SWI/SNF-dependent chromatin remodeling ofRNR3requires TAF_IIs and the general transcription machinery

Abstract

Gene expression requires the recruitment of chromatin remodeling activities and general transcription factors (GTFs) to promoters. Whereas the role of activators in recruiting chromatin remodeling activities has been clearly demonstrated, the contributions of the transcription machinery have not been firmly established. Here we demonstrate that the remodeling of the RNR3 promoter requires a number of GTFs, mediator and RNA polymerase II. We also show that remodeling is dependent upon the SWI/SNF complex, and that TFIID and RNA polymerase II are required for its recruitment to the promoter. In contrast, Gcn5p-dependent histone acetylation occurs independently of TFIID and RNA polymerase II function, and we provide evidence that acetylation increases the extent of nucleosome remodeling, but is not required for SWI/SNF recruitment. Thus, the general transcription machinery can contribute to nucleosome remodeling by mediating the association of SWI/SNF with promoters, thereby revealing a novel pathway for the recruitment of chromatin remodeling activities.[Keywords: Chromatin remodeling; SWI/SNF; TAFs; RNR3; SAGA; TFIID] Supplemental material is available at http://www.genesdev.org.

Genetic Screens for Enhancers of brahma Reveal Functional Interactions Between the BRM Chromatin-Remodeling Complex and the Delta-Notch Signal Transduction Pathway in Drosophila

“…For example, the MOF histone acetyltransferase functionthat the BRM complex may interact more closely than previously thought with the general transcriptional maally antagonizes the Drosophila ISWI chromatin-remodeling factor (Corona et al 2002); bromodomains within chinery. These findings are consistent with the observation that yeast TFIID and RNA pol II are required for the yeast RSC chromatin-remodeling complex recognize acetylated histone H3 (Kasten et al 2004); and the recruitment of SWI/SNF to the RNR3 promoter (Sharma et al 2003). We have been unable to detect a methylation of lysines 4 and 9 of H3 and lysine 20 of H4 by Ash1 may recruit the BRM complex (Beisel et physical interaction between RNA pol II and the BRM complex by co-immunoprecipitation (Armstrong et al al.…”

“…The ATPase subcruits the BRM complex to chromatin in vitro (Kal et al 2000) and in vivo (Dejardin and Cavalli 2004). units of chromatin-remodeling complexes facilitate these reactions by functioning as ATP-dependent DNA SWI/SNF also interacts with the general transcriptional machinery (Sharma et al 2003;Yoon et al 2003), and translocases (Saha et al 2002;Whitehouse et al 2003). The ability of SWI/SNF complexes to remodel chromamutations in genes encoding components of RNA polymerase II impair the recruitment of SWI/SNF to the tin in vitro is inhibited by PRC1, suggesting a potential mechanism for PcG repression in vivo (Francis et al GAL1 promoter (Lemieux and Gaudreau 2004).…”

Mediator, TATA-binding Protein, and RNA Polymerase II Contribute to Low Histone Occupancy at Active Gene Promoters in Yeast

“…PIC components contribute to Swi/Snf recruitment to the induced RNR3 promoter (8), suggesting that the increased H3 occupancy seen in Mediator, Pol II, and TBP mutants could occur indirectly via deficient Swi/Snf recruitment. Two arguments can be made against this scenario: first, Swi/Snf recruitment occurs normally at the CHA1 promoter under inducing conditions in srb4/med17 ts yeast, but histone H3 eviction does not (11); thus, Swi/Snf is not sufficient for histone eviction.…”

“…To test this model, we used ChIP to measure histone H3 association in the temperature-sensitive mutants rpb1-1 and tbp ts-1 (48,49), which show defective association of Pol II and TBP, respectively, with target genes at 37°C (8,50,51). Wild type and mutant strains were grown at 24°C, shifted to 37°C for 30 min, and CHA1 induced by addition of serine for an additional 30 min while maintaining cultures at 37°C prior to ChIP (11).…”

Direct interactions promote eviction of the Sir3 heterochromatin protein by the SWI/SNF chromatin remodeling enzyme

“…Yeast strains that lack SWI/SNF show a variety of phenotypes, including growth defects on rich medium or medium containing alternative carbon sources (e.g., galactose or raffinose), inositol auxotrophy (25,33) and sensitivity to DNA-damaging and replication stress agents (26,30). Consistent with the intact chromatin-remodeling activities of the SWI/SNF-Δ10R enzyme, strains harboring the swi2-Δ10R allele showed normal growth on nearly every condition tested.…”