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hRRN3 is essential in the SL1‐mediated recruitment of RNA Polymerase I to rRNA gene promoters
Author(s) -
Miller Gail,
Panov Kostya I.,
Friedrich J.Karsten,
TrinkleMulcahy Laura,
Lamond Angus I.,
Zomerdijk Joost C.B.M.
Publication year - 2001
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/20.6.1373
Subject(s) - biology , rna polymerase ii , promoter , transcription factor ii d , rna polymerase iii , general transcription factor , rna polymerase i , sigma factor , transcription factor ii f , transcription (linguistics) , rna polymerase , transcription factor ii e , genetics , microbiology and biotechnology , gene , rna , gene expression , linguistics , philosophy
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 (Iα) are transcriptionally inactive, hRRN3 defines a distinct subpopulation of Pol I complexes (Iβ) 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 β 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.