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The study of chromatin occupancy other mitotically bound factors upon the mitotic depletion of SMARCE1 in mouse ES cells.

ABSTRACT: The study of chromatin occupancy other mitotically bound factors upon the mitotic depletion of SMARCE1 in mouse ES cells.

PROVIDER: PRJNA894705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22059322_1.fastq.gz	Fastqsanger.gz
	SRR22059322_2.fastq.gz	Fastqsanger.gz
	SRR22059323_1.fastq.gz	Fastqsanger.gz
	SRR22059323_2.fastq.gz	Fastqsanger.gz
	SRR22059324_1.fastq.gz	Fastqsanger.gz

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The study of chromatin occupancy other mitotically bound factors upon the mitotic depletion of SMARCE1 in mouse ES cells.

Project description:We executed CUT&RUN-seq for SOX2, ESRRB, and EZH2 upon the mitotic depletion of SMARCE1 in mouse ES cells.

2023-03-19 | GSE216661 | GEO

Mitotic bookmarking by SWI/SNF subunits

Project description:For cells to initiate and sustain a differentiated state, it is necessary that a “memory” of this state is transmitted through mitosis to the daughter cells. Mammalian SWItch/ Sucrose Non- Fermentable (SWI/SNF) complexes, also called Brg1/ Brg- associated factors (BAF), control cell identity by modulating chromatin architecture to regulate gene expression, but whether they participate in cell fate memory is unclear. Here, we provide evidence that subunits of SWI/SNF act as mitotic bookmarks to safeguard cell identity during cell division. The SWI/SNF core subunits SMARCE1 and SMARCB1 are displaced from enhancers but bound on promoters during mitosis and we show that this binding is required for appropriate reactivation of bound genes after mitotic exit. Ablation of SMARCE1 during a single mitosis in mouse embryonic stem cells is sufficient to disrupt gene expression, impair the occupancy of several established bookmarks at a subset of their targets, and cause aberrant neural differentiation. Thus, SWI/SNF subunit SMARCE1 plays a mitotic bookmarking role and is essential for heritable epigenetic fidelity during transcriptional reprogramming.

2023-03-18 | GSE189563 | GEO

Transcription profiling of Smarce1- MD (R42A) and Smarce1- MD mESCs with BMP4 rescue.

Project description:To evaluate the effects of mitotic degradation of SMARCE1 upon gene expression, we performed RNA-sequencing (RNA-seq) of cultures of four independent subclones each of Smarce1-MD and control Smarce1-MD (R42A) mESCs. We found that transcription of the core pluripotency regulatory network was not disrupted. In contrast, GO analysis showed that neural differentiation-associated terms were enriched among genes upregulated in Smarce1-MD mESCs. To better understand the difference in neural fates in the neural induction experiments, we performed differential gene expression analysis and gene set enrichment analysis (GSEA) studies. Mitotic degradation of SMARCE1 resulted in higher expression of GABA receptors and hyper-activation of synaptic signaling on neural induction, indicating the aberrant neural cell fate commitment compared to SMARCE1-MD (R42A) cultures. And then we add back BMP4 to partically rescue the phenotype and very small amount of BMP4 will rescue the phenotype.

2023-03-19 | GSE216656 | GEO

Transcription profiling of Smarce1- MD (R42A) and Smarce1- MD mESCs, and their derived cell cultures at day 06 after neural induction.

2023-03-19 | GSE189557 | GEO

The study of nascent RNA transcripts in asynchronous cells and cells released from mitosis at the indicated timepoints between Smarce1- MD (R42A) and Smarce1- MD mESCs.

Project description:SMARCE1 binding on mitotic chromatin is required for the timely reinitiation of expression of SMARCE1-bookmarked genes and maintaining identity memory in cell division.

2023-03-19 | GSE189559 | GEO

The study of SWI/SNF subunits and other transcription factors deposition in asynchronous and mitotic mESCs and cells released from mitosis

Project description:We executed CUT&RUN-seq for SWI/SNF components ARID1A, BRD9, SMARCA4, SMARCB1, SMARCE1, as well as ESRRB, SOX2, and EZH2 in asynchronous and mitotic cells and reported that, in asynchronous cells, ARID1A localized primarily at enhancer regions and EZH2 preferentially deposited at bivalent promoters and silent enhancer domains. The remaining factors were enriched at both TSS/promoters and to varying degrees at active enhancers. Unexpectedly, in mitosis, the chromatin regulatory factors almost all tethered at proximal gene regions with very little binding at enhancers. While the SWI/SNF subunits were bound principally at promoters, EZH2, the catalytic subunit of Polycomb Repressive Complex 2 was bound at both promoters and silent enhancers in mitotic cells. Moreover, we reported that upon the degradation of SMARCE1 in mitosis, the occupancy of SOX2, ESRRB, and EZH2 on mitotic chromatin was disrupted.

2023-03-19 | GSE189560 | GEO

The study of SMARCE1 and SOX2 deposition in DMSO or BRM014 treated Smarce1-MD(R42A) and Smarce1-MD cells at 90 min after releasing from mitosis.

Project description:We executed CUT&RUN-seq for SMARCE1 and SOX2 in BRG1 inhibitor BRM014 treated ,in MD or MD mutatnt mouse embryonic stem cells at 90 min from mitotic release.

2023-03-19 | GSE216657 | GEO

ChIP-seq for SMARCE1 and SMARCC1 in non-invasive and invasive HMLE-Twist-ER cells

Project description:We find that in invasive HMLE-Twist-ER cells, SMARCE1 binds to ILF3 and is localized to ILF motifs. In contrast, ILF motifs were not enriched at SMARCE1-bound sites in noninvasive HMLE-Twist-ER cells or at SMARCC1-bound sites.

2017-03-23 | GSE96933 | GEO

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Project description:To evaluate the differential potential affected by SMARCE1 -MD/MD(R42A) , we performed RNA-sequencing (RNA-seq) of Smarce1-MD and control Smarce1-MD (R42A) embrynoic body.

2023-03-19 | GSE216662 | GEO

The study of nascent RNA transcripts in asynchronous cells and cells released from mitosis at the indicated timepoints between IAA or dmso treatment in the SMARCE1 - AID system

Project description:SMARCE1 binding on mitotic chromatin is required for the timely reinitiation of expression of SMARCE1-bookmarked genes and maintaining identity memory in cell division.

2023-06-05 | GSE234094 | GEO

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