Article

  • The EMBO Journal (2008) 27, 100 - 110
  • doi:10.1038/sj.emboj.7601946

Published online: 6 December 2007

RSC regulates nucleosome positioning at Pol II genes and density at Pol III genes

Timothy J Parnell1, Jason T Huff1 and Bradley R Cairns1

  1. Howard Hughes Medical Institute and Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA

Correspondence to:

Bradley R Cairns, Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT 84112, USA. Tel.: +1 801 585 1822; Fax: +1 801 585 6410; E-mail: brad.cairns@hci.utah.edu

Received 9 August 2007; Accepted 7 November 2007


Nucleosomes can restrict the access of transcription factors to chromatin. RSC is a SWI/SNF-family chromatin-remodeling complex from yeast that repositions and ejects nucleosomes in vitro. Here, we examined these activities and their importance in vivo. We utilized array-based methods to examine nucleosome occupancy and positioning at more than 200 locations in the genome following the controlled destruction of the catalytic subunit of RSC, Sth1. Loss of RSC function caused pronounced and general reductions in new transcription from Pol I, II, and III genes. At Pol III genes, Sth1 loss conferred a general reduction in RNA Pol III occupancy and a gain in nucleosome density. Notably at the one Pol III gene examined, histone restoration was partly replication-dependent. In contrast, at Pol II promoters we observed primarily single nucleosome changes, including movement. Importantly, alterations near the transcription start site were more common at RSC-occupied promoters than at non-occupied promoters. Thus, RSC action affects both nucleosome density and positioning in vivo, but applies these remodeling modes differently at Pol II and Pol III genes.

  • Keywords:

    • chromatin,
    • nucleosome,
    • RSC,
    • transcription
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