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

TY - JOUR

T1 - hRRN3 is essential in the SL1-mediated recruitment of RNA Polymerase I to rRNA gene promoters

AU - Miller, Gail

AU - Panov, Kostya I.

AU - Friedrich, J. Karsten

AU - Trinkle-Mulcahy, Laura

AU - Lamond, Angus I.

AU - Zomerdijk, Joost C. B. M.

N1 - dc.publisher: Nature Publishing Group dc.description.sponsorship: Wellcome Trust Biotechnology and Biological Sciences Research Council

PY - 2001/3

Y1 - 2001/3

N2 - 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 (Ia) are transcriptionally inactive, hRRN3 defines a distinct subpopulation of Pol I complexes (Iß) that supports specific initiation of transcription. Human RRN3 interacts directly with TAF1110 and TAF163 of promoter-selectivity factor SL1. Blocking this connection prevents recruitment of Pol Iß 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.

AB - 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 (Ia) are transcriptionally inactive, hRRN3 defines a distinct subpopulation of Pol I complexes (Iß) that supports specific initiation of transcription. Human RRN3 interacts directly with TAF1110 and TAF163 of promoter-selectivity factor SL1. Blocking this connection prevents recruitment of Pol Iß 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.

KW - Growth control

KW - Holoenzyme

KW - Nucleolus

KW - rRNA

KW - Transcription

U2 - 10.1093/emboj/20.6.1373

DO - 10.1093/emboj/20.6.1373

M3 - Article

C2 - 11250903

SN - 0261-4189

VL - 20

SP - 1373

EP - 1382

JO - The EMBO Journal

JF - The EMBO Journal

IS - 6

ER -