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Involvement of yeast carboxy-terminal domain kinase I (CTDK-I) in transcription elongation in vivo.


pharmacology, Acetyltransferases, genetics, Cell Division, drug effects, Gene Deletion, Genes, Lethal, Histone Acetyltransferases, Mutation, Protein Kinases, metabolism, Saccharomyces cerevisiae, growth & development, Saccharomyces cerevisiae Proteins, Transcription Factors, Transcription Factors, General, Transcription, Genetic, Transcriptional Elongation Factors, Uracil, analogs & derivatives

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      Yeast cells lacking transcription elongation factor genes such as PPR2 (TFIIS) and ELP (Elongator) are viable and show deleterious phenotypes only when transcription is rendered less effective by RNA polymerase mutations or by decreasing nucleotide pools. Here we demonstrate that deletion of the CTK1 gene, encoding the kinase subunit of RNA polymerase II carboxy-terminal domain kinase I (CTDK-I), is synthetically lethal when combined with deletion of PPR2 or ELP genes. The inviability of ctk1 elp3 double mutants can be rescued by expression of an Elp3 mutant that has retained its ability to form the Elongator complex but has severely diminished histone acetyltransferase activity, suggesting that the functional overlap between CTDK-I and Elongator is in assembly of RNA polymerase II elongation complexes. Our results suggest that CTDK-I plays an important role in transcriptional elongation in vivo, possibly by creating a form of RNA polymerase that is less prone to transcriptional arrest.

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