Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (257K) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (22)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Liu, J.
Right arrow Articles by Doetsch, P. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, J.
Right arrow Articles by Doetsch, P. W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, Vol 26, Issue 7 1707-1712, Copyright © 1998 by Oxford University Press

ARTICLES

Escherichia coli RNA and DNA polymerase bypass of dihydrouracil: mutagenic potential via transcription and replication

J Liu and PW Doetsch
Department of Biochemistry and Division of Cancer Biology, Emory University School of Medicine, Atlanta, GA 30322, USA.

Dihydrouracil (DHU) is a DNA base damage product produced in significant amounts by ionizing radiation damage to cytosine under anoxic conditions. DHU represents a model for pyrimidine base damage (ring saturation products) of the type recognized and repaired by Escherichia coli endonuclease III and its homologs in other species. We have built this lesion into synthetic oligonucleotides, with DHU placed at a single location downstream from an E.coli RNA polymerase promoter. This construct was used to determine the effect of DHU when encountered on a DNA template strand by either E.coli RNA or DNA polymerase (Klenow fragment). Single round transcription experiments or primer extension- type replication experiments were conducted in order to make a direct comparison between RNA and DNA polymerases with DHU placed within the same sequence context. Both DNA and RNA polymerase efficiently bypass DHU and insert adenine opposite this lesion. These results suggest that DHU is mutagenic with respect to both replication and transcription and have implications for DNA repair as well the routes leading to generation of mutant proteins in dividing and non-dividing cells.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
S. D. Kathe, G.-P. Shen, and S. S. Wallace
Single-Stranded Breaks in DNA but Not Oxidative DNA Base Damages Block Transcriptional Elongation by RNA Polymerase II in HeLa Cell Nuclear Extracts
J. Biol. Chem., April 30, 2004; 279(18): 18511 - 18520.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
A. Viswanathan, H. J. You, and P. W. Doetsch
Phenotypic Change Caused by Transcriptional Bypass of Uracil in Nondividing Cells
Science, April 2, 1999; 284(5411): 159 - 162.
[Abstract] [Full Text]

Home page
 J. Biol. Chem.Home page
A. Viswanathan and P. W. Doetsch
Effects of Nonbulky DNA Base Damages on Escherichia coli RNA Polymerase-mediated Elongation and Promoter Clearance
J. Biol. Chem., August 14, 1998; 273(33): 21276 - 21281.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.