ArticleJournal of bacteriology1998
Stimulation of transcription by mutations affecting conserved regions of RNA polymerase II.
Article in Journal of bacteriology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- 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
- High-Resolution Phenotypic Landscape of the RNA Polymerase II Trigger Loop.PLoS genetics · 2016Article
- Basic mechanisms of RNA polymerase II activity and alteration of gene expression in Saccharomyces cerevisiae.Biochimica et biophysica acta · 2013Review
- Dissection of Pol II trigger loop function and Pol II activity-dependent control of start site selection in vivo.PLoS genetics · 2012Article
- Amino Acid Substitutions in the Caenorhabditis elegans RNA Polymerase II Large Subunit AMA-1/RPB-1 that Result in α-Amanitin Resistance and/or Reduced Function.G3 (Bethesda, Md.) · 2011Article
- RNA polymerase II trigger loop residues stabilize and position the incoming nucleotide triphosphate in transcription.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Article
- The RNA polymerase II trigger loop functions in substrate selection and is directly targeted by alpha-amanitin.Molecular cell · 2008Article
- Structural basis of transcription: role of the trigger loop in substrate specificity and catalysis.Cell · 2006Article
- Mutations in the Saccharomyces cerevisiae RPB1 gene conferring hypersensitivity to 6-azauracil.Genetics · 2006Article
- Structural perspective on mutations affecting the function of multisubunit RNA polymerases.Microbiology and molecular biology reviews : MMBR · 2006Review
- Functional interaction between TFIIB and the Rpb2 subunit of RNA polymerase II: implications for the mechanism of transcription initiation.Molecular and cellular biology · 2004Article
- Genetic interactions of DST1 in Saccharomyces cerevisiae suggest a role of TFIIS in the initiation-elongation transition.Genetics · 2004Article
- Functional interaction between Ssu72 and the Rpb2 subunit of RNA polymerase II in Saccharomyces cerevisiae.Molecular and cellular biology · 2000Article
- Transcription elongation factor SII.BioEssays : news and reviews in molecular, cellular and developmental biology · 2000Review
- Mechanism and regulation of transcriptional elongation by RNA polymerase II.Current opinion in cell biology · 1999Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations that increase the low-level transcription of the Saccharomyces cerevisiae HIS4 gene, which results from deletion of the genes encoding transcription factors BAS1, BAS2, and GCN4, were isolated previously in SIT1 (also known as RPO21, RPB1, and SUA8), the gene encoding the largest subunit of RNA polymerase II (RNAPII). Here we show that sit1 substitutions cluster in two conserved regions of the enzyme which form part of the active site. Six sit1 mutations, affect region F, a region that is involved in transcriptional elongation and in resistance to alpha-aminatin. Four sit1 substitutions lie in another region involved in transcriptional elongation, region D, which binds Mg2+ ions essential for RNA catalysis. One region D substitution is lethal unless suppressed by a substitution in region G and interacts genetically with PPR2, the gene encoding transcription elongation factor IIS. Some sit1 substitutions affect the selection of transcriptional start sites at the CYC1 promoter in a manner reminiscent of that of sua8 (sua stands for suppression of upstream ATG) mutations. Together with previous findings which indicate that regions D and G are in close proximity to the 3' end of the nascent transcript and that region F is involved in the translocation process, our results suggest that transcriptional activation by the sit1 mutations results from alteration of the RNAPII active center.
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