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TATA binding protein discriminates between different lesions on DNA, resulting in a transcription decrease

F Coin1, P Frit, B Viollet

  • 1Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, F-67404 Illkirch Cedex, Université Louis Pasteur, Strasbourg, France.

Molecular and Cellular Biology
|June 25, 1998
PubMed
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General transcription factor TFIIH recognizes various DNA lesions, while TATA binding protein (TBP)-TFIID selectively targets DNA damage causing kinks, impacting transcription inhibition rates.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Basal transcription factors play a crucial role in DNA damage recognition.
  • Different transcription factors exhibit varying mechanisms for detecting DNA damage.
  • Understanding these mechanisms is key to comprehending cellular responses to genotoxic stress.

Purpose of the Study:

  • To investigate the differential DNA damage recognition mechanisms of transcription factors TFIIH and TBP-TFIID.
  • To elucidate the specific types of DNA lesions recognized by TBP-TFIID.
  • To correlate DNA damage recognition with transcription inhibition rates.

Main Methods:

  • Transcription-competition assays
  • Nitrocellulose filter binding assays

Related Experiment Videos

  • DNase I footprinting assays to map protein-DNA interactions

    • Main Results:

    • TFIIH recognizes a broad range of DNA lesions repairable by nucleotide excision repair (NER).
    • TBP-TFIID exhibits selectivity, recognizing DNA damage that induces kinked structures, similar to TATA box binding.
    • DNase I footprinting confirmed TBP protection patterns at promoter sites and cisplatin-induced cross-links.

    Conclusions:

    • TFIIH and TBP-TFIID employ distinct DNA damage recognition strategies.
    • TBP-TFIID's selectivity for kinked DNA structures influences transcription inhibition.
    • These findings offer insights into differential transcription inhibition rates following DNA damage.