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Different forms of TFIIH for transcription and DNA repair: Holo-TFIIH and a nucleotide excision repairosome

  • Jesper Q. Svejstrup
  • , Zhigang Wang
  • , William J. Feave
  • , Xiahua Wu
  • , David A. Bushnell
  • , Thomas F. Donahue
  • , Errol C. Friedberg
  • , Roger D. Kornberg

Producción científica: Articlerevisión exhaustiva

249 Citas (Scopus)

Resumen

Yeast TFIIH that is active in transcription can be dissociated into three components: a 5-subunit core, the SSL2 gene product, and a complex of 47 kDa, 45 kDa, and 33 kDa polypeptides that possesses protein kinase activity directed towards the C-terminal repeat domain of RNA polymerase II. These three components can reconstitute fully functional TFIIH, and all three are required for transcription in vitro. By contrast, TFIIH that is highly active in nucleotide excision repair (NER) lacks the kinase complex and instead contains the products of all other genes known to be required for NER in yeast: RAD1, RAD2, RAD4, RAD10, and RAD14. This repairosome is not active in reconstituted transcription in vitro and is significantly more active than any of the constituent polypeptides in correcting defective repair in extracts from strains mutated in NER genes.

Idioma originalEnglish
Páginas (desde-hasta)21-28
Número de páginas8
PublicaciónCell
Volumen80
N.º1
DOI
EstadoPublished - ene 13 1995

Nota bibliográfica

Funding Information:
R. D. K. is the corresponding author for this study. We thank L. Prakash for anti-RAD14 antibodies and S. Bj6rklund and J. LaPointe for purified transcription factors. J, Q. S. was supported by a fellowship from the Danish Medical Research Council. W, J. F. was supported by a Medical Research Council of Canada Studentship. This work was supported by National Institutes of Health grants GM36659 to R. D. K., GM32263 to T. F. D., and CA12428 to E. C. F.

Financiación

R. D. K. is the corresponding author for this study. We thank L. Prakash for anti-RAD14 antibodies and S. Bj6rklund and J. LaPointe for purified transcription factors. J, Q. S. was supported by a fellowship from the Danish Medical Research Council. W, J. F. was supported by a Medical Research Council of Canada Studentship. This work was supported by National Institutes of Health grants GM36659 to R. D. K., GM32263 to T. F. D., and CA12428 to E. C. F.

FinanciadoresNúmero del financiador
National Institutes of Health (NIH)GM36659, CA12428
National Institute of General Medical SciencesR01GM032263
Sundhed og Sygdom, Det Frie Forskningsråd
Medical Research Council Canada

    ASJC Scopus subject areas

    • General Biochemistry, Genetics and Molecular Biology

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