Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell Architecture and Functional Requirement of Alternative Splicing during Hematopoietic Stem Cell Emergence

ABSTRACT: Single-cell Architecture and Functional Requirement of Alternative Splicing during Hematopoietic Stem Cell Emergence

PROVIDER: PRJNA769627 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR12129200_1.fastq.gz	Fastqsanger.gz
	SRR12129200_2.fastq.gz	Fastqsanger.gz
	SRR12129201_1.fastq.gz	Fastqsanger.gz
	SRR12129201_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 95

Similar Datasets

Single-cell architecture and functional requirement of alternative splicing during hematopoietic stem cell formation

Project description:Single-cell architecture and functional requirement of alternative splicing during hematopoietic stem cell formation

| PRJNA643551 | ENA

Single-cell Architecture and Functional Requirement of Alternative Splicing during Hematopoietic Stem Cell Emergence

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

2021-10-15 | GSE185555 | GEO

Single-cell architecture and functional requirement of alternative splicing during hematopoietic stem cell formation.

Project description:[Figure: see text].

| S-EPMC8741192 | biostudies-literature

Single-cell Architecture and Functional Requirement of Alternative Splicing during Hematopoietic Stem Cell Emergence [RNA-Seq]

Project description:Hematopoietic stem cells (HSCs) are well known to generate from a rare hemogenic population of embryonic endothelial cells through a dynamic fate transition, accompanied by widespread changes in gene regulatory networks. Nevertheless, RNA splicing, a striking feature in shaping transcriptome and enabling the generation of vast transcripts and diverse proteins, has never been illustrated in this transient endothelial to HSC conversion. Here, we constructed an isoform-based transcriptome landscape during HSC development at single-cell resolution, which enables the identification of hemogenic signature isoforms, as well as stage-specific splicing events. Combining with functional screening, we showed that the inclusion of such hemogenic-specific exons was essential for hemogenic function in vitro. Moreover, their gradual appearance along with HSC specification from endothelial cells was orchestrated by the splicing regulator Srsf2. Therefore, early Srsf2 deficiency from endothelia cells dramatically impaired the HSC generation, which was accompanied by changes in the splicing pattern of several master hematopoietic regulators. These results redefine our understanding of the dynamic transcriptome diversity and demonstrate that the elaborate control of splicing governs cell fate in HSC formation.

2023-10-01 | GSE185554 | GEO

Single-cell architecture and functional requirement of alternative splicing during hematopoietic stem cell formation

Project description:Hematopoietic stem cells (HSCs) are well known to generate from a rare hemogenic population of embryonic endothelia cells through a dynamic fate transition, accompanied by widespread changes in gene regulatory networks. Nevertheless, RNA splicing, a striking feature in shaping transcriptome and enabling the generation of vast transcripts and diverse proteins, has never been illustrated in this transient endothelial to HSC conversion. Here, we constructed an isoform-based transcriptome landscape during HSC development at single-cell resolution, which enables the identification of hemogenic signature isoforms, as well as stage-specific splicing events. Combining with functional screening, we showed that the inclusion of such hemogenic-specific exons was essential for hemogenic function in vitro. Moreover, their gradual appearance along with HSC specification from endothelia cells was orchestrated by the splicing regulator Srsf2. Therefore, early Srsf2 deficiency from endothelia cells dramatically impaired the HSC generation, which was accompanied by changes in splicing pattern of several master hematopoietic regulators. These results redefine our understanding of the dynamic transcriptome diversity and demonstrate that the elaborate control of splicing governs cell fate in HSC formation.

2021-10-13 | GSE153653 | GEO

Stage-specific requirement for Mettl3-dependent m6A mRNA methylation during hematopoietic stem cell differentiation

Project description:Stage-specific requirement for Mettl3-dependent m6A mRNA methylation during hematopoietic stem cell differentiation

| PRJNA509123 | ENA

A CLK3-HMGA2 Alternative Splicing Axis Impacts Human Hematopoietic Stem Cell Molecular Identity throughout Development.

Project description:While gene expression dynamics have been extensively cataloged during hematopoietic differentiation in the adult, less is known about transcriptome diversity of human hematopoietic stem cells (HSCs) during development. To characterize transcriptional and post-transcriptional changes in HSCs during development, we leveraged high-throughput genomic approaches to profile miRNAs, lincRNAs, and mRNAs. Our findings indicate that HSCs manifest distinct alternative splicing patterns in key hematopoietic regulators. Detailed analysis of the splicing dynamics and function of one such regulator, HMGA2, identified an alternative isoform that escapes miRNA-mediated targeting. We further identified the splicing kinase CLK3 that, by regulating HMGA2 splicing, preserves HMGA2 function in the setting of an increase in let-7 miRNA levels, delineating how CLK3 and HMGA2 form a functional axis that influences HSC properties during development. Collectively, our study highlights molecular mechanisms by which alternative splicing and miRNA-mediated post-transcriptional regulation impact the molecular identity and stage-specific developmental features of human HSCs.

| S-EPMC5957284 | biostudies-literature

Temporal requirement of the alternative-splicing factor Sfrs1 for the survival of retinal neurons.

Project description:Alternative splicing is the primary mechanism by which a limited number of protein-coding genes can generate proteome diversity. We have investigated the role of the alternative-splicing factor Sfrs1, an arginine/serine-rich (SR) protein family member, during mouse retinal development. Loss of Sfrs1 function during embryonic retinal development had a profound effect, leading to a small retina at birth. In addition, the retina underwent further degeneration in the postnatal period. Loss of Sfrs1 function resulted in the death of retinal neurons that were born during early to mid-embryonic development. Ganglion cells, cone photoreceptors, horizontal cells and amacrine cells were produced and initiated differentiation. However, these neurons subsequently underwent cell death through apoptosis. By contrast, Sfrs1 was not required for the survival of the neurons generated later, including later-born amacrine cells, rod photoreceptors, bipolar cells and Müller glia. Our results highlight the requirement of Sfrs1-mediated alternative splicing for the survival of retinal neurons, with sensitivity defined by the window of time in which the neuron was generated.

| S-EPMC3593640 | biostudies-literature

Proinflammatory signaling regulates hematopoietic stem cell emergence.

Project description:Hematopoietic stem cells (HSCs) underlie the production of blood and immune cells for the lifetime of an organism. In vertebrate embryos, HSCs arise from the unique transdifferentiation of hemogenic endothelium comprising the floor of the dorsal aorta during a brief developmental window. To date, this process has not been replicated in vitro from pluripotent precursors, partly because the full complement of required signaling inputs remains to be determined. Here, we show that TNFR2 via TNF? activates the Notch and NF-?B signaling pathways to establish HSC fate, indicating a requirement for inflammatory signaling in HSC generation. We determine that primitive neutrophils are the major source of TNF?, assigning a role for transient innate immune cells in establishing the HSC program. These results demonstrate that proinflammatory signaling, in the absence of infection, is utilized by the developing embryo to generate the lineal precursors of the adult hematopoietic system.

| S-EPMC4243083 | biostudies-literature

The human XPG gene: gene architecture, alternative splicing and single nucleotide polymorphisms.

Project description:Defects in the XPG DNA repair endonuclease gene can result in the cancer-prone disorders xeroderma pigmentosum (XP) or the XP-Cockayne syndrome complex. While the XPG cDNA sequence was known, determination of the genomic sequence was required to understand its different functions. In cells from normal donors, we found that the genomic sequence of the human XPG gene spans 30 kb, contains 15 exons that range from 61 to 1074 bp and 14 introns that range from 250 to 5763 bp. Analysis of the splice donor and acceptor sites using an information theory-based approach revealed three splice sites with low information content, which are components of the minor (U12) spliceosome. We identified six alternatively spliced XPG mRNA isoforms in cells from normal donors and from XPG patients: partial deletion of exon 8, partial retention of intron 8, two with alternative exons (in introns 1 and 6) and two that retained complete introns (introns 3 and 9). The amount of alternatively spliced XPG mRNA isoforms varied in different tissues. Most alternative splice donor and acceptor sites had a relatively high information content, but one has the U12 spliceosome sequence. A single nucleotide polymorphism has allele frequencies of 0.74 for 3507G and 0.26 for 3507C in 91 donors. The human XPG gene contains multiple splice sites with low information content in association with multiple alternatively spliced isoforms of XPG mRNA.

| S-EPMC31292 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data