Format

Send to

Choose Destination
Sci Rep. 2018 Mar 15;8(1):4630. doi: 10.1038/s41598-018-22879-5.

Zinc knuckle of TAF1 is a DNA binding module critical for TFIID promoter occupancy.

Author information

1
Department of Pharmacology, University of Washington, Seattle, WA, 98195, USA.
2
Howard Hughes Medical Institute, University of Washington, Box 357280, Seattle, WA, 98195, USA.
3
Department of Pharmacology, University of Washington, Seattle, WA, 98195, USA. nzheng@uw.edu.
4
Howard Hughes Medical Institute, University of Washington, Box 357280, Seattle, WA, 98195, USA. nzheng@uw.edu.
5
Department of Pharmacology, University of Washington, Seattle, WA, 98195, USA. ehwang@uw.edu.

Abstract

The general transcription factor IID (TFIID) is the first component of the preinitiation complex (PIC) to bind the core promoter of RNA polymerase II transcribed genes. Despite its critical role in protein-encoded gene expression, how TFIID engages promoter DNA remains elusive. We have previously revealed a winged-helix DNA-binding domain in the N-terminal region of the largest TFIID subunit, TAF1. Here, we report the identification of a second DNA-binding module in the C-terminal half of human TAF1, which is encoded by a previously uncharacterized conserved zinc knuckle domain. We show that the TAF1 zinc knuckle aids in the recruit of TFIID to endogenous promoters vital for cellular proliferation. Mutation of the TAF1 zinc knuckle with defects in DNA binding compromises promoter occupancy of TFIID, which leads to a decrease in transcription and cell viability. Together, our studies provide a foundation to understand how TAF1 plays a central role in TFIID promoter binding and regulation of transcription initiation.

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center