Open AccessThe Paf1 Complex Represses SER3 Transcription in Saccharomyces cerevisiae by Facilitating Intergenic Transcription-Dependent Nucleosome Occupancy of the SER3 Promoter
Author(s) -
Justin A. Pruneski,
Sarah J. Hainer,
Kostadin Petrov,
Joseph A. Martens
Publication year - 2011
Publication title -
eukaryotic cell
Language(s) - English
Resource type - Journals
eISSN - 1535-9778
pISSN - 1535-9786
DOI - 10.1128/ec.05141-11
Subject(s) - biology , microbiology and biotechnology , transcription (linguistics) , nucleosome , rna polymerase ii , transcription coregulator , general transcription factor , promoter , transcription factor , chromatin , chromatin remodeling , genetics , gene expression , gene , philosophy , linguistics
Previous studies have shown that repression of theSaccharomyces cerevisiae SER3 gene is dependent on transcription ofSRG1 from noncoding DNA initiating within the intergenic region 5′ ofSER3 and extending across theSER3 promoter region. By a mechanism dependent on the activities of the Swi/Snf chromatin remodeling factor, the HMG-like factor Spt2, and the Spt6 and Spt16 histone chaperones,SRG1 transcription deposits nucleosomes over theSER3 promoter to prevent transcription factors from binding and activatingSER3 . In this study, we uncover a role for the Paf1 transcription elongation complex inSER3 repression. We find thatSER3 repression is primarily dependent on the Paf1 and Ctr9 subunits of this complex, with minor contributions by the Rtf1, Cdc73, and Leo1 subunits. We show that the Paf1 complex localizes to theSRG1 transcribed region under conditions that repressSER3 , consistent with it having a direct role in mediatingSRG1 transcription-dependentSER3 repression. Importantly, we show that the defect inSER3 repression in strains lacking Paf1 subunits is not a result of reducedSRG1 transcription or reduced levels of known Paf1 complex-dependent histone modifications. Rather, we find that strains lacking subunits of the Paf1 complex exhibit reduced nucleosome occupancy and reduced recruitment of Spt16 and, to a lesser extent, Spt6 at theSER3 promoter. Taken together, our results suggest that Paf1 and Ctr9 repressSER3 by maintainingSRG1 transcription-dependent nucleosome occupancy.