1. Distinction and relationship between elongation rate and processivity of RNA polymerase II in vivo.
- Author
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Mason PB and Struhl K
- Subjects
- Antibiotics, Antineoplastic pharmacology, Antimetabolites pharmacology, Chromatin metabolism, Mutation genetics, Mycophenolic Acid pharmacology, Nuclear Proteins genetics, Nuclear Proteins metabolism, Protein Kinases genetics, Protein Kinases metabolism, Protein Subunits chemistry, Protein Subunits genetics, Protein Subunits metabolism, Saccharomyces cerevisiae metabolism, Saccharomyces cerevisiae Proteins genetics, Saccharomyces cerevisiae Proteins metabolism, Transcription Initiation Site, Transcriptional Elongation Factors genetics, Transcriptional Elongation Factors metabolism, Uracil metabolism, Uracil pharmacology, Gene Expression Regulation, Fungal, Peptide Chain Elongation, Translational, RNA Polymerase II genetics, RNA Polymerase II metabolism, Saccharomyces cerevisiae genetics, Transcription, Genetic physiology, Uracil analogs & derivatives
- Abstract
A number of proteins and drugs have been implicated in the process of transcriptional elongation by RNA polymerase (Pol) II, but the factors that govern the elongation rate (nucleotide additions per min) and processivity (nucleotide additions per initiation event) in vivo are poorly understood. Here, we show that a mutation in the Rpb2 subunit of Pol II reduces both the elongation rate and processivity in vivo. In contrast, none of the putative elongation factors tested affect the elongation rate, although mutations in the THO complex and in Spt4 significantly reduce processivity. The drugs 6-azauracil and mycophenolic acid reduce both the elongation rate and processivity, and this processivity defect is aggravated by mutations in Spt4, TFIIS, and CTDK-1. Our results suggest that, in vivo, a reduced rate of Pol II elongation leads to premature dissociation along the chromatin template and that Pol II processivity can be uncoupled from elongation rate.
- Published
- 2005
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