoint Proteins Rescues Replication Fork Defects Of Mcm10 .” 2009. Web. 24 Feb 2020.

Vancouver:

Lee C. Interplay Between Mcm Helicase And Checkpoint Proteins Rescues Replication Fork Defects Of Mcm10 . [Internet] [Thesis]. Cornell University; 2009. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/1813/14066.

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

Council of Science Editors:

Lee C. Interplay Between Mcm Helicase And Checkpoint Proteins Rescues Replication Fork Defects Of Mcm10 . [Thesis]. Cornell University; 2009. Available from: http://hdl.handle.net/1813/14066

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

Vanderbilt University

25. Wells, Christina Elizabeth. Elucidating the mechanism of action of selective histone deacetylase inhibitors in cancer.

Degree: PhD, Biochemistry, 2013, Vanderbilt University

URL: http://etd.library.vanderbilt.edu//available/etd-03202013-133129/ ;

► Given the fundamental roles of histone deacetylases (HDACs) in the regulation of DNA repair, replication, transcription and chromatin structure, it is fitting that therapies targeting… (more)

Subjects/Keywords: DNA replication; HDIs; small molecule

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APA (6^th Edition):

Wells, C. E. (2013). Elucidating the mechanism of action of selective histone deacetylase inhibitors in cancer. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-03202013-133129/ ;

Chicago Manual of Style (16^th Edition):

Wells, Christina Elizabeth. “Elucidating the mechanism of action of selective histone deacetylase inhibitors in cancer.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed February 24, 2020. http://etd.library.vanderbilt.edu//available/etd-03202013-133129/ ;.

MLA Handbook (7^th Edition):

Wells, Christina Elizabeth. “Elucidating the mechanism of action of selective histone deacetylase inhibitors in cancer.” 2013. Web. 24 Feb 2020.

Vancouver:

Wells CE. Elucidating the mechanism of action of selective histone deacetylase inhibitors in cancer. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2020 Feb 24]. Available from: http://etd.library.vanderbilt.edu//available/etd-03202013-133129/ ;.

Council of Science Editors:

Wells CE. Elucidating the mechanism of action of selective histone deacetylase inhibitors in cancer. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu//available/etd-03202013-133129/ ;

University of Waterloo

26. DaSilva, Lance. Functional Characterization of the Origin Recognition Complex (ORC) in S. cerevisiae.

Degree: 2008, University of Waterloo

URL: http://hdl.handle.net/10012/3518

► The origin recognition complex (Orc1-6) plays a fundamental role in the initiation of DNA replication by binding replication origins throughout the budding yeast cell cycle.… (more)

Subjects/Keywords: DNA Replication

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APA (6^th Edition):

DaSilva, L. (2008). Functional Characterization of the Origin Recognition Complex (ORC) in S. cerevisiae. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/3518

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):

DaSilva, Lance. “Functional Characterization of the Origin Recognition Complex (ORC) in S. cerevisiae.” 2008. Thesis, University of Waterloo. Accessed February 24, 2020. http://hdl.handle.net/10012/3518.

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

MLA Handbook (7^th Edition):

DaSilva, Lance. “Functional Characterization of the Origin Recognition Complex (ORC) in S. cerevisiae.” 2008. Web. 24 Feb 2020.

Vancouver:

DaSilva L. Functional Characterization of the Origin Recognition Complex (ORC) in S. cerevisiae. [Internet] [Thesis]. University of Waterloo; 2008. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/10012/3518.

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

Council of Science Editors:

DaSilva L. Functional Characterization of the Origin Recognition Complex (ORC) in S. cerevisiae. [Thesis]. University of Waterloo; 2008. Available from: http://hdl.handle.net/10012/3518

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

Princeton University

27. Haye, Joanna E. DYNAMICS OF THE MISMATCH REPAIR COMPLEXES DURING DNA REPLICATION .

Degree: PhD, 2014, Princeton University

URL: http://arks.princeton.edu/ark:/88435/dsp01vm40xt80m

► DNA mismatch repair (MMR) functions mainly to correct mispaired bases that escape the proofreading activity of the DNA polymerase during replication. Defects in MMR genes… (more)

▼ DNA mismatch repair (MMR) functions mainly to correct mispaired bases that escape the proofreading activity of the DNA polymerase during replication. Defects in MMR genes have been linked to compromised genome stability and diseases including cancer. MMR is a highly conserved process and the yeast Saccharomyces cerevisiae is an ideal model organism to explore aspects of MMR because of the ease of manipulation and homology to the human system. MMR initiates when a mismatch in the DNA helix is recognized by MutS homologs. Subsequent events include excision of the error-containing strand followed by re-synthesis. A critical step in this process is directing repair to the newly synthesized strand, which requires a strand discrimination signal. Current data suggest that transient discontinuities in the DNA backbone, known as nicks, generated during replication serve as the strand discrimination signal. Additionally, histones have the capacity to block mismatch recognition and are known to rapidly assemble behind the replication fork. Thus, there must be a short window of opportunity for the MutS homologs to scan for mismatches and access the strand discrimination signals during replication. To address these unresolved issues, we hypothesize that the MMR machinery tracks with the replisome to allow for efficient scanning and access to the strand discrimination signal. We employed chromatin immunoprecipitation and DNA tiling microarrays (ChIP-chip) to determine the distribution of the eukaryotic MutS complexes during replication. The data indicate that during S-phase of the cell cycle MutS binds origins of replication and shows bi-directional occupancy of regions flanking the origins over time with timing consistent with fork progression. Importantly, MutS displays the same origin binding and spreading pattern as the leading strand DNA polymerase over multiple experiments. In sum, our data supports the hypothesis of the MMR machinery tracking with the replisome. There are two MutS complexes that occur in eukaryotes, MutSα (Msh2/Msh6) and MutSβ (Msh2/Msh3). Both complexes recognize the different types of mismatches that arise during DNA replication. Reporter constructs have traditionally been utilized to assay the types of mismatches targeted by each complex. With the availability of new techniques, we can now analyze the functions of MutSα and MutSβ on a genome wide scale. In this work, we used next generation sequencing to determine the mutation spectra in strains lacking MSH2, MSH3 or MSH6. Our studies confirm the findings of previous genetic experiments that MutSα and MutSβ are functionally redundant for repair at HPRs; however, each complex is essential for ~6-7% of the mismatches generated during replication. In this work, we provide evidence that both complexes should be in the vicinity of the replisome to ensure that majority of the mutations can be avoided during replication. Advisors/Committee Members: Gammie, Alison E (advisor), Rose, Mark D (advisor).

Subjects/Keywords: DNA mismatch repair; Replication

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

APA (6^th Edition):

Haye, J. E. (2014). DYNAMICS OF THE MISMATCH REPAIR COMPLEXES DURING DNA REPLICATION . (Doctoral Dissertation). Princeton University. Retrieved from http://arks.princeton.edu/ark:/88435/dsp01vm40xt80m

Chicago Manual of Style (16^th Edition):

Haye, Joanna E. “DYNAMICS OF THE MISMATCH REPAIR COMPLEXES DURING DNA REPLICATION .” 2014. Doctoral Dissertation, Princeton University. Accessed February 24, 2020. http://arks.princeton.edu/ark:/88435/dsp01vm40xt80m.

MLA Handbook (7^th Edition):

Haye, Joanna E. “DYNAMICS OF THE MISMATCH REPAIR COMPLEXES DURING DNA REPLICATION .” 2014. Web. 24 Feb 2020.

Vancouver:

Haye JE. DYNAMICS OF THE MISMATCH REPAIR COMPLEXES DURING DNA REPLICATION . [Internet] [Doctoral dissertation]. Princeton University; 2014. [cited 2020 Feb 24]. Available from: http://arks.princeton.edu/ark:/88435/dsp01vm40xt80m.

Council of Science Editors:

Haye JE. DYNAMICS OF THE MISMATCH REPAIR COMPLEXES DURING DNA REPLICATION . [Doctoral Dissertation]. Princeton University; 2014. Available from: http://arks.princeton.edu/ark:/88435/dsp01vm40xt80m

Hong Kong University of Science and Technology

28. Cheung, Man Hei. The role of NOC3 in DNA replication in human cells.

Degree: 2015, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-80225 ; https://doi.org/10.14711/thesis-b1514893 ; http://repository.ust.hk/ir/bitstream/1783.1-80225/1/th_redirect.html

► Noc3 (Nucleolar complex associated protein) was originally identified by a genetic screen in budding yeast Saccharomyces cerevisiae. It was reported that it plays crucial roles… (more)

Subjects/Keywords: DNA replication ; Nuclear proteins

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

APA (6^th Edition):

Cheung, M. H. (2015). The role of NOC3 in DNA replication in human cells. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-80225 ; https://doi.org/10.14711/thesis-b1514893 ; http://repository.ust.hk/ir/bitstream/1783.1-80225/1/th_redirect.html

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):

Cheung, Man Hei. “The role of NOC3 in DNA replication in human cells.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed February 24, 2020. http://repository.ust.hk/ir/Record/1783.1-80225 ; https://doi.org/10.14711/thesis-b1514893 ; http://repository.ust.hk/ir/bitstream/1783.1-80225/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Cheung, Man Hei. “The role of NOC3 in DNA replication in human cells.” 2015. Web. 24 Feb 2020.

Vancouver:

Cheung MH. The role of NOC3 in DNA replication in human cells. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2020 Feb 24]. Available from: http://repository.ust.hk/ir/Record/1783.1-80225 ; https://doi.org/10.14711/thesis-b1514893 ; http://repository.ust.hk/ir/bitstream/1783.1-80225/1/th_redirect.html.

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

Council of Science Editors:

Cheung MH. The role of NOC3 in DNA replication in human cells. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: http://repository.ust.hk/ir/Record/1783.1-80225 ; https://doi.org/10.14711/thesis-b1514893 ; http://repository.ust.hk/ir/bitstream/1783.1-80225/1/th_redirect.html

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

Hong Kong University of Science and Technology

29. Qin, Yan LIFS. The role of hNOC3 in human DNA replication.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html

► Noc3p (nucleolar complex-associated protein) is highly conserved in eukaryotes, and it plays a critical role in the initiation of DNA replication in budding yeast. Noc3p… (more)

Subjects/Keywords: DNA replication ; Cell cycle

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

APA (6^th Edition):

Qin, Y. L. (2013). The role of hNOC3 in human DNA replication. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html

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):

Qin, Yan LIFS. “The role of hNOC3 in human DNA replication.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed February 24, 2020. http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Qin, Yan LIFS. “The role of hNOC3 in human DNA replication.” 2013. Web. 24 Feb 2020.

Vancouver:

Qin YL. The role of hNOC3 in human DNA replication. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Feb 24]. Available from: http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html.

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

Council of Science Editors:

Qin YL. The role of hNOC3 in human DNA replication. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html

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

University of Gothenburg / Göteborgs Universitet

30. Posse, Viktor. Molecular insights into mitochondrial transcription and its role in DNA replication.

Degree: 2016, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/50132

► The mitochondrion is an organelle of the eukaryotic cell responsible for the production of most of the cellular energy-carrying molecule adenosine triphosphate (ATP), through the… (more)

▼ The mitochondrion is an organelle of the eukaryotic cell responsible for the production of most of the cellular energy-carrying molecule adenosine triphosphate (ATP), through the process of oxidative phosphorylation. The mitochondrion contains its own genome, a small circular DNA molecule (mtDNA), encoding essential subunits of the oxidative phosphorylation system. Initiation of mitochondrial transcription involves three proteins, the mitochondrial RNA polymerase, POLRMT, and its two transcription factors, TFAM and TFB2M. Even though the process of transcription has been reconstituted in vitro, a full molecular understanding is still missing. Initiation of mitochondrial DNA replication is believed to be primed by transcription prematurely terminated at a sequence known as CSBII. The mechanisms of replication initiation have however not been fully defined. In this thesis we have studied transcription and replication of mtDNA. In the first part of this thesis we demonstrate that the transcription initiation machinery is recruited in discrete steps. Furthermore, we find that a large domain of POLRMT known as the N-terminal extension is dispensable for transcription initiation, and instead functions in suppressing initiation events from non-promoter DNA. Additionally we demonstrate that TFB2M is the last factor that is recruited to the initiation complex and that it induces melting of the mitochondrial promoters. In this thesis we also demonstrate that POLRMT is a non-processive polymerase that needs the presence of the elongation factor TEFM for processive transcription. TEFM increases the affinity of POLRMT for an elongation-like RNA-DNA template and decreases the probability of premature transcription termination. Our data also suggest that TEFM might be of importance for mitochondrial replication initiation, since it affects termination at CSBII. In the last part of this thesis we study the RNA-DNA hybrids (R-loops) that can be formed by the CSBII terminated transcript. We characterize these R-loops and demonstrate that they can be processed by RNaseH1 to form replicative primers that can be used by the mitochondrial replication machinery.

Subjects/Keywords: mitochondrion; mtDNA; transcription; DNA replication

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APA (6^th Edition):

Posse, V. (2016). Molecular insights into mitochondrial transcription and its role in DNA replication. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/50132

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):

Posse, Viktor. “Molecular insights into mitochondrial transcription and its role in DNA replication.” 2016. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed February 24, 2020. http://hdl.handle.net/2077/50132.

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

MLA Handbook (7^th Edition):

Posse, Viktor. “Molecular insights into mitochondrial transcription and its role in DNA replication.” 2016. Web. 24 Feb 2020.

Vancouver:

Posse V. Molecular insights into mitochondrial transcription and its role in DNA replication. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2016. [cited 2020 Feb 24]. Available from: http://hdl.handle.net/2077/50132.

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

Council of Science Editors:

Posse V. Molecular insights into mitochondrial transcription and its role in DNA replication. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2016. Available from: http://hdl.handle.net/2077/50132

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

Open Access Theses and Dissertations