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Mol Cell Biol, July 1998, p. 4023-4031, Vol. 18, No. 7
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

DA-Complex Assembly Activity Required for VP16C Transcriptional Activation

Naoko Kobayashi,1 Peter J. Horn,2 Susan M. Sullivan,2 Steven J. Triezenberg,2 Thomas G. Boyer,1 and Arnold J. Berk1 *

Department of Microbiology and Molecular Genetics, Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California 90095-1570,1 and Department of Biochemistry, Michigan State University, East Lansing, Michigan 48824-13192

Received 6 March 1998/Returned for modification 31 March 1998/Accepted 15 April 1998

One class of transcriptional activation domains stimulates the concerted binding of TFIIA and TFIID to promoter DNA. To test whether this DA-complex assembly activity contributes significantly to the overall mechanism of activation in vivo, we analyzed mutants of the 38-amino-acid residue VP16C activation subdomain from herpes simplex virus. An excellent correlation was observed between the in vivo activation function of these mutants and their in vitro DA-complex assembly activity. Mutants severely defective for in vivo activation also showed reduced in vitro binding to native TFIIA. No significant correlation between in vivo activation function and in vitro binding to human TATA binding protein, human TFIIB, or Drosophila melanogaster TAFII40 was observed for this set of VP16C mutants. These results argue that the ability of VP16C to increase the rate and extent of DA-complex assembly makes a significant contribution to the overall mechanism of transcriptional activation in vivo.

* Corresponding author. Mailing address: Molecular Biology Institute, UCLA, Los Angeles, CA 90095-1570. Phone: (310) 206-6298. Fax: (310) 206-7286. E-mail: berk{at}mbi.ucla.edu.

Mol Cell Biol, July 1998, p. 4023-4031, Vol. 18, No. 7
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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