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Mol Cell Biol, July 1998, p. 3907-3914, Vol. 18, No. 7
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

TATA Binding Protein Discriminates between Different Lesions on DNA, Resulting in a Transcription Decrease

Frédéric Coin,1 Philippe Frit,2 Benoit Viollet,1 Bernard Salles,2 and Jean-Marc Egly1 *

Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, F-67404 Illkirch Cedex, Université Louis Pasteur, Strasbourg,1 and Institut de Pharmacologie et de Biologie Structurale, CNRS, 31077 Toulouse Cedex,2 France

Received 8 January 1998/Returned for modification 23 February 1998/Accepted 24 April 1998

DNA damage recognition by basal transcription factors follows different mechanisms. Using transcription-competition, nitrocellulose filter binding, and DNase I footprinting assays, we show that, although the general transcription factor TFIIH is able to target any kind of lesion which can be repaired by the nucleotide excision repair pathway, TATA binding protein (TBP)-TFIID is more selective in damage recognition. Only genotoxic agents which are able to induce kinked DNA structures similar to the one for the TATA box in its TBP complex are recognized. Indeed, DNase I footprinting patterns reveal that TBP protects equally 4 nucleotides upstream and 6 nucleotides downstream from the A-T (at position -29 of the noncoding strand) of the adenovirus major late promoter and from the G-G of a cisplatin-induced 1,2-d(GpG) cross-link. Together, our results may partially explain differences in transcription inhibition rates following DNA damage.

* Corresponding author. Mailing address: Institut de Génétique et de Biologie Moléculaire et Cellulaire, BP 163, F-67404 Illkirch Cedex, Université Louis Pasteur, Strasbourg, France. Phone: 33 (03)88 65 34 47. Fax: 33 (03)88 65 32 01. E-mail: egly{at}igbmc.u-strasbg.fr.

Mol Cell Biol, July 1998, p. 3907-3914, Vol. 18, No. 7
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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