ArticlePloS one2010
Single cell analysis of transcriptional activation dynamics.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023Review
- Studying DNA Double-Strand Break Repair: An Ever-Growing Toolbox.Frontiers in molecular biosciences · 2020Review
- PML is recruited to heterochromatin during S phase and represses DAXX-mediated histone H3.3 chromatin assembly.Journal of cell science · 2019Article
- NELF-E is recruited to DNA double-strand break sites to promote transcriptional repression and repair.EMBO reports · 2017Article
- HJURP interaction with the condensin II complex during G1 promotes CENP-A deposition.Molecular biology of the cell · 2017Article
- RNase P protein subunit Rpp29 represses histone H3.3 nucleosome deposition.Molecular biology of the cell · 2016Article
- Mechanistic analysis of the role of bromodomain-containing protein 4 (BRD4) in BRD4-NUT oncoprotein-induced transcriptional activation.The Journal of biological chemistry · 2015Article
- Regulation of RNA polymerase II activation by histone acetylation in single living cells.Nature · 2014Article
- Seeing is believing: visualizing transcriptional dynamics in single cells.Journal of cellular physiology · 2014Review
- Novel method for site-specific induction of oxidative DNA damage reveals differences in recruitment of repair proteins to heterochromatin and euchromatin.Nucleic acids research · 2014Article
- RNA imaging in living cells - methods and applications.RNA biology · 2014Review
- Pin1 promotes histone H1 dephosphorylation and stabilizes its binding to chromatin.The Journal of cell biology · 2013Article
- Single cell analysis of RNA-mediated histone H3.3 recruitment to a cytomegalovirus promoter-regulated transcription site.The Journal of biological chemistry · 2013Article
- Zooming in on single active genes in living mammalian cells.Histochemistry and cell biology · 2013Review
- The dynamics of HCF-1 modulation of herpes simplex virus chromatin during initiation of infection.Viruses · 2013Review
- Sp100A promotes chromatin decondensation at a cytomegalovirus-promoter-regulated transcription site.Molecular biology of the cell · 2013Article
- The Epstein-Barr virus nuclear antigen-1 reprograms transcription by mimicry of high mobility group A proteins.Nucleic acids research · 2013Article
- ATRX: the case of a peculiar chromatin remodeler.Epigenetics · 2013Review
- Single-cell analysis of Daxx and ATRX-dependent transcriptional repression.Journal of cell science · 2012Article
- A combination of H2A.Z and H4 acetylation recruits Brd2 to chromatin during transcriptional activation.PLoS genetics · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGene activation is thought to occur through a series of temporally defined regulatory steps. However, this process has not been completely evaluated in single living mammalian cells. METHODOLOGY/PRINCIPAL
findingsTo investigate the timing and coordination of gene activation events, we tracked the recruitment of GCN5 (histone acetyltransferase), RNA polymerase II, Brd2 and Brd4 (acetyl-lysine binding proteins), in relation to a VP16-transcriptional activator, to a transcription site that can be visualized in single living cells. All accumulated rapidly with the VP16 activator as did the transcribed RNA. RNA was also detected at significantly more transcription sites in cells expressing the VP16-activator compared to a p53-activator. After alpha-amanitin pre-treatment, the VP16-activator, GCN5, and Brd2 are still recruited to the transcription site but the chromatin does not decondense. CONCLUSIONS/SIGNIFICANCE: This study demonstrates that a strong activator can rapidly overcome the condensed chromatin structure of an inactive transcription site and supercede the expected requirement for regulatory events to proceed in a temporally defined order. Additionally, activator strength determines the number of cells in which transcription is induced as well as the extent of chromatin decondensation. As chromatin decondensation is significantly reduced after alpha-amanitin pre-treatment, despite the recruitment of transcriptional activation factors, this provides further evidence that transcription drives large-scale chromatin decondensation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.