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Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit (scRNA-Seq)

ABSTRACT: Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit (scRNA-Seq)

PROVIDER: PRJNA934465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23447845_1.fastq.gz	Fastqsanger.gz
	SRR23447845_2.fastq.gz	Fastqsanger.gz
	SRR23447846_1.fastq.gz	Fastqsanger.gz
	SRR23447846_2.fastq.gz	Fastqsanger.gz

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Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit

Project description:Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit

| PRJNA934393 | ENA

Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit (RNA-Seq)

Project description:Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit (RNA-Seq)

| PRJNA934460 | ENA

Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit (scRNA-Seq)

Project description:Many lincRNAs have been identified as essential regulators for ESC pluripotency through siRNA-based screening. However, the biological and molecular functions of the large intergenic noncoding RNAs (lincRNAs) remain unclear. Here, we employed CRISPR/Cas9-mediated knockout technology to explore the functions of 8 previously annotated lincRNAs in ESCs. Unexpectedly, it was found that most lincRNAs are dispensable for pluripotency maintenance, cloning formation ability, proliferation and apoptosis in ESCs when we disrupted these lincRNAs individually or in combinations. Single-cell transcriptomic analysis of a set of lncRNA knockout ESCs showed consistent results, indicating that previously observed functions of lincRNAs on ESC pluripotency maintenance may be due to off-targeted effects. Interestingly, deletion and transcriptional repression of linc1343 disrupts embryoid body (EB) differentiation in ESC. Notably, GM17300 and two small RNAs (Snora73a, Snora73b) derived from the lnc1343 locus are highly expressed in ESCs. Further overexpression of Snora73a and Snora73b in linc1343 knockout cells rescue the phenotype, suggesting that snoRNAs derived from linc1343 are the responders for EB differentiation. Taken together, our results demonstrate the divergent effects of lincRNAs on regulating ESC pluripotency and EB differentiation.

2024-08-07 | GSE225238 | GEO

Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit (RNA-Seq)

2024-08-07 | GSE225237 | GEO

lincRNAs act in the circuitry controlling pluripotency and differentiation

Project description:While thousands of large intergenic non-coding RNAs (lincRNAs) have been identified in mammals, few have been functionally characterized leading to debate about their biological role. To address this, we performed loss-of-function studies on most lincRNAs expressed in mouse embryonic stem cells (ESC) and characterized the effects on gene expression. Here we show that knockdown of lincRNAs have major consequences on gene expression patterns, comparable to knockdown of well-known ESC regulators. Notably, lincRNAs primarily affect gene expression in trans. We identify dozens of lincRNAs whose knockdown causes an exit from the pluripotent state or upregulation of lineage commitment programs. We integrate lincRNAs into the molecular circuitry of ESCs and show that lincRNA genes are regulated by key transcription factors and that lincRNA transcripts physically bind to multiple chromatin regulatory proteins to affect shared gene expression programs. Together, the results demonstrate that lincRNAs have key roles in the circuitry controlling ESC state. We generated five lentiviral-based shRNAs targeting each of the 237 lincRNAs previously identified in ESCs. These shRNAs successfully targeted 147 lincRNAs and reduced their expression by an average of ~75% compared to endogenous levels in ESCs. As positive controls, we generated shRNAs targeting ~50 genes encoding regulatory proteins, including both transcription factor and chromatin factor genes that have been shown to play critical roles in ESC regulation; we obtained validated hairpins against 40 of these genes. As negative controls, we performed independent infections with lentiviruses containing 27 different shRNAs with no known cellular target RNA.

2011-08-29 | E-GEOD-30245 | biostudies-arrayexpress

lincRNAs act in the circuitry controlling pluripotency and differentiation

2011-08-30 | GSE30245 | GEO

Reevaluation by CRISPR-Cas9 approach reveals multiple lincRNAs dispensable for pluripotency maintenance and SNORA73 essential for pluripotency exit

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-07 | GSE225240 | GEO

Mesenchymal-Epithelial Transition Regulates Initiation of Pluripotency Exit before Gastrulation

Project description:The pluripotent epiblast gives rise to all tissues and organs in an adult body. Its differentiation starts at gastrulation when the epiblast generates mesoderm and endoderm germ layers through a process called epithelial-mesenchymal transition (EMT). Although gastrulation EMT coincides with loss of epiblast pluripotency, pluripotent cells in development and in culture can adopt either mesenchymal or epithelial morphology. The relationship between epiblast pluripotency and epiblast morphology is not well understood. In this work, using chicken epiblast and human induced pluripotent stem cell (hiPSC) models, we show that pluripotent cells undergo an obligatory mesenchymal-epithelial transition (MET) prior to EMT-associated pluripotency loss. Epiblast MET and the subsequent EMT are two distinct processes. The former, a partial MET, is associated with reversible pluripotency exit; whereas the latter, a full EMT, is associated with complete and irreversible pluripotency loss. We provide evidence that integrin-mediated cell-matrix interaction, but not E-cadherin-mediated cell-cell interaction, is a key player in pluripotency exit regulation. We propose that epiblast partial MET is an evolutionarily conserved process among all amniotic vertebrates and its developmental function is to mediate planar symmetry-breaking within an epithelialized epiblast, taking place after epiblast MET but before gastrulation EMT.

2018-12-31 | GSE114476 | GEO

Transient upregulation of IRF1 during the exit from naive pluripotency confers viral protection

Project description:IRF1 in exit from naive pluripotency

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Jun-mediated changes in cell adhesion contribute to embryonic stem cell exit from ground state pluripotency

Project description:Embryonic stem cells (ESC) are able to give rise to any somatic cell type. A lot is known about how ESC pluripotency is maintained, but comparatively less is known about how differentiation is promoted. Cell fate decisions are regulated by interactions between signalling and transcriptional networks. Recent studies have shown that the overexpression or downregulation of the transcription factor Jun can affect the ESC fate. Here we have focussed on the role of the Jun in the exit of mouse ESCs from ground state pluripotency and the onset of early differentiation. Transcriptomic analysis of differentiating ESCs reveals that Jun is required to upregulate a programme of genes associated with cell adhesion as ESCs exit the pluripotent ground state.

2015-12-07 | E-MTAB-4068 | biostudies-arrayexpress

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