The SWI/SNF chromatin remodeling complex influences transcription by RNA polymerase I in Saccharomyces cerevisiae

• Published in: PloS one 2013-02, Vol.8 (2), p.e56793
• Main Authors: Zhang, Yinfeng, Anderson, Susan J, French, Sarah L, Sikes, Martha L, Viktorovskaya, Olga V, Huband, Jacalyn, Holcomb, Katherine, Hartman, 4th, John L, Beyer, Ann L, Schneider, David A
• Format: Article
• Language: English
• Subjects: Biology; Chromatin; Chromatin Assembly and Disassembly; Chromatin remodeling; Clonal deletion; Comparative analysis; Deoxyribonucleic acid; DNA; DNA, Ribosomal - metabolism; DNA-directed RNA polymerase; Elongation; Epistasis, Genetic; Gene Deletion; Gene Dosage; Gene Expression Regulation, Fungal; Genes; Genetic aspects; Mutation; Protein Binding; Protein Subunits - genetics; Protein Subunits - metabolism; Ribonucleic acid; RNA; RNA polymerase; RNA Polymerase I - metabolism; RNA polymerase II; RNA, Ribosomal - genetics; RNA, Ribosomal - metabolism; rRNA; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - metabolism; Saccharomyces cerevisiae Proteins - genetics; Saccharomyces cerevisiae Proteins - metabolism; Transcription (Genetics); Transcription elongation; Transcription initiation; Transcription, Genetic; Yeast
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0056793

SWI/SNF is a chromatin remodeling complex that affects transcription initiation and elongation by RNA polymerase II. Here we report that SWI/SNF also plays a role in transcription by RNA polymerase I (Pol I) in Saccharomyces cerevisiae. Deletion of the genes encoding the Snf6p or Snf5p subunits of SWI/SNF was lethal in combination with mutations that impair Pol I transcription initiation and elongation. SWI/SNF physically associated with ribosomal DNA (rDNA) within the coding region, with an apparent peak near the 5' end of the gene. In snf6Δ cells there was a ∼2.5-fold reduction in rRNA synthesis rate compared to WT, but there was no change in average polymerase occupancy per gene, the number of rDNA gene repeats, or the percentage of transcriptionally active rDNA genes. However, both ChIP and EM analyses showed a small but reproducible increase in Pol I density in a region near the 5' end of the gene. Based on these data, we conclude that SWI/SNF plays a positive role in Pol I transcription, potentially by modifying chromatin structure in the rDNA repeats. Our findings demonstrate that SWI/SNF influences the most robust transcription machinery in proliferating cells.