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Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos [ChIP-seq]

ABSTRACT: Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos [ChIP-seq]

PROVIDER: PRJNA732404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14633961.fastq.gz	Fastqsanger.gz
	SRR14633962.fastq.gz	Fastqsanger.gz
	SRR14633963.fastq.gz	Fastqsanger.gz
	SRR14633964.fastq.gz	Fastqsanger.gz
	SRR14633965.fastq.gz	Fastqsanger.gz

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Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos [RNA-seq]

Project description:Brg1 and Brm function as alternative core enzymatic ATPases of SWI/SNF complex in vertebrates, with clear homologs in zebrafish. Brg1 (but not Brm) is required for early cleavage-stage transcription in mice, but where and how Brg1 or Brm impact chromatin in early embryos remains unexplored. Here, we utilize zebrafish embryos to provide the first simultaneous genome-wide profiling of Brg1 and Brm occupancy in any organism/cell type, alongside our profiling of open chromatin and RNA polymerase II. We reveal shared and unique loci for Brg1 and Brm, their shared occupancy of open chromatin and particular developmental promoters, and higher transcription at co-occupied genes. Interestingly, only Brg1 is strongly associated with active histone modifications. Strikingly, only Brm commonly occupies gene bodies, overlapping precisely with Pol II. Functional experiments involving Pol II elongation inhibition alongside bioinformatic analyses suggest that Brm travels with Pol II into gene bodies, primarily at short, very highly-transcribed genes with few introns. Taken together, our results support roles for Brg1 primarily at promoters and enhancers, and for Brm in association with Pol II in elongation through chromatin within gene bodies during genome-wide transcriptional activation

2024-05-24 | GSE175446 | GEO

Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos [ChIP-seq]

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Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos

Project description:Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos

| PRJNA732402 | ENA

Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos [RNA-seq]

Project description:Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos [RNA-seq]

| PRJNA732405 | ENA

Superior preclinical efficacy of co-treatment with BRG1/BRM and FLT3 inhibitor against AML cells with FLT3 mutations

Project description:Although treatment with standard frontline therapies, including a FLT3 inhibitor (FLT3i) reduces AML burden and achieves clinical remissions, most patients with AML with FLT3 mutation relapse due to therapy-resistant stem/progenitor cells. The core ATPases, BRG1 (SMARCA4) and BRM (SMARCA2) of the canonical (c) BAF (BRG1/BRM-associated factor) complex is a dependency in AML cells, including those harboring FLT3 mutations. We have previously reported that treatment with FHD-286, a BRG1/BRM ATPases inhibitor, induces differentiation and loss of viability of AML stem/progenitor cells. Findings of present studies demonstrate that treatment with FHD-286 induces lethality in AML cells, regardless of sensitivity or resistance to FLT3i. This efficacy is associated with the induction of gene-expression perturbations responsible for growth inhibition, differentiation, as well as a reduced AML-initiating potential of the AML cells. Additionally, co-treatment with FHD-286 and FLT3i exerts superior pre-clinical efficacy against AML cells and patient-derived (PD) xenograft (PDX) models of AML with FLT3 mutations.

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Distinctive roles for the chromatin remodeling ATPases Brg1 and Brm in early zebrafish embryos

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-24 | GSE175447 | GEO

Project title: Effect of FHD-286 or BRG1/BRM degrader AU15330 on protein expressions in MLL1-rearranged AML cells

Project description:MOLM13 cells and patient-derived de novo AML cells with MLL1 rearrangement were treated with 100 nM of FHD-286 or 100 nM of AU15330, a dual BRG1/BRM protein degrader for 48 hours. The goal was to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and/or lethal effects of treatment with a chromatin remodeling inhibitor, FHD-286, or a BRG1/BRM protein degrader in MLL1-rearranged AML cells.

2025-04-28 | PXD055994 | Pride

Highly effective combination of BRG1/BRM inhibitor with BET inhibitor or decitabine for high-risk MECOM-rearranged AML [RNA-seq]

Project description:In AML with 3q26.2 rearrangements (r) the distal GATA2 hematopoietic enhancer becomes aberrantly relocated leading to activation of EVI1 expression EVI1 is a transcriptional regulator that plays a role in proliferation and maintenance of a stem cell-like phenotype in AML. BRG1 (SMARCA4) and BRM (SMARCA2) are the mutually exclusive ATPases of the BAF (BRG1/BRM-associated factor) chromatin remodeling complexes. They regulate access to enhancers/promoters and gene-expressions orchestrating AML stem/progenitor cell proliferation and differentiation. AML with 3q26.2 rearrangements are clinically challenging and prognosis remains very poor. FHD-286 is an orally bioavailable, selective inhibitor of BRG1/BRM under clinical development in AML. Present studies show that FHD-286 induced differentiation and lethality in AML cells with MECOM-r, perturbed chromatin accessibility and depleted expression of EVI1, c-Myc, CD44 and CDK4. Co-treatment with FHD-286 and decitabine, BET inhibitor (BETi) or HAT inhibitor synergistically induced in vitro lethality in patient-derived AML cells with MECOM-r. In patient-derived xenograft (PDX) models of AML with MECOM-r, compared to each drug, co-treatment with FHD-286 and BETi OTX015 significantly reduced AML burden and improved survival, without inducing significant toxicity. These findings highlight the FHD-286-based combinations as promising therapy of AML with chromosome 3q26.2 rearrangement and EVI1 overexpression.

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Highly effective combination of BRG1/BRM inhibitor with BET inhibitor or decitabine for high-risk MECOM-rearranged AML [ChIP-Seq]

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Highly effective combination of BRG1/BRM inhibitor with BET inhibitor or decitabine for high-risk MECOM-rearranged AML [ATAC-seq]

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