NoRC-a novel member of mammalian ISWI-containing chromatin remodeling machines
Transcription by RNA polymerase I on nucleosomal templates requires binding of the transcription termination factor TTF‐I to a cognate site 160 bp upstream of the transcription start site. Binding of TTF‐I is accompanied by changes in the chromatin architecture which suggests that TTF‐I recruits a r...
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Published in | The EMBO journal Vol. 20; no. 17; pp. 4892 - 4900 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Chichester, UK
John Wiley & Sons, Ltd
03.09.2001
Blackwell Publishing Ltd Oxford University Press |
Subjects | |
Online Access | Get full text |
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Summary: | Transcription by RNA polymerase I on nucleosomal templates requires binding of the transcription termination factor TTF‐I to a cognate site 160 bp upstream of the transcription start site. Binding of TTF‐I is accompanied by changes in the chromatin architecture which suggests that TTF‐I recruits a remodeling activity to the rDNA promoter. We have cloned a cDNA that encodes TIP5 (TTF‐I‐interacting protein 5), a 205 kDa protein that shares a number of important protein domains with WSTF (Williams syndrome transcription factor) and hAcf1/WCRF180, the largest subunits of human chromatin remodeling complexes hCHRAC and WCRF. TIP5 co‐localizes with the basal RNA polymerase I transcription factor UBF in the nucleolus and is associated with SNF2h. The cellular TIP5–SNF2h complex, termed NoRC (nucleolar remodeling complex), induces nucleosome sliding in an ATP‐ and histone H4 tail‐dependent fashion. The results suggest that NoRC is a novel nucleolar chromatin remodeling machine that may serve a role in the regulation of the rDNA locus. |
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Bibliography: | istex:81CEA7488876FC8BA5C30712D0611FF53AED61F0 ArticleID:EMBJ7593985 ark:/67375/WNG-69NJX6GX-X ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0261-4189 1460-2075 1460-2075 |
DOI: | 10.1093/emboj/20.17.4892 |