TFIIIB placement on a yeast U6 RNA gene in vivo is directed primarily by TFIIIC rather than by sequence-specific DNA contacts
Author(s) -
Valerie L. Gerlach,
Simon K. Whitehall,
E. Peter Geiduschek,
David A. Brow
Publication year - 1995
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.15.3.1455
Subject(s) - rna polymerase iii , biology , upstream activating sequence , tata box , genetics , chromatin , transcription (linguistics) , microbiology and biotechnology , transcription factor , rna , gene , promoter , enhancer , rna polymerase , gene expression , linguistics , philosophy
The Saccharomyces cerevisiae U6 RNA gene (SNR6), which is transcribed by RNA polymerase III, has an unusual combination of promoter elements: an upstream TATA box, an intragenic A block, and a downstream B block. In tRNA genes, the A and B blocks are binding sites for the transcription initiation factor TFIIIC, which positions TFIIIB a fixed distance upstream of the A block. However, in vitro transcription of SNR6 with purified components requires neither TFIIIC nor the A and B blocks, presumably because TFIIIB recognizes the upstream sequences directly. Here we demonstrate that TFIIIB placement on SNR6 in vivo is directed primarily by the TFIIIC-binding elements rather than by upstream sequences. We show that the A block is a stronger start site determinant than the upstream sequences when the two are uncoupled by an insertion mutation. Furthermore, while TFIIIC-independent in vitro transcription of SNR6 is highly sensitive to TATA box point mutations, in vivo initiation on SNR6 is only marginally sensitive to such mutations unless the A block is mutated. Intriguingly, a deletion downstream of the U6 RNA coding region that reduces A-to-B block spacing also increases in vivo dependence on the TATA box. Moreover, this deletion results in the appearance of micrococcal nuclease-hypersensitive sites in the TFIIIB chromatin footprint, indicating that TFIIIB binding is disrupted by a mutation 150 bp distant. This and additional chromatin footprinting data suggest that SNR6 is assembled into a nucleoprotein complex that facilitates the TFIIIC-dependent binding of TFIIIB.
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