SWI/SNF regulates half of its targets without the need of ATP-driven nucleosome remodeling by Brahma

Abstract

BackgroundBrahma (BRM) is the only catalytic subunit of the SWI/SNF chromatin-remodeling complex of Drosophila melanogaster. The function of SWI/SNF in transcription has long been attributed to its ability to remodel nucleosomes, which requires the ATPase activity of BRM. However, recent studies have provided evidence for a non-catalytic function of BRM in the transcriptional regulation of a few specific genes.ResultsHere we have used RNA-seq and ChIP-seq to identify the BRM target genes in S2 cells, and we have used a catalytically inactive BRM mutant (K804R) that is unable to hydrolyze ATP to investigate the magnitude of the non-catalytic function of BRM in transcription regulation. We show that 49% of the BRM target genes in S2 cells are regulated through mechanisms that do not require BRM to have an ATPase activity. We also show that the catalytic and non-catalytic mechanisms of SWI/SNF regulation operate on two subsets of genes that differ in promoter architecture and are linked to different biological processes.ConclusionsThis study shows that the non-catalytic role of SWI/SNF in transcription regulation is far more prevalent than previously anticipated and that the genes that are regulated by SWI/SNF through ATPase-dependent and ATPase-independent mechanisms have specialized roles in different cellular and developmental processes.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4746-2) contains supplementary material, which is available to authorized users.

The SWI/SNF ATP-Dependent Chromatin Remodeling Complex in Arabidopsis Responds to Environmental Changes in Temperature-Dependent Manner

“…Decreased positioning of nucleosomes in the gene body and slight fuzziness of nucleosomes in the promoter region correlate with enhanced transcription of CBF1 and MYB15 genes under normal growth condition in the swi3c mutant. These findings are in line with the results showing that the presence of SWI/SNF CRCs in the gene body plays an important role in the control of nucleosome density during transcriptional elongation in Drosophila [46]. The contrasting situation was observed under a lower growth temperature where the chromatin structure on ICE1 did not differ from the wild type, whereas only some fuzziness of nucleosomes was detected on MYB15, while the expression of these genes was not altered in the swi3c mutant compared to wild type.…”

“…Although unexpected, this observation is in line with recent mapping studies of human [44] and Arabidopsis [45] SWI/SNF CRCs, which were located in various gene regions. Similarly, SWI/SNF CRCs in Drosophila were observed to bind gene body regions affecting transcription elongation [46] and RNA polymerase II pausing [47]. The location of SWI3C on the ICE1, CBF1 and MYB15 loci has remarkably changed in a temperature-dependent manner and was shifted 5 -upstream of TSSs in the promoter regions of ICE1, MYB15 and CBF1 genes.…”

Both IDO1 and TDO contribute to the malignancy of gliomas via the Kyn–AhR–AQP4 signaling pathway

“…The fixed cells were lysed and sonicated, the lysates were cleared by centrifugation, and an antibody against AhR was added and incubated overnight under rotation. 55,56 After reversal of the cross-linking, precipitated DNA was purified with a column and eluted in 20 μL of water. Precipitated DNA fragments were amplified by qPCR.…”

SWI/SNF interacts with cleavage and polyadenylation factors and facilitates pre-mRNA 3′ end processing

“…ChIP-seq experiments were carried out by Jordán-Pla et al. ( 7 ) using an antibody against the endogenous dBRM protein ( 27 ). The ChIP-seq data are available at GEO with accession number GSE95236 (datasets ‘endogenous BRM input replicates 1 and 2’ and ‘endogenous BRM IP replicates 1 and 2).…”