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hRRN3 is essential in the SL1-mediated recruitment of RNA Polymerase I to rRNA gene promoters.

A crucial step in transcription is the recruitment of RNA polymerase to promoters. In the transcription of human rRNA genes by RNA Polymerase I (Pol I), transcription factor SL1 has a role as the essential core promoter binding factor. Little is known about the mechanism by which Pol I is recruited. We provide evidence for an essential role for hRRN3, the human homologue of a yeast Pol I transcription factor, in this process. We find that whereas the bulk of human Pol I complexes (I alpha) are transcriptionally inactive, hRRN3 defines a distinct subpopulation of Pol I complexes (I beta) that supports specific initiation of transcription. Human RRN3 interacts directly with TAF(I)110 and TAF(I)63 of promoter-selectivity factor SL1. Blocking this connection prevents recruitment of Pol I beta to the rDNA promoter. Furthermore, hRRN3 can be found in transcriptionally autonomous Pol I holoenzyme complexes. We conclude that hRRN3 functions to recruit initiation-competent Pol I to rRNA gene promoters. The essential role for hRRN3 in linking Pol I to SL1 suggests a mechanism for growth control of Pol I transcription.

Pubmed ID: 11250903

Authors

  • Miller G
  • Panov KI
  • Friedrich JK
  • Trinkle-Mulcahy L
  • Lamond AI
  • Zomerdijk JC

Journal

The EMBO journal

Publication Data

March 15, 2001

Associated Grants

None

Mesh Terms

  • Binding Sites
  • Cell Nucleolus
  • DNA-Binding Proteins
  • Gene Expression Regulation
  • Holoenzymes
  • Humans
  • Models, Genetic
  • Pol1 Transcription Initiation Complex Proteins
  • Promoter Regions, Genetic
  • Protein Binding
  • RNA Polymerase I
  • RNA, Ribosomal
  • Transcription Factors
  • Transcription, Genetic