Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TASOR expression in naive embryonic stem cells safeguards their developmental potential [CUT&TAG]

ABSTRACT: TASOR expression in naive embryonic stem cells safeguards their developmental potential [CUT&TAG]

PROVIDER: PRJNA1090603 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28413303_1.fastq.gz	Fastqsanger.gz
	SRR28413303_2.fastq.gz	Fastqsanger.gz
	SRR28413304_1.fastq.gz	Fastqsanger.gz
	SRR28413304_2.fastq.gz	Fastqsanger.gz
	SRR28413305_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

TASOR expression in naive embryonic stem cells safeguards their developmental potential [CUT&TAG]

Project description:The seamless transition through stages of pluripotency relies on a delicate balance between transcription factor networks and epigenetic silencing mechanisms that ensure proper regulation of the developmental program, critical for normal development. Here, we uncover the pivotal role of the transgene activation suppressor (TASOR), a component of the human silencing hub (HUSH) complex, in sustaining cell viability during the transition from naive to primed pluripotency, despite its rapid downregulation during this transition. Loss of TASOR in naive cells triggers replication stress, disrupts H3K9me3 heterochromatin formation, and compromise the transcriptional and post-transcriptional silencing of LINE-1 (L1) transposable elements (TEs), with these effects become more pronounced in primed cells. Remarkably, the survival of Tasor-knockout cells during naive to primed transition can be restored through the inhibition of cysteine-aspartic acid protease (Caspase) or deletion of mitochondrial antiviral signaling protein (MAVS). This suggests that unscheduled L1 expression activates an innate immune response, leading to programmed cell death, specifically in cells exiting naïve pluripotency. Additionally, we propose that HUSH-promoted H3K9me3 in naïve PSCs sets the stage for ensuing DNA methylation in primed cells, establishing long-term silencing during differentiation. Our findings shed insights on the crucial impact of epigenetic programs established in early developmental stages on subsequent phases, underscoring their significance in the developmental process.

2024-09-16 | GSE262194 | GEO

Epigenomic profiling of TASOR in Hela cells using CUT&RUN and CUT&Tag

Project description:Targeted epigenomic profiling methods CUT&RUN and CUT&Tag were used to examine TASOR genome binding and TASOR-regulated H3K9me3 deposition on chromatin.

2020-08-05 | GSE155693 | GEO

TASOR expression in naive embryonic stem cells safeguards their developmental potential [RNA-seq]

2024-09-16 | GSE262195 | GEO

TASOR expression in naive embryonic stem cells safeguards their developmental potential [ATAC-seq]

2024-09-16 | GSE262193 | GEO

TASOR expression in naive embryonic stem cells safeguards their developmental potential [RNA-seq]

Project description:TASOR expression in naive embryonic stem cells safeguards their developmental potential [RNA-seq]

| PRJNA1090604 | ENA

TASOR expression in naive embryonic stem cells safeguards their developmental potential [ATAC-seq]

Project description:TASOR expression in naive embryonic stem cells safeguards their developmental potential [ATAC-seq]

| PRJNA1090605 | ENA

TASOR expression in naive embryonic stem cells safeguards their developmental potential.

Project description:The seamless transition through stages of pluripotency relies on a balance between transcription factor networks and epigenetic mechanisms. Here, we reveal the crucial role of the transgene activation suppressor (TASOR), a component of the human silencing hub (HUSH) complex, in maintaining cell viability during the transition from naive to primed pluripotency. TASOR loss in naive pluripotent stem cells (PSCs) triggers replication stress, disrupts H3K9me3 heterochromatin, and impairs silencing of LINE-1 (L1) transposable elements, with more severe effects in primed PSCs. Notably, the survival of Tasor knockout PSCs during this transition can be restored by inhibiting caspase or deleting the mitochondrial antiviral signaling protein (MAVS). This suggests that unscheduled L1 expression activates an innate immune response, leading to cell death specifically in cells exiting naive pluripotency. Our findings highlight the importance of epigenetic programs established in naive pluripotency for normal development.

| S-EPMC11646706 | biostudies-literature

Epigenomic profiling of TASOR in Hela cells using CUT&RUN and CUT&Tag

Project description:Epigenomic profiling of TASOR in Hela cells using CUT&RUN and CUT&Tag

| PRJNA655230 | ENA