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.
Institut de Génétique et de
Biologie Moléculaire et Cellulaire,
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.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|