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ATAC-seq in TX1072 XXΔXic and XO mESCs during differentiation

ABSTRACT: ATAC-seq in TX1072 XXΔXic and XO mESCs during differentiation

PROVIDER: PRJNA704380 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13771250_1.fastq.gz	Fastqsanger.gz
	SRR13771250_2.fastq.gz	Fastqsanger.gz
	SRR13771251_1.fastq.gz	Fastqsanger.gz
	SRR13771251_2.fastq.gz	Fastqsanger.gz
	SRR13771252_1.fastq.gz	Fastqsanger.gz

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TT-seq and RNA-seq in TX1072 XXΔXic and XO mESCs during differentiation

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ATAC-seq in TX1072 XXΔXic and XO mESCs during differentiation

Project description:Developmental genes are controlled by complex cis-regulatory landscapes that integrate multiple signals to ensure the correct spatio-temporal expression pattern. To investigate the underlying regulatory principles, we use the Xist locus as a model, which encodes the master regulator of X-chromosome inactivation. Xist is upregulated at the primed pluripotent state in a female-specific manner, thus integrating developmental cues and X-dosage information. It remains poorly understood how these signals are decoded by the ~800kb genomic region that controls Xist. While a series of repressive cis-regulatory elements have been identified, the distal enhancers that activate Xist transcription remain largely unknown. Here we use ATAC-seq to profile DNA accessibility within the X inactivation center at the onset of random X-chromosome inactivation using an endogenous cell model of the inactive (TX 1072 XXΔXic) and active (TX 1072 XO) X chromosome.

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CUT&Tag on H3K4me3, H3K27ac, H3K4me1, H3K9me3, H3K27me3, H3K36me3 and H2AK119ub in TX1072 XXΔXic and XO mESCs during differentiation

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Project description:Developmental genes are controlled by complex cis-regulatory landscapes that integrate multiple signals to ensure the correct spatio-temporal expression pattern. To investigate the underlying regulatory principles, we use the Xist locus as a model, which encodes the master regulator of X-chromosome inactivation. Xist is upregulated at the primed pluripotent state in a female-specific manner, thus integrating developmental cues and X-dosage information. It remains poorly understood how these signals are decoded by the ~800kb genomic region that controls Xist. While a series of repressive cis-regulatory elements have been identified, the distal enhancers that activate Xist transcription remain largely unknown. Here we use TT-seq and RNA-seq to profile nascent and processed RNA transcription within the X inactivation center at the onset of random X-chromosome inactivation using an endogenous cell model of the inactive (TX 1072 XXΔXic) and active (TX 1072 XO) X chromosome.

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