ArticlePLoS genetics2012
Dissection of Pol II trigger loop function and Pol II activity-dependent control of start site selection in vivo.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed.
- RNA polymerase inhibitors reveal active-site motions essential for the nucleotide addition cycle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Sub-2 Å cryo-EM structures of transcribing RNA polymerase II reveal critical roles of water molecules in catalysis.Molecular cell · 2026Article
- RNA polymerase inhibitors reveal active-site motions essential for the nucleotide-addition cycle.bioRxiv : the preprint server for biology · 2026Article
- Genetic dissection of transcription start site selection by RNA polymerase II in Saccharomyces cerevisiae.Genetics · 2026Article
- Important role in transcription start site selection for the RNA polymerase II-TFIIE-TFIIH interface in Saccharomyces cerevisiae.Genetics · 2026Article
- RNA polymerase II-TFIIE-TFIIH interface functions in transcription start site selection inbioRxiv : the preprint server for biology · 2025Article
- Genetic dissection of transcription start site selection by RNA Polymerase II inbioRxiv : the preprint server for biology · 2025Article
- mRNA initiation and termination are spatially coordinated.Science (New York, N.Y.) · 2025Article
- Widespread epistasis shapes RNA polymerase II active site function and evolution.Nature communications · 2025Article
- Inherent asymmetry of Rpd3S coordinates its nucleosome engagement and association with elongating RNA polymerase II.Nature structural & molecular biology · 2025Article
- RNA Polymerase II Activity Control of Gene Expression and Involvement in Disease.Journal of molecular biology · 2025Review
- Transcription start site scanning requires the fungi-specific hydrophobic loop of Tfb3.Nucleic acids research · 2024Article
- Article
- Higher-order epistasis within Pol II trigger loop haplotypes.bioRxiv : the preprint server for biology · 2024Article
- Structural basis of transcription: RNA polymerase II substrate binding and metal coordination using a free-electron laser.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Thiolutin has complex effects in vivo but is a direct inhibitor of RNA polymerase II in vitro.Nucleic acids research · 2024Article
- mRNA initiation and termination are spatially coordinated.bioRxiv : the preprint server for biology · 2024Article
- Quantitative analysis of transcription start site selection reveals control by DNA sequence, RNA polymerase II activity and NTP levels.Nature structural & molecular biology · 2024Article
- Flap endonuclease Rad27 cleaves the RNA of R-loop structures to suppress telomere recombination.Nucleic acids research · 2023Article
- Plant terminators: the unsung heroes of gene expression.Journal of experimental botany · 2023Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Structural and biochemical studies have revealed the importance of a conserved, mobile domain of RNA Polymerase II (Pol II), the Trigger Loop (TL), in substrate selection and catalysis. The relative contributions of different residues within the TL to Pol II function and how Pol II activity defects correlate with gene expression alteration in vivo are unknown. Using Saccharomyces cerevisiae Pol II as a model, we uncover complex genetic relationships between mutated TL residues by combinatorial analysis of multiply substituted TL variants. We show that in vitro biochemical activity is highly predictive of in vivo transcription phenotypes, suggesting direct relationships between phenotypes and Pol II activity. Interestingly, while multiple TL residues function together to promote proper transcription, individual residues can be separated into distinct functional classes likely relevant to the TL mechanism. In vivo, Pol II activity defects disrupt regulation of the GTP-sensitive IMD2 gene, explaining sensitivities to GTP-production inhibitors, but contrasting with commonly cited models for this sensitivity in the literature. Our data provide support for an existing model whereby Pol II transcriptional activity provides a proxy for direct sensing of NTP levels in vivo leading to IMD2 activation. Finally, we connect Pol II activity to transcription start site selection in vivo, implicating the Pol II active site and transcription itself as a driver for start site scanning, contravening current models for this process.
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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.