Blog
About

8
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

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

      Genes

      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

      Read this article at

      ScienceOpenPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Author and article information

          Journal
          11311553

          Comments

          Comment on this article