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PMID: 15494395 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

TDP1 overexpression in human cells counteracts DNA damage mediated by topoisomerases I and II.

The Journal of biological chemistry ·Vol. 279 ·No. 53 ·2004-12-31 ·Pages 55618-25

Barthelmes HU, Habermeyer M, Christensen MO, Mielke C, Interthal H, Pouliot JJ, Boege F, Marko D

Abstract

Tyrosyl DNA phosphodiesterase 1 (TDP1) is a repair enzyme that removes adducts, e.g. of topoisomerase I from the 3'-phosphate of DNA breaks. When expressed in human cells as biofluorescent chimera, TDP1 appeared more mobile than topoisomerase I, less accumulated in nucleoli, and not chromosome-bound at early mitosis. Upon exposure to camptothecin both proteins were cleared from nucleoli and rendered less mobile in the nucleoplasm. However, with TDP1 this happened much more slowly reflecting most likely the redistribution of nucleolar structures upon inhibition of rDNA transcription. Thus, a steady association of TDP1 with topoisomerase I seems unlikely, whereas its integration into repair complexes assembled subsequently to the stabilization of DNA.topoisomerase I intermediates is supported. Cells expressing GFP-tagged TDP1 > 100-fold in excess of endogenous TDP1 exhibited a significant reduction of DNA damage induced by the topoisomerase I poison camptothecin and could be selected by that drug. Surprisingly, DNA damage induced by the topoisomerase II poison VP-16 was also diminished to a similar extent, whereas DNA damage independent of topoisomerase I or II was not affected. Overexpression of the inactive mutant GFP-TDP1(H263A) at similar levels did not reduce DNA damage by camptothecin or VP-16. These observations confirm a requirement of active TDP1 for the repair of topoisomerase I-mediated DNA damage. Our data also suggest a role of TDP1 in the repair of DNA damage mediated by topoisomerase II, which is less clear. Since overexpression of TDP1 did not compromise cell proliferation, it could be a pleiotropic resistance mechanism in cancer therapy.

MeSH Terms
Bacterial Proteins/metabolism Binding Sites Blotting, Western Camptothecin/chemistry,pharmacology Cell Line Cell Line, Tumor Cell Nucleolus/metabolism Cell Nucleus/metabolism Cell Proliferation Cloning, Molecular DNA/metabolism DNA Damage DNA Topoisomerases, Type I/metabolism DNA Topoisomerases, Type II/metabolism DNA, Ribosomal/chemistry Etoposide/pharmacology Green Fluorescent Proteins/metabolism Humans Immunoblotting Luminescent Proteins/metabolism Methylnitronitrosoguanidine/pharmacology Microscopy, Fluorescence Mitosis Mutation Phosphoric Diester Hydrolases/metabolism,physiology Time Factors
Chemicals
Bacterial Proteins DNA, Ribosomal Luminescent Proteins yellow fluorescent protein, Bacteria Methylnitronitrosoguanidine Green Fluorescent Proteins Etoposide DNA Phosphoric Diester Hydrolases TDP1 protein, human tyrosyl-DNA phosphodiesterase DNA Topoisomerases, Type I DNA Topoisomerases, Type II Camptothecin
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Barthelmes Hans U
Institute of Clinical Chemistry and Laboratory Diagnostics, Heinrich-Heine-University, Medical School, Moorenstrasse 5, D-40225 Düsseldorf, Germany.
Habermeyer Michael
Christensen Morten O
Mielke Christian
Interthal Heidrun
Pouliot Jeffrey J
Boege Fritz
Marko Doris
Article Info
Journal
The Journal of biological chemistry
Abbr.
J Biol Chem
ISSN
0021-9258
Published
2004-12-31
Epub
2004-00-19
Pages
55618-25
Language
English
Region
United States
NLM ID
2985121R
Subset
IM
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