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Mechanistic Studies of DNA Replicati...

Raper, Austin Tyler.

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Mechanistic Studies of DNA Replication, Lesion Bypass, and Editing.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mechanistic Studies of DNA Replication, Lesion Bypass, and Editing./
作者:	Raper, Austin Tyler.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	436 p.
附註:	Source: Dissertation Abstracts International, Volume: 80-04(E), Section: B.
Contained By:	Dissertation Abstracts International80-04B(E).
標題:	Biochemistry. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=11011022
ISBN:	9780438648814

Mechanistic Studies of DNA Replication, Lesion Bypass, and Editing.
Raper, Austin Tyler.

Mechanistic Studies of DNA Replication, Lesion Bypass, and Editing. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 436 p.

Source: Dissertation Abstracts International, Volume: 80-04(E), Section: B.

Thesis (Ph.D.)--The Ohio State University, 2018.

DNA acts as a molecular blueprint for life. Adenosine, cytidine, guanosine, and thymidine nucleotides serve as the building blocks of DNA and can be arranged in near-endless combinations. These unique sequences of DNA may encode genes that when expressed produce RNA, proteins, and enzymes responsible for executing diverse tasks necessary for biological existence. Accordingly, careful maintenance of the molecular integrity of DNA is paramount for the growth, development, and functioning of organisms. However, DNA is damaged upon reaction with pervasive chemicals generated by normal cellular metabolism or encountered through the environment. The resulting DNA lesions act as roadblocks to high-fidelity A- and B-family DNA polymerases responsible for replicating DNA in preparation for cell division which may lead to programmed cell death. Additionally, these lesions may fool the polymerase into making errors during DNA replication, leading to genetic mutations and cancer. Fortunately, the cell has evolved DNA damage tolerance as an emergency response to such lesions.

ISBN: 9780438648814Subjects--Topical Terms:

518028
Biochemistry.

Mechanistic Studies of DNA Replication, Lesion Bypass, and Editing.
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520 $a DNA acts as a molecular blueprint for life. Adenosine, cytidine, guanosine, and thymidine nucleotides serve as the building blocks of DNA and can be arranged in near-endless combinations. These unique sequences of DNA may encode genes that when expressed produce RNA, proteins, and enzymes responsible for executing diverse tasks necessary for biological existence. Accordingly, careful maintenance of the molecular integrity of DNA is paramount for the growth, development, and functioning of organisms. However, DNA is damaged upon reaction with pervasive chemicals generated by normal cellular metabolism or encountered through the environment. The resulting DNA lesions act as roadblocks to high-fidelity A- and B-family DNA polymerases responsible for replicating DNA in preparation for cell division which may lead to programmed cell death. Additionally, these lesions may fool the polymerase into making errors during DNA replication, leading to genetic mutations and cancer. Fortunately, the cell has evolved DNA damage tolerance as an emergency response to such lesions.
520 $a During DNA damage tolerance, a damage-stalled high-fidelity polymerase is substituted for a specialized Y-family polymerase, capable of bypassing the offending DNA lesion, for replication to continue. However, the ability of the specialized polymerase to bypass DNA lesions occurs at the expense of replication fidelity. Hence, tight regulation of polymerase exchange during DNA damage tolerance is imperative to ensure timely bypass of a lesion by the Y-family member, as well as prompt polymerase replacement by an A- or B-family member to limit DNA replication errors (i.e. mutations). Nevertheless, mistakes during DNA damage tolerance that evade DNA repair pathways are intimately connected to mutagenesis and may lead to cancer or numerous other genetic diseases. Until recently, making corrections to erroneous DNA sequences in the cell was prohibitively time-consuming, expensive, and laborious. However, the advent of clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated (Cas) proteins as a convenient technology for gene editing has opened the door for revolutionary cures to genetic diseases and state-of-the-art research into complex disease states.
520 $a Here I have investigated the functions of enzymes and associated cofactors critical for DNA replication, lesion bypass, and editing. Through pre-steady-state gel- and fluorescence-based kinetic techniques, as well as single-molecule fluorescence spectroscopy, I identified and characterized discrete steps of the kinetic mechanisms of these enzymes to better understand how they execute their unique activities, interact with protein partners, and potentially contribute to disease.
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