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

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

PROVIDER: PRJNA732405 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14633956_1.fastq.gz	Fastqsanger.gz
	SRR14633956_2.fastq.gz	Fastqsanger.gz
	SRR14633957_1.fastq.gz	Fastqsanger.gz
	SRR14633957_2.fastq.gz	Fastqsanger.gz
	SRR14633958_1.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

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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

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

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

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BRG1/BRM inhibitor targets AML stem cells and exerts superior preclinical efficacy combined with BET or Menin inhibitor (scRNA-Seq)

Project description:BRG1 (SMARCA4) and BRM (SMARCA2) are the mutually exclusive core ATPases of the chromatin remodeling BAF (BRG1/BRM-associated factor) complexes. They enable transcription factors/co-factors to access enhancers/promoter and modulate gene-expressions responsible for cell growth and differentiation of AML stem/progenitor cells. In AML with MLL1r (MLL1 rearrangement) or mutant (mt) NPM1, although Menin inhibitor (MI) treatment induces clinical remissions, most patients either fail to respond or relapse, some harboring Menin mutations. FHD-286 is an orally bioavailable, selective inhibitor of BRG1/BRM under clinical development in AML. Present studies show that FHD-286 induces differentiation and lethality in AML cells with MLL1r or mtNPM1, concomitantly causing perturbed chromatin accessibility and repression of c-Myc, PU.1 and CDK4/6. Co-treatment with FHD-286 and decitabine, BET inhibitor (BETi) or MI, or venetoclax synergistically induced in vitro lethality in AML cells with MLL1r or mtNPM1. In patient-derived xenograft (PDX) models of AML with MLL1r or mtNPM1, FHD-286 treatment reduced AML burden, improved survival, and attenuated AML-initiating potential of stem-progenitor cells. Compared to each drug, co-treatment with FHD-286 and BETi, MI, decitabine or venetoclax 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 MLL1r or mtNPM1.

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