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At least 307 records · Page 17Linked to original sources
PubMed2001

TATA box occupancy in the SV40 transcription elongation complex.

In order to gain insight into requirements for template activation and commitment in mammalian transcription, TATA site occupancy was measured in native SV40 viral transcription complexes that were in the process of transcription elongation at the time of cell lysis. This was accomplished by quantifying resistance to restriction enzyme digestion of transcription complexes in nuclear lysate. The rate of cleavage at the TATA site of the late gene in the native complex was slower than that of a bare DNA control, both for wild-type virus and for a virus containing a TATA consensus sequence. These results suggest that the TATA site in the transcription elongation complex in vivo is occupied with transcription factor TBP/TFIID. When considered in light of previous work, these findings support a model in which transcription activation involves reinitiation from a promoter that contains both activator and TFIID bound in a stable complex.

Cell Line↗
PubMed1993

The DNA-binding subunit of human transcription factor IID can interact with the TATA box as a multimer.

Transcription initiation from eukaryotic protein-coding genes is a complex process that minimally requires RNA polymerase (pol) II (B) and at least seven general transcription factors. The 38-kDa subunit (TBP) of the human general transcription factor TFIID recognizes the TATA sequence element and initiates the assembly of the other general transcription factors and RNA pol II. It is believed, based on experiments with yeast recombinant protein, that TBP binds as a monomer to DNA. Using purified recombinant human TBP protein we find that TBP interacts with the TATA element as both a monomer and a dimer. The multimeric binding of TBP to DNA revealed by this study has important implications for the role of TBP in transcription initiation and suggests novel mechanisms whereby other transcription factors may interact with a RNA pol II preinitiation complex.

Base Sequence↗
PubMed1997

Transcription reinitiation rate: a special role for the TATA box.

Promoters need to specify both the timing of transcriptional induction and the amount of transcript synthesized. In order to explore each of these effects separately, in vitro assays for the level of active preinitiation complex formation and for the rate of continuous RNA production were done. The effects were found to be influenced differently by different promoter elements. A consensus TATA element had a very strong effect on the rate of continuous RNA production, whereas two types of activators were important primarily in forming active transcription preinitiation complexes. Consensus TATA promoters exhibited high rates of continuous transcription; they assembled active preinitiation transcription complexes slowly but then produced transcripts continuously at an approximately fivefold-higher rate. Initiator-containing TATA-less promoters produced continuous transcripts slowly. Point mutations in the TATA element led to lower levels of transcription by reducing the number of preinitiation complexes and amplifying this reduction by lowering the apparent reinitiation rate. The results allow understanding of the sequence diversity of promoter elements in terms of specifying separate controls over the sensitivity of gene induction and over the strength of the induced promoter.

Cell-Free System↗
PubMed1995

Overlapping initiator and TATA box functions in the basal core promoter of hepatitis B virus.

The regulation of transcription of the hepatitis B virus core promoter is an important event in the viral life cycle. Two messages, precore and pregenomic RNAs, that are initiated 30 nucleotides apart are produced by the core promoter. Precore RNA encodes nucleocapsid protein and pregenomic RNA core and polymerase. The latter transcript also serves as a template for viral genome replication via reverse transcription. We have previously defined a basal core promoter, which contains four TA-rich sequences (TA1 through TA4) but no canonical TATA element, that can direct transcription of both messages. In this study, we demonstrated that a stretch of 15 nucleotides containing TA4 is sufficient to direct precise initiation of both precore and pregenomic transcripts. This sequence can function as both an initiator and a TATA element. Mutational analysis further revealed that sequences essential for either function are colocalized. The significance of this finding with respect to the basal transcription mechanism and regulation of viral gene expression is discussed.

Base Sequence↗
PubMed1994

Inhibition by insulin of protein kinase A-induced transcription of the phosphoenolpyruvate carboxykinase gene. Mediation by the activation domain of cAMP response element-binding protein (CREB) and factors bound to the TATA box.

The minimal promoter/transcription factor requirements for induction of phosphoenolpyruvate carboxykinase (PEPCK) transcription by cAMP-activated protein kinase A (PKA) and inhibition of this induction by insulin were investigated. H4 hepatoma cells were treated with or without insulin following cotransfection with chloramphenicol acetyltransferase reporter genes and expression vectors coding for the cAMP response element-binding protein (CREB) activation domain fused to the GAL4 DNA binding domain (CRG) and the catalytic subunit of PKA. Mutation of the PEPCK CRE to a GAL4 binding site (G4-PEPCK) within the fully responsive PEPCK promoter (-600/+69) made induction by PKA dependent upon cotransfection of CRG and this induction by CRG+PKA was inhibited by insulin. Mutation of the insulin regulatory sequence (delta IRS-G4-PEPCK) did not prevent induction by cAMP or inhibition by insulin. Fusion of GAL4 binding sites to the PEPCK TATA region (-40/+1, G4-PT) allowed induction by CRG+PKA and inhibition by insulin. However, inhibition by insulin was not observed when the CREB activation domain in CRG was replaced with the activation domain of VP16 (G4-VP16) or when the PEPCK TATA region was replaced with TATA regions from other genes. Our results indicate that the minimal requirements for induction of PEPCK by PKA and inhibition by insulin include: 1) the CREB activation domain, 2) the PEPCK TATA sequence, and 3) insulin-responsive hepatoma cells. These data suggest that specific factors interacting with both the PEPCK TATA region and the CREB activation domain are required for insulin inhibition of PKA-induced transcription.

Animals↗