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ChIP-Seq of ES-E14 mouse embryonic stem cells investigating changes in Sall4

ABSTRACT: ChIP-Seq of ES-E14 mouse embryonic stem cells investigating changes in Sall4

PROVIDER: PRJEB38752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4210450.fastq.gz	Fastqsanger.gz
	ERR4210441.fastq.gz	Fastqsanger.gz
	ERR4210451.fastq.gz	Fastqsanger.gz
	ERR4210442.fastq.gz	Fastqsanger.gz
	ERR4210452.fastq.gz	Fastqsanger.gz

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ChIP-Seq of ES-E14 mouse embryonic stem cells investigating changes in Sall4

Project description:Sall4 is a stem cell factor which is important for embryogenesis. We have genetically modified Sall4 in mouse embryonic stem cells to access the preference of Sall4 binding site. There are three different genetic modifications for the ES cells in the form of Sall4 Knockout (KO), Sall4 Zinc Finger Cluster 4 Mutation (ZFC4mut) and Sall4 Zinc Finger Cluster 1-2 Deletion (ZFC1-2Δ) respectively that we have considered for our study.

2021-01-05 | E-MTAB-9197 | biostudies-arrayexpress

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Titration of Sall4 by the NuRD complex facilitates neural differentiation of ES cells

Project description:Sall4 is a transcription factor essential for early mammalian development. Though it is reported to play an important role in embryonic stem (ES) cell self-renewal, whether it is an essential pluripotency factor has been disputed. Though Sall4 is known to associate with the Nucleosome Remodeling and Deacetylase (NuRD) complex, the nature of this interaction is unclear as NuRD and Sall4 serve opposing functions in ES cells. Here we use defined culture conditions and single-cell gene expression analyses to show that Sall4 prevents activation of the neural gene expression programme in ES cells but is dispensable for maintaining the pluripotency gene regulatory network. We further show using genome-wide analyses that while Sall4 interacts with NuRD, it neither recruits NuRD to chromatin nor influences transcription via NuRD. Rather we propose a model where, by titrating Sall4 protein, NuRD limits the differentiation-inhibiting activity of Sall4 in ES cells to enable lineage commitment.

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Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder ES cells were cultured with or without mouse embryonic fibroblast (MEF) feeder cells in LIF-supplemented medium as described. To maintain the expression of Oct3/4, all ES cells were cultured in the presence of Blasticidin. Four samples were analyzed. GSM356329, GSM356330 : cultured in the absence of feeders GSM356331, GSM356332 : cultured on the feeders

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Project description:This SuperSeries is composed of the following subset Series: GSE21054: Differential roles of Sall4 isoforms in ES cell pluripotency: expression GSE21055: Differential Role of Sall4 isoforms in ES cell pluripotency: ChIP-chip Refer to individual Series

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