Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

ABSTRACT: Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

PROVIDER: PRJNA954782 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24144089_1.fastq.gz	Fastqsanger.gz
	SRR24144089_2.fastq.gz	Fastqsanger.gz
	SRR24144090_1.fastq.gz	Fastqsanger.gz
	SRR24144090_2.fastq.gz	Fastqsanger.gz
	SRR24144091_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

Project description:To investigate the role of RNA methyltransferase-like 3 (Mettl3)-mediated m6A modification in pancreatic endocrine differentiation in early embryonic period. We then performed m6A MeRIP-seq (GenSeq®️ m6A MeRIP Kit) at E15.5 Mettl3pKO pancreas group and E15.5 WT pancreas group

2023-04-16 | GSE229502 | GEO

Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass [scRNA-seq]

Project description:To investigate the role of RNA methyltransferase-like 3 (Mettl3)-mediated m6A modification in pancreatic endocrine differentiation in early embryonic period. We then performed single cell RNA-seq at E15.5 Mettl3pKO pancreas group and E15.5 WT pancreas group

2024-03-18 | GSE234256 | GEO

Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass [scRNA-seq]

Project description:Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass [scRNA-seq]

| PRJNA980632 | ENA

Characterization and reduction of non-endocrine cells accompanying islet-like endocrine cells differentiated from human iPSC

Project description:The differentiation of pancreatic endocrine cells from human pluripotent stem cells has been thoroughly investigated for their application in cell therapy against diabetes. Although non-endocrine cells are inevitable contaminating by-products of the differentiation process, a comprehensive profile of such cells is lacking. Therefore, we characterized non-endocrine cells in iPSC-derived pancreatic islet cells (iPIC) using single-cell transcriptomic analysis. We found that non-endocrine cells consist of 1) heterogeneous proliferating cells, and 2) cells with not only pancreatic traits but also liver or intestinal traits marked by FGB or AGR2. Non-endocrine cells specifically expressed FGFR2, PLK1, and LDHB. We demonstrated that inhibition of pathways involving these genes selectively reduced the number of non-endocrine cells in the differentiation process. These findings provide useful insights into cell purification approaches and contribute to the improvement of the mass production of endocrine cells for stem cell-derived cell therapy for diabetes.

2022-09-16 | GSE213290 | GEO

The effects of METTL3 on islet β-cell function

Project description:Purpose: The goal of this study is to investigate how METTL3 regulates islet β-cell function. Methods: Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany) from pancreatic islets of Mettl3flox/flox and β-Mettl3-KO mice at 8 weeks old. Each RNA sample was pooled from four Mettl3flox/flox and β-Mettl3-KO mice, respectively. Three independent biological replicates for each group were used for RNA-seq. RNA-seq was performed by deep sequencing using an Illumina Novaseq 6000 platform. Paired-end clean reads were aligned to the mouse reference genome(GRCm38.p6) with Hisat2 v2.0.5, and the aligned reads were used to quantify mRNA expression by using featureCounts v1.5.0-p3. Conclusion: Our study represents the first detailed analysis of islet transcriptomes from Mettl3flox/flox and β-Mettl3-KO mice, generated by RNA-seq technology. The RNA-seq analysis showed that 2560 genes were downregulated and 3408 genes were upregulated in the pancreatic islets of β-Mettl3-KO mice. GO analysis showed that the downregulated genes were primarily related to insulin secretion, SNARE binding, and mitochondrial respiratory chain, whereas the upregulated genes were associated with the immune response, B cell activation, and antigen binding.

2020-11-13 | GSE155612 | GEO

Synaptotagmin 13 drives pancreatic endocrine cell egression and islet morphogenesis: BioID

Project description:Identification of protein intreactions for the synaptotagmin 13 protein from MDCK cells by BioID-based proximity labelling and LFQ mass spectrometry. Epithelial cell egression is important for organ development and cell differentiation, but also drives cancer metastasis. The tightly connected pancreatic epithelial differentiation and morphogenesis generate islets of Langerhans. However, the morphogenetic drivers and molecular mechanisms are largely unresolved. Here we identify the uncharacterized Synaptotagmin 13 (Syt13) as a major regulator of endocrine cell egression and islet morphogenesis and differentiation. We detected upregulation of Syt13 in endocrine precursors that associates with increased expression of several unique cytoskeletal components. High-resolution imaging reveals a previously unidentified apical-basal to front-rear repolarization during endocrine cell egression. Strikingly, Syt13 directly interacts with acetylated tubulin and phosphoinositide phospholipids to be recruited to the leading edge of egressing cells. Knockout of Syt13 discloses the impairment in endocrine cell egression and skews the α-to-β-cell ratio. At mechanistic levels, Syt13 regulates protein endocytosis to remodel the basement membrane and modulate cell-matrix adhesion at the leading edge of egressing endocrine cells. Altogether, these findings implicate that Ca2+-independent atypical Syt13 vesicular protein functions in regulating cell polarity to orchestrate endocrine cell egression and tissue morphogenesis.

2022-06-23 | PXD026699 | Pride

Synaptotagmin 13 drives pancreatic endocrine cell egression and islet morphogenesis: Affinity purification

Project description:Identification of protein complexes for the synaptotagmin 13 protein from MDCK cells by Strep affinity purificaiton and LFQ mass spectrometry. Epithelial cell egression is important for organ development and cell differentiation, but also drives cancer metastasis. The tightly connected pancreatic epithelial differentiation and morphogenesis generate islets of Langerhans. However, the morphogenetic drivers and molecular mechanisms are largely unresolved. Here we identify the uncharacterized Synaptotagmin 13 (Syt13) as a major regulator of endocrine cell egression and islet morphogenesis and differentiation. We detected upregulation of Syt13 in endocrine precursors that associates with increased expression of several unique cytoskeletal components. High-resolution imaging reveals a previously unidentified apical-basal to front-rear repolarization during endocrine cell egression. Strikingly, Syt13 directly interacts with acetylated tubulin and phosphoinositide phospholipids to be recruited to the leading edge of egressing cells. Knockout of Syt13 discloses the impairment in endocrine cell egression and skews the α-to-β-cell ratio. At mechanistic levels, Syt13 regulates protein endocytosis to remodel the basement membrane and modulate cell-matrix adhesion at the leading edge of egressing endocrine cells. Altogether, these findings implicate that Ca2+-independent atypical Syt13 vesicular protein functions in regulating cell polarity to orchestrate endocrine cell egression and tissue morphogenesis.

2023-12-28 | PXD026698 | Pride

Endocrine islet beta-cell subtypes with differential function are derived from biochemically distinct embryonic endocrine islet progenitors that are regulated by maternal nutrients

Project description:Endocrine islet beta cells comprise heterogenous cell subsets. Yet the origin, stability, and physiological significance of these subsets remain largely unknown. Using combinatorial cell lineage tracing, scRNA-seq, and DNA methylation analysis, we show here that embryonic islet progenitors with differential gene expression and DNA methylation produce stable beta-cell subtypes of different function and viability in adult mice. Differentially expressed genes, including the Myt transcription factors, voltage-gated channels, and Ca2+-sensor synaptotagmins, contribute to the functional differences of these subtypes. Maternal overnutrition, a major diabetes risk factor, reduces the proportion of endocrine progenitors of the better-functionality beta-cell subtype. Intriguingly, the gene signature that defines mouse beta-cell subtypes can reliably divide human cells into two populations, with the proportion of better-functionality beta cells reduced in diabetic donors. These results establish that some beta-cell subtypes are determined via DNA methylation in embryonic islet progenitors, which is regulated by diabetes-causing maternal factors. The implication is that modulating DNA methylation in islet progenitors can be explored to improve beta-cell function in the prevention and therapy of diabetes.

2025-02-01 | GSE254955 | GEO

The effects of METTL3 on islet β-cell function

Project description:The effects of METTL3 on islet β-cell function

| PRJNA650497 | ENA

Comparison of endocrine enriched genes in islet beta cells versus induced beta cells

Project description:Endocrine enriched genes in adult islet beta cells were identified and compared with that of induced beta cells (with M3 transcription factors) in adult. The control sample is non-beta pancreatic cells.

2008-07-08 | GSE12025 | GEO

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