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Transcription factor Znf2 coordinates with the chromatin remodeling SWI/SNF complex to regulate differentiation in Cryptococcus neoformans

ABSTRACT: Cellular differentiation is instructed by development regulators in coordination with chromatin remodeling complexes. Much information about their coordination comes from studies in the model ascomycetous yeasts. It is not clear, however, of the kind of information that can be extrapolated to species of other phyla in Kingdom Fungi. In the basidiomycete Cryptococcus neoformans, the transcription factor Znf2 controls yeast-to-hypha differentiation. Through a forward genetic screen, we identified the basidiomycete-specific factor Brf1 and discovered that it works together with Snf5 in the SWI/SNF chromatin remodeling complex in concert with existent Znf2 to execute cellular differentiation. We demonstrated that SWI/SNF assists Znf2 opening up the promoter regions of hyphal specific genes, including the ZNF2 gene itself. In addition, this complex supports Znf2 to fully associate with its target regions. Importantly, our findings revealed key differences in composition and biological function of the SWI/SNF complex in the two major phyla of Kingdom Fungi.

ORGANISM(S): Cryptococcus neoformans

PROVIDER: GSE137248 | GEO | 2019/09/12

REPOSITORIES: GEO

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Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodeling complex

Project description:Tissue-specific transcription factors initiate differentiation toward a specialized cell type by inducing transcription-permissive chromatin modifications at target gene promoters, through the recruitment of the SWI/SNF chromatin-remodeling complex (1, 2). The molecular mechanism that regulates the chromatin re-distribution of SWI/SNF in response to differentiation signals is currently unknown. Here we show that the muscle determination factor MyoD and the SWI/SNF structural sub-unit, BAF60c (SMARCD3), form a complex on the regulatory elements of MyoD-target genes in undifferentiated myoblasts, prior to the activation of gene expression. MyoD-BAF60c complex is devoid of the ATP-dependent enzymatic sub-units Brg1 and Brm, is required for stable MyoD binding to Ebox sequences, and marks the chromatin for signal-dependent recruitment of the SWI/SNF core complex to muscle loci. BAF60c phosphorylation on a conserved threonine by differentiation-activated p38 signalling promotes the incorporation of MyoD-BAF60c into a Brg1-based SWI/SNF complex, which is competent to remodel the chromatin and activates transcription of MyoD-target genes. Our data support an unprecedented two-step model, by which pre-assembled BAF60c-MyoD complex directs the SWI/SNF complex chromatin re-distribution to muscle loci in response to differentiation cues. Differentiation of C2C12 cells individually interfered for BRG1, BAF60B, BAF60C

2011-03-07 | E-GEOD-24573 | biostudies-arrayexpress

Analysis of proteins that bind promoter of the PDR5 multidrug transporter gene in Saccharomyces cerevisiae using minichromosome isolation and LC-MS/MS

Project description:The Pleiotropic Drug Resistance (PDR) network is central to the drug response in fungi, and its overactivation is associated with drug resistance. However, gene regulation of the PDR network is not well understood. Here, we established a method to identify proteins that bind promoter of the PDR5 multidrug transporter gene in Saccharomyces cerevisiae using minichromosome isolation and SILAC-based quantitative proteomics, and identified the SWI/SNF chromatin remodelling complex as a PDR5 promoter-binding complex. We also purified the SWI/SNF complex from S. cerevisiae by immunoprecipitating Flag-tagged Snf6, a subunit of SWI/SNF, and identified the subunits of SWI/SNF and its binding proteins by LC-MS/MS.

2022-02-22 | PXD028798 | Pride

Transcription factor Znf2 coordinates with the chromatin remodeling SWI/SNF complex to regulate differentiation in Cryptococcus neoformans

Project description:Transcription factor Znf2 coordinates with the chromatin remodeling SWI/SNF complex to regulate differentiation in Cryptococcus neoformans

| PRJNA564926 | ENA

Brd7, a novel PBAF-specific SWI/SNF subunit, is required for gene activation and repression in embryonic stem cells

Project description:The composition of chromatin remodeling complexes dictates how these enzymes control transcriptional programs and cellular identity. Here, we investigate the composition of SWI/SNF complexes in embryonic stem cells (ESCs). In contrast to differentiated cells, ESCs have a biased incorporation of certain paralogous SWI/SNF subunits, with low levels of Brm, BAF170 and ARID1B. Upon differentiation, the expression of these subunits increases, resulting in a higher diversity of compositionally distinct SWI/SNF enzymes. We also identify Brd7 as a novel component of the PBAF complex in both ESCs and differentiated cells. Using shRNA-mediated depletion of Brg1, we show that SWI/SNF can function as both a repressor and an activator in pluripotent cells, regulating expression of developmental modifiers and signaling components such as Nodal, ADAMTS1, Bmi-1, CRABP1 and TRH. Knock-down studies of PBAF-specific Brd7 and of a signature subunit within the BAF complex, ARID1A, show that these two sub-complexes affect SWI/SNF target genes differentially, in some cases even antagonistically. This may be due to their different biochemical properties. Finally, we examine the role of SWI/SNF in regulating its target genes during differentiation. We find that SWI/SNF affects recruitment of components of the pre-initiation complex in a promoter-specific manner, to modulate transcription positively or negatively. Taken together, our results provide insight into the function of compositionally diverse SWI/SNF enzymes that underlie their inherent gene-specific mode of action. R1 ESCs were infected in duplicates with shRNA targeting Brg1 or GLUT4 (as a control). Knockdown of Brg1 mRNA affected Brg1 protein levels efficiently. RNA was isolated 67 hours post-infection and analyzed using microarrays.

2010-03-04 | E-GEOD-7791 | biostudies-arrayexpress

The SWI/SNF Complex Regulates the PRDM Protein Hamlet to Ensure Lineage Directionality in Drosophila Neural Stem Cells

Project description:Members of the SWI/SNF chromatin-remodeling complex are among the most frequently mutated genes in human cancer. SWI/SNF complex controls self-renewal and differentiation in stem cell lineages but how this function relates to tumorigenesis is currently unclear. Here, we use Drosophila neuroblasts to demonstrate that the SWI/SNF component Osa (ARID1) prevents tumorigenesis in stem cell lineages by ensuring correct unidirectional lineage progression. Our transcriptome anaysis identifies Ham as a key Osa target gene. comparison of transcriptomes of wild type Drosophila melanogaster larval type II NB lineages (excluding neurons) and osa RNAi type II lineages containing mainly NB-like cells and INPs

2014-03-13 | E-GEOD-48242 | biostudies-arrayexpress

siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

The Swi/Snf chromatin remodeling complex promotes Th17 differentiation by coordinating RORγt-driven epigenetic program

Project description:TH17 cells play a critical role in mucosal immunity and also in multiple autoimmune diseases. The differentiation of TH17 cells is dictated by a master transcription factor, RORγt; however, the mechanism by which RORγt controls target genes is poorly understood. Here we identify the Swi/Snf chromatin remodeling complex as an essential regulator of TH17 cell differentiation. Loss of the expression of SRG3/mBAF155, a core subunit of the Swi/Snf complex, results in a specific downregulation of RORγt target genes such as IL-17A, IL-17F and IL-23R. Importantly, the comparative transcriptional analysis reveals a high similarity between RORγt and the Swi/Snf complex in the control of TH17-related gene expression. Mechanistically, the Swi/Snf complex partners with RORγt and coordinates a variety of RORγt–mediated epigenetic modifications, including both permissive and repressive ones. These results provide a basis for the understanding of how a master transcription factor RORγt cooperates with the Swi/Snf complex to govern the Th17 cell differentiation.

2020-05-06 | GSE129132 | GEO

Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodeling complex

2011-03-07 | GSE24573 | GEO

SWI/SNF is positively auto-regulated by an AT-hook in the catalytic subunit

Project description:The SWI/SNF ATP-dependent chromatin remodeler is a master regulator of the epigenome; controlling pluripotency, cell fate determination and differentiation. There is a sparsity of information on the autoregulation of SWI/SNF, the domains involved and their mode of action. We find a DNA or RNA binding module conserved from yeast to humans located in the C-terminus of the catalytic subunit of SWI/SNF called the AT-hook that positively regulates the chromatin remodeling activity of yeast and mouse SWI/SNF. The AT-hook in yeast SWI/SNF interacts with the SnAC and ATPase domains, which after binding to nucleosome switches to contacting the N-terminus of histone H3. Deletion of the AT-hooks in yeast SWI/SNF and mouse esBAF complexes reduces the remodeling activity of SWI/SNF without affecting complex integrity or its recruitment to nucleosomes. In addition, deletion of the AT-hook impairs the ATPase and nucleosome mobilizing activities of yeast SWI/SNF without disrupting the interactions of the ATPase domain with nucleosomal DNA. The AT-hook is also important in vivo for SWI/SNF-dependent response to amino acid starvation in yeast and for cell lineage priming in mouse embryonic stem cells. In summary, the AT-hook is shown to be an evolutionarily conserved autoregulatory domain of SWI/SNF that positively regulates SWI/SNF both in vitro and in vivo.

2023-06-15 | PXD040664 | Pride

ACTL6a Enforces the Epidermal Progenitor State by Suppressing SWI/SNF-Dependent Induction of KLF4

Project description:Somatic progenitors suppress differentiation to maintain tissue self-renewal. While epigenetic regulators of DNA and histone modifications can support such repression, a role for nuclear actin-like proteins is unclear. In epidermis, ACTL6a/BAF53A was found enriched in progenitors and down-regulated during differentiation. Conditional ACTL6a deletion abolished epidermal self-renewal and induced terminal differentiation, whereas ectopically expressed ACTL6a suppressed differentiation. Among known activators of epidermal differentiation, KLF4 was found to control 227 genes also regulated by ACTL6a. ACTL6a loss upregulated KLF4 and its target genes, effects that were blocked by KLF4 depletion. Among multiple ACTL6a-interacting epigenetic regulators, the SWI/SNF complex was required for KLF4 activation and differentiation. In progenitors, ACTL6a loss led to enhanced SWI/SNF binding to the promoters of KLF4 and other differentiation genes. ACTL6a thus maintains the undifferentiated progenitor state, in part by suppressing SWI/SNF complex-enabled induction of KLF4. Gene expression analysis: To identify the gene set controlled by ACTL6a in human keratinocyte. Total RNA was isolated in biologic duplicate from cells with ACTL6a loss as compared to controls, and hybridized to Affymetrix HG-U133 2.0 Plus arrays.

2012-11-30 | E-GEOD-36222 | biostudies-arrayexpress

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