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Strand specific DNA repair in UV irr...

Lommel, Lori.

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Strand specific DNA repair in UV irradiated human and Chinese hamster cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Strand specific DNA repair in UV irradiated human and Chinese hamster cells./
Author:	Lommel, Lori.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 1993,
Description:	192 p.
Notes:	Source: Dissertation Abstracts International, Volume: 54-05, Section: B, page: 2363.
Contained By:	Dissertation Abstracts International54-05B.
Subject:	Molecular biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9326512

Strand specific DNA repair in UV irradiated human and Chinese hamster cells.
Lommel, Lori.

Strand specific DNA repair in UV irradiated human and Chinese hamster cells. - Ann Arbor : ProQuest Dissertations & Theses, 1993 - 192 p.

Source: Dissertation Abstracts International, Volume: 54-05, Section: B, page: 2363.

Thesis (Ph.D.)--Stanford University, 1993.

My goals were to investigate the mechanism and biological significance of preferential repair of UV-induced cyclobutane pyrimidine dimers (CPD) in the transcribed strand of active genes relative to the nontranscribed strand, and to determine the cell cycle-dependent nature of this strand bias in repair in mammalian cells. I analyzed the repair of CPDs in each strand of the dihydrofolate reductase gene, (1) in several human and Chinese hamster ovary (CHO) cell mutants that differ from each other in their degree of UV sensitivity and DNA repair capacity, and (2) in cell cycle selected subpopulations of a repair proficient human cell line. To assay repair in the mutants I used a method to quantitate the CPD content in specific restriction fragments. To assay repair through the cell cycle, I first sorted the cells into subpopulations with G1; early, middle, and late S; and G2/M phase DNA contents. My analyses of the human and CHO cell mutants demonstrated a consistent correlation between the degree of UV sensitivity and the proficiency of CPD removal from the transcribed strand of an active gene. This is strong evidence that the removal of CPDs is essential, and it clears up some misleading conclusions, regarding the biological importance of the CPD, that were reached by others based upon their analyses of repair in the genome overall. In my analysis of repair during the cell cycle the induction of CPDs was similar in all the subpopulations, indicating that the DNA is similarly susceptible to the formation of CPDs in all phases of the cell cycle. Furthermore, there was essentially no strand bias in CPD induction. However, within 4 hours after UV, there were significantly fewer lesions remaining in the transcribed strand than in the non-transcribed strand in each of the subpopulations, indicating that preferential repair of the transcribed strand occurs in all phases. Furthermore, the magnitude of the strand bias was relatively constant through the cell cycle.Subjects--Topical Terms:

517296
Molecular biology.

Strand specific DNA repair in UV irradiated human and Chinese hamster cells.
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035 $a (MiAaPQ)AAI9326512
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100 1 $a Lommel, Lori. $3 3285239
245 1 0 $a Strand specific DNA repair in UV irradiated human and Chinese hamster cells.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 1993
300 $a 192 p.
500 $a Source: Dissertation Abstracts International, Volume: 54-05, Section: B, page: 2363.
500 $a Adviser: Philip C. Hanawalt.
502 $a Thesis (Ph.D.)--Stanford University, 1993.
520 $a My goals were to investigate the mechanism and biological significance of preferential repair of UV-induced cyclobutane pyrimidine dimers (CPD) in the transcribed strand of active genes relative to the nontranscribed strand, and to determine the cell cycle-dependent nature of this strand bias in repair in mammalian cells. I analyzed the repair of CPDs in each strand of the dihydrofolate reductase gene, (1) in several human and Chinese hamster ovary (CHO) cell mutants that differ from each other in their degree of UV sensitivity and DNA repair capacity, and (2) in cell cycle selected subpopulations of a repair proficient human cell line. To assay repair in the mutants I used a method to quantitate the CPD content in specific restriction fragments. To assay repair through the cell cycle, I first sorted the cells into subpopulations with G1; early, middle, and late S; and G2/M phase DNA contents. My analyses of the human and CHO cell mutants demonstrated a consistent correlation between the degree of UV sensitivity and the proficiency of CPD removal from the transcribed strand of an active gene. This is strong evidence that the removal of CPDs is essential, and it clears up some misleading conclusions, regarding the biological importance of the CPD, that were reached by others based upon their analyses of repair in the genome overall. In my analysis of repair during the cell cycle the induction of CPDs was similar in all the subpopulations, indicating that the DNA is similarly susceptible to the formation of CPDs in all phases of the cell cycle. Furthermore, there was essentially no strand bias in CPD induction. However, within 4 hours after UV, there were significantly fewer lesions remaining in the transcribed strand than in the non-transcribed strand in each of the subpopulations, indicating that preferential repair of the transcribed strand occurs in all phases. Furthermore, the magnitude of the strand bias was relatively constant through the cell cycle.
590 $a School code: 0212.
650 4 $a Molecular biology. $3 517296
650 4 $a Medical imaging. $3 3172799
690 $a 0307
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710 2 $a Stanford University. $3 754827
773 0 $t Dissertation Abstracts International $g 54-05B.
790 $a 0212
791 $a Ph.D.
792 $a 1993
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9326512