ArticleMolecular and cellular biology2001
Heterozygous disruption of the TATA-binding protein gene in DT40 cells causes reduced cdc25B phosphatase expression and delayed mitosis.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- TATA-Box Binding Protein O-GlcNAcylation at T114 Regulates Formation of the B-TFIID Complex and Is Critical for Metabolic Gene Regulation.Molecular cell · 2020Article
- Article
- Elevated TATA-binding protein expression drives vascular endothelial growth factor expression in colon cancer.Oncotarget · 2017Article
- Relevance of HCN2-expressing human mesenchymal stem cells for the generation of biological pacemakers.Stem cell research & therapy · 2016Article
- Article
- A specific E3 ligase/deubiquitinase pair modulates TBP protein levels during muscle differentiation.eLife · 2015Article
- TBP-related factors: a paradigm of diversity in transcription initiation.Cell & bioscience · 2011Article
- Epidermal growth factor receptor 1 (EGFR1) and its variant EGFRvIII regulate TATA-binding protein expression through distinct pathways.Molecular and cellular biology · 2008Article
- Enhanced RNA polymerase III-dependent transcription is required for oncogenic transformation.The Journal of biological chemistry · 2008Article
- Variations in intracellular levels of TATA binding protein can affect specific genes by different mechanisms.Molecular and cellular biology · 2008Article
- TBP is differentially regulated by c-Jun N-terminal kinase 1 (JNK1) and JNK2 through Elk-1, controlling c-Jun expression and cell proliferation.Molecular and cellular biology · 2007Article
- Cell-specific nucleolar localization of TBP-related factor 2.Molecular biology of the cell · 2004Article
- Epidermal growth factor enhances cellular TATA binding protein levels and induces RNA polymerase I- and III-dependent gene activity.Molecular and cellular biology · 2004Article
- TATA-binding protein-like protein (TLP/TRF2/TLF) negatively regulates cell cycle progression and is required for the stress-mediated G(2) checkpoint.Molecular and cellular biology · 2003Article
- Increased expression of TATA-binding protein, the central transcription factor, can contribute to oncogenesis.Molecular and cellular biology · 2003Article
- The DT40 web site: sampling and connecting the genes of a B cell line.Nucleic acids research · 2002Article
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
TATA-binding protein (TBP) is a key general transcription factor required for transcription by all three nuclear RNA polymerases. Although it has been intensively analyzed in vitro and in Saccharomyces cerevisiae, in vivo studies of vertebrate TBP have been limited. We applied gene-targeting techniques using chicken DT40 cells to generate heterozygous cells with one copy of the TBP gene disrupted. Such TBP-heterozygous (TBP-Het) cells showed unexpected phenotypic abnormalities, resembling those of cells with delayed mitosis: a significantly lower growth rate, larger size, more G2/-M- than G1-phase cells, and a high proportion of sub-G1, presumably apoptotic, cells. Further evidence for delayed mitosis in TBP-Het cells was provided by the differential effects of several cell cycle-arresting drugs. To determine the cause of these defects, we first examined the status of cdc2 kinase, which regulates the G2/M transition, and unexpectedly observed more hyperphosphorylated, inactive cdc2 in TBP-Het cells. Providing an explanation for this, mRNA and protein levels of cdc25B, the trigger cdc2 phosphatase, were significantly and specifically reduced. These properties were all due to decreased TBP levels, as they could be rescued by expression of exogeneous TBP, including, in most but not all cases, a mutant form lacking the species-specific N-terminal domain. Our results indicate that small changes in TBP concentration can have profound effects on cell growth in vertebrate cells.
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