Skip Navigation

This Article
Right arrow Print PDF (752K)
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 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 arrowRequest Permissions
Citing Articles
Right arrowScopus Links
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Oleson, F. B.
Right arrow Articles by Lieberman, M. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Oleson, F. B.
Right arrow Articles by Lieberman, M. W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1979, Vol. 7, No. 5 1343-1362
© 1979

Articles

Distribution of DNA damage in chromatin and its relation to repair in human cells treated with 7-bromomethylbenz(a) anthracene1

Frederick B. Oleson2, Bonnie L Mitchell3, Anthony Dipple* and Michael W. Lieberman

Department of Pathology, Washington University School of Medicine St. Louis, MO 63110, USA *The Frederick Cancer Research Center Frederick, MD 21701, USA

Received August 15, 1979.

We have examined the relationship between the distribution of DNA damage and repair in chromatin from confluent human fibroblasts treated with the carcinogen 7-bromomethy lbenz (a)anthracene. Analysis of staphylococcal nuclease (SN)4 digestion kinetics and gel electrophoresis revealed that more total damage occurs in nucleosome core DNA (~80–85% of chromatin DNA) than in SN sensitive DNA (~15–20%). Furthermore, over a 24 hr period, damage is removed at about the same rate from these two regions. In contrast, virtually all of the nucleotides incorporated during repair synthesis are initially SN sensitive even when measured at 12 hr after damage. With time many repair-incorporated nucleotides become SN resistant and coelectrophorese with nucleosome core DNA. To explain these data we propose a model whereby excision repair occurs in both linker and core DNA, however, in core DNA the repair process induces conformational changes resulting in temporarily increased SN sensitivity; subsequently, rearrangement occurs and results in the re-establishment of native or near-native nucleosome conformation and SN resistance.

1This study was supported by NIH Grant CA 20513 and by the following companies: Brown and Williamson Tobacco Corp.; Larus and Brother Co., Inc.; Philip Morris, Inc.; Lorillard, a Division of Loews Theatres, Inc.; Liggett & Myers, Inc.; R.J. Reynolds Tobacco Co.; United States Tobacco Co.; and Tobacco Associates, Inc. Media and cells were provided by the Washington University Cancer Center (supported by NIH Grant CE 16217). Additional support was provided by NCI under contract NO1-CO-75380 with Litton Bionetics, Inc.

2Recipient of NIH Postdoctoral Fellowship CA 09118. Present address: Division of Medicine and Environmental Health, Monsanto Company, St. Louis, Mo. 63166.

3Recipient of a Cancer Research Fellowship from the Ladies Auxiliary to the Veterans of Foreign Wars.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




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.