Yeast cells lacking transcription elongation factor genes such as PPR2 (TFIIS) and ELF (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 LI carboxy-terminal domain kinase I (CTDK-I), is synthetically lethal when combined with deletion of PPR2 or ELF 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. (C) 2001 Elsevier Science B.V. All rights reserved.
机构:
Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, Div Nucle Acids Enzymol, Piscataway, NJ 08854 USAUniv Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, Div Nucle Acids Enzymol, Piscataway, NJ 08854 USA
机构:
Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, Div Nucle Acids Enzymol, Piscataway, NJ 08854 USAUniv Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, Div Nucle Acids Enzymol, Piscataway, NJ 08854 USA