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Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome

ABSTRACT: Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome

PROVIDER: PRJNA756240 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15526384.fastq.gz	Fastqsanger.gz
	SRR15526385.fastq.gz	Fastqsanger.gz
	SRR15526386.fastq.gz	Fastqsanger.gz
	SRR15526387.fastq.gz	Fastqsanger.gz
	SRR15526388.fastq.gz	Fastqsanger.gz

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Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome

Project description:We performed RNA-seq to investigate global changes in gene expression in proliferating myoblasts transduced with either the scramble, Baf250A, Brd9 or Baf180 shRNAs. This study revelaed that the Baf250-containing BAF complex and the Brd9-containing ncBAF complex contribute to myoblast proliferation but the Baf180-containing PBAF subfamily does not.

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Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

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Project description:Testicular germ cell tumors (TGCT) are the predominant tumor in younger males. Usually, curation rates are quite high, but 15-20 % of patients with metastatic non-seminomas are resistant to standard cisplatin-based therapy. Interfering with the epigenetic landscape has already been shown to be effective in prostate cancer. BRD9 is an epigenetic reader which is part of the SWI-SNF chromatin-remodeling complex involved in regulation of gene expression. Alternative treatment options for therapy-resistant TGCT patients need to be investigated. BRD9 seems to be a promising target for analyzing the effect of BRD9 inhibition in TGCT cell lines. BRD9 expression was analyzed by meta-analysis of microarray data as well as by Western Blot and immunohistochemistry of tissue microarrays in TGCT cell lines and TGCT tissues. Viability was assessed by performing XTT-assay to determine the effect of BRD9 inhibition in TGCT cell lines. FACS analysis was used to display changes in cell cycle distribution as well as apoptosis. The impact on transcriptome level of BRD9 inhibition was analyzed by 3’mRNA-sequencing. BRD9 was heterogeneously expressed in TGCT cell lines and tissues. Nevertheless, inhibition of BRD9 led to strong decrease in viability. I-BRD9 induced apoptosis as well as cell cycle arrest in G1-phase. On transcriptome level, prominent downregulation of pluripotency markers (NANOG, PRMD14 and KLF4) and upregulation of genes involved in epithelium development were detected. I-BRD9 treatment of GCT cell lines reduced viability, induced apoptosis and cell cycle arrest while control cells remain mainly unaffected. Transcriptomic data indicate exit of pluripotency and differentiation towards the epithelial fate. In fact, loss of pluripotency and differentiation seems to be a common aspect of GCT reacting to drug application. The data implicate I-BRD9 as a possible treatment alternative for TGCTs.

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Project description:The hierarchical organization of hematopoietic stem cells (HSCs) governing adult hematopoiesis has been extensively investigated. However, the dynamic epigenomic transition from fetal to adult hematopoiesis remains incompletely understood, particularly regarding the involvement of epigenetic factors. In this study, we investigate the roles of BRD9, an essential component of the non-canonical BAF (ncBAF) complex known to govern the fate of adult HSCs, in fetal hematopoiesis. Consistent with observations in adult hematopoiesis, BRD9 loss impairs fetal HSC stemness and disturbs erythroid maturation. Intriguingly, the impact on myeloid lineage was discrepant: BRD9 loss inhibited and promoted myeloid differentiation in fetal and adult models, respectively. Through comprehensive transcriptomic and epigenomic analyses, we elucidate the differential roles of BRD9 in a context- and lineage-dependent manner. Our data uncover how BRD9/ncBAF complex modulates transcription in a stage-specific manner, providing deeper insights into the epigenetic regulation underlying the transition from fetal to adult hematopoiesis.

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