SWI/SNF can activate transcription through an alternative mechanism that is independent of the nucleosome remodeling activity of Brahma
(English)Manuscript (preprint) (Other academic)
SWI/SNF is a chromatin-remodeling complex with a well-established role in transcription regulation. SWI/SNF facilitates nucleosome remodeling in an ATPase-dependent manner, and regulates the recruitment of transcription regulators to gene promoters. We show here that the SWI/SNF complex of Drosophila melanogater has the ability to regulate transcription through an alternative mechanism that does not require the chromatin remodeling capacity of the core ATPase subunit Brahma (BRM). The expression of the genes CG44250 and CG44251 is regulated by BRM in Drosophila melanogaster S2 cells, as shown by RNA interference experiments and over-expression of recombinant BRM. ChIP data confirm that the cellular levels of BRM influence the density and the phosphorylation state of RNA polymerase II at the CG44250/51. Interestingly, a mutant BRM with an inactive ATPase domain does mimic the effect of the active recombinant BRM on the expression of CG44250/51, which suggests that the regulation of CG44250/51 by BRM does not require the chromatin remodeling activity of SWI/SNF. There are two main SWI/SNF complexes in Drosophila melanogaster: BAP and PBAP. They both harbor the ATPase subunit BRM and additional core subunits, and they are characterized by specific signature subunits that confer differential substrate preferences. Data from microarray experiments in SWI/SNF knock- down S2 cells suggest that the PBAP complex is specifically involved in the regulation of the transcription of the CG44250/51 genes. Taken together, our results show that the PBAP complex regulates gene expression by a mechanism different from chromatin remodeling.
Research subject Molecular Biology
IdentifiersURN: urn:nbn:se:su:diva-94621OAI: oai:DiVA.org:su-94621DiVA: diva2:654591