Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (551 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A conserved A-T rich sequence which is contained in promoters for RNA polymerase II. The segment is seven base pairs long and the nucleotides most commonly found are tataaaa.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Box, TATA; Hogness Box; Box, Hogness.
Where it fits in the MeSH classification
- Broader topics
- Promoter Regions, Genetic
Related concepts
- Tataaaa
Research landscape
PubMed indexes 3,263 records tagged with the MeSH heading “TATA Box” (counts retrieved 2026-10-29). 75 of them (2.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,189 records.
Reviews account for 134 records (4.1%) and meta-analyses for 0. Randomized controlled trials number 0 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,189 |
| 2000-2009 | 729 |
| 2010-2019 | 270 |
| 2020 onward | 75 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 134 | 4.1% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "TATA Box"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Transcriptional and structural impact of TATA-initiation site spacing in mammalian core promoters | 2006 | Research article Design not recorded in structured metadata | 93 | cc by PMID 16916456 · DOI · PMC1779604 |
| Quantitative imaging of transcription in living Drosophila embryos reveals the impact of core promoter motifs on promoter state dynamics | 2021 | Research article Design not recorded in structured metadata | 84 | cc by PMID 34301936 · DOI · PMC8302612 |
| Targeted PMP22 TATA-box editing by CRISPR/Cas9 reduces demyelinating neuropathy of Charcot-Marie-Tooth disease type 1A in mice | 2020 | Research article Design not recorded in structured metadata | 53 | cc by PMID 31713617 · DOI · PMC7145652 |
Transcriptional and structural impact of TATA-initiation site spacing in mammalian core promoters [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThe TATA box, one of the most well studied core promoter elements, is associated with induced, context-specific expression.
- Closing excerpt
- The coupling of spacing to tissue specificity at the transcriptome level provides important clues as to the function of core promoters and the choice of TSS by the pre-initiation complex.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (250 words)
BackgroundThe TATA box, one of the most well studied core promoter elements, is associated with induced, context-specific expression. The lack of precise transcription start site (TSS) locations linked with expression information has impeded genome-wide characterization of the interaction between TATA and the pre-initiation complex.ResultsUsing a comprehensive set of 5.66 x 10(6) sequenced 5' cDNA ends from diverse tissues mapped to the mouse genome, we found that the TATA-TSS distance is correlated with the tissue specificity of the downstream transcript. To achieve tissue-specific regulation, the TATA box position relative to the TSS is constrained to a narrow window (-32 to -29), where positions -31 and -30 are the optimal positions for achieving high tissue specificity. Slightly larger spacings can be accommodated only when there is no optimally spaced initiation signal; in contrast, the TATA box like motifs found downstream of position -28 are generally nonfunctional. The strength of the TATA binding protein-DNA interaction plays a subordinate role to spacing in terms of tissue specificity. Furthermore, promoters with different TATA-TSS spacings have distinct features in terms of consensus sequence around the initiation site and distribution of alternative TSSs. Unexpectedly, promoters that have two dominant, consecutive TSSs are TATA depleted and have a novel GGG initiation site consensus.ConclusionIn this report we present the most comprehensive characterization of TATA-TSS spacing and functionality to date. The coupling of spacing to tissue specificity at the transcriptome level provides important clues as to the function of core promoters and the choice of TSS by the pre-initiation complex.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 16916456 · DOI · PMC1779604
Quantitative imaging of transcription in living Drosophila embryos reveals the impact of core promoter motifs on promoter state dynamics [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Genes are expressed in stochastic transcriptional bursts linked to alternating active and inactive promoter states.
- Closing excerpt
- Overall, our results provide a rationale for promoter switching during zygotic genome activation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (152 words)
Genes are expressed in stochastic transcriptional bursts linked to alternating active and inactive promoter states. A major challenge in transcription is understanding how promoter composition dictates bursting, particularly in multicellular organisms. We investigate two key Drosophila developmental promoter motifs, the TATA box (TATA) and the Initiator (INR). Using live imaging in Drosophila embryos and new computational methods, we demonstrate that bursting occurs on multiple timescales ranging from seconds to minutes. TATA-containing promoters and INR-containing promoters exhibit distinct dynamics, with one or two separate rate-limiting steps respectively. A TATA box is associated with long active states, high rates of polymerase initiation, and short-lived, infrequent inactive states. In contrast, the INR motif leads to two inactive states, one of which relates to promoter-proximal polymerase pausing. Surprisingly, the model suggests pausing is not obligatory, but occurs stochastically for a subset of polymerases. Overall, our results provide a rationale for promoter switching during zygotic genome activation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34301936 · DOI · PMC8302612
Targeted PMP22 TATA-box editing by CRISPR/Cas9 reduces demyelinating neuropathy of Charcot-Marie-Tooth disease type 1A in mice [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Charcot-Marie-Tooth 1A (CMT1A) is the most common inherited neuropathy without a known therapy, which is caused by a 1.
- Closing excerpt
- Collectively, our data present a proof-of-concept that CRISPR/Cas9-mediated targeting of TATA-box can be utilized to treat CMT1A.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Charcot-Marie-Tooth 1A (CMT1A) is the most common inherited neuropathy without a known therapy, which is caused by a 1.4 Mb duplication on human chromosome 17, which includes the gene encoding the peripheral myelin protein of 22 kDa (PMP22). Overexpressed PMP22 protein from its gene duplication is thought to cause demyelination and subsequently axonal degeneration in the peripheral nervous system (PNS). Here, we targeted TATA-box of human PMP22 promoter to normalize overexpressed PMP22 level in C22 mice, a mouse model of CMT1A harboring multiple copies of human PMP22. Direct local intraneural delivery of CRISPR/Cas9 designed to target TATA-box of PMP22 before the onset of disease, downregulates gene expression of PMP22 and preserves both myelin and axons. Notably, the same approach was effective in partial rescue of demyelination even after the onset of disease. Collectively, our data present a proof-of-concept that CRISPR/Cas9-mediated targeting of TATA-box can be utilized to treat CMT1A.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31713617 · DOI · PMC7145652
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Sp1: emerging roles--beyond constitutive activation of TATA-less housekeeping genes [4]
- Research article TATA-binding protein is a classless factor [5]
- Research article Regulation of gene expression by TBP-associated proteins [6]
- Research article Three in one and one in three: it all depends on TBP [7]
- Research article Eukaryotic coactivators associated with the TATA box binding protein [8]
- Research article Mechanisms of transcriptional activation in vivo: two steps forward [9]
References
- Ponjavic J, Lenhard B, Kai C, Kawai J, Carninci P, Hayashizaki Y, et al.. Transcriptional and structural impact of TATA-initiation site spacing in mammalian core promoters. . 2006. PMID 16916456 · DOI · PMC1779604
- Pimmett VL, Dejean M, Fernandez C, Trullo A, Bertrand E, Radulescu O, et al.. Quantitative imaging of transcription in living Drosophila embryos reveals the impact of core promoter motifs on promoter state dynamics. . 2021. PMID 34301936 · DOI · PMC8302612
- Lee JS, Lee JY, Song DW, Bae HS, Doo HM, Yu HS, et al.. Targeted PMP22 TATA-box editing by CRISPR/Cas9 reduces demyelinating neuropathy of Charcot-Marie-Tooth disease type 1A in mice. . 2020. PMID 31713617 · DOI · PMC7145652
- Wierstra I. Sp1: emerging roles--beyond constitutive activation of TATA-less housekeeping genes. Biochem Biophys Res Commun. 2008. PMID 18364237 · DOI
- Sharp PA. TATA-binding protein is a classless factor. Cell. 1992. PMID 1547484 · DOI
- Lee TI, Young RA. Regulation of gene expression by TBP-associated proteins. Genes Dev. 1998. PMID 9585500 · DOI
- Rigby PW. Three in one and one in three: it all depends on TBP. Cell. 1993. PMID 8422684 · DOI
- Gill G, Tjian R. Eukaryotic coactivators associated with the TATA box binding protein. Curr Opin Genet Dev. 1992. PMID 1638117 · DOI
- Stargell LA, Struhl K. Mechanisms of transcriptional activation in vivo: two steps forward. Trends Genet. 1996. PMID 8783941 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.