ArticleBMC molecular biology2010
Regulation of TFIIIB during F9 cell differentiation.
Article in BMC molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Pooled it
- BDP1 as a biomarker in serous ovarian cancer.Cancer medicine · 2023Article
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- Brf1 loss and not overexpression disrupts tissues homeostasis in the intestine, liver and pancreas.Cell death and differentiation · 2019Article
- Differential Phosphorylation of RNA Polymerase III and the Initiation Factor TFIIIB in Saccharomyces cerevisiae.PloS one · 2015Article
- Nutrient/TOR-dependent regulation of RNA polymerase III controls tissue and organismal growth in Drosophila.The EMBO journal · 2012Article
- tRNA genes protect a reporter gene from epigenetic silencing in mouse cells.Cell cycle (Georgetown, Tex.) · 2011Article
- Different sequence signatures in the upstream regions of plant and animal tRNA genes shape distinct modes of regulation.Nucleic acids research · 2011Article
- Cell growth- and differentiation-dependent regulation of RNA polymerase III transcription.Cell cycle (Georgetown, Tex.) · 2010Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDifferentiation of F9 embryonal carcinoma (EC) cells into parietal endoderm (PE) provides a tractable model system for studying molecular events during early and inaccessible stages of murine development. PE formation is accompanied by extensive changes in gene expression both in vivo and in culture. One of the most dramatic is the ~10-fold decrease in transcriptional output by RNA polymerase (pol) III. This has been attributed to changes in activity of TFIIIB, a factor that is necessary and sufficient to recruit pol III to promoters. The goal of this study was to identify molecular changes that can account for the low activity of TFIIIB following F9 cell differentiation.
resultsThree essential subunits of TFIIIB decrease in abundance as F9 cells differentiate; these are Brf1 and Bdp1, which are pol III-specific, and TBP, which is also used by pols I and II. The decreased levels of Brf1 and Bdp1 proteins can be explained by reduced expression of the corresponding mRNAs. However, this is not the case for TBP, which is regulated post-transcriptionally. In proliferating cells, pol III transcription is stimulated by the proto-oncogene product c-Myc and the mitogen-activated protein kinase Erk, both of which bind to TFIIIB. However, c-Myc levels fall during differentiation and Erk becomes inactive through dephosphorylation. The diminished abundance of TFIIIB is therefore likely to be compounded by changes to these positive regulators that are required for its full activity. In addition, PE cells have elevated levels of the retinoblastoma protein RB, which is known to bind and repress TFIIIB.
conclusionThe low activity of TFIIIB in PE can be attributed to a combination of changes, any one of which could be sufficient to inhibit pol III transcription. Declining levels of essential TFIIIB subunits and of activators that are required for maximal TFIIIB activity are accompanied by an increase in a potent repressor of TFIIIB. These events provide fail-safe guarantees to ensure that pol III output is appropriate to the diminished metabolic requirements of terminally differentiated cells.
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