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The impact of maternal diet on endocrine islet progenitor cells in mice

ABSTRACT: The impact of maternal diet on endocrine islet progenitor cells in mice

PROVIDER: PRJNA1071543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27799800_1.fastq.gz	Fastqsanger.gz
	SRR27799800_2.fastq.gz	Fastqsanger.gz
	SRR27799801_1.fastq.gz	Fastqsanger.gz
	SRR27799801_2.fastq.gz	Fastqsanger.gz
	SRR27799802_1.fastq.gz	Fastqsanger.gz

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The impact of maternal diet on endocrine islet progenitor cells in mice

Project description:The goal of this study is to examine how altering maternal diet, including poor- or over-nutrition, impacts the gene expression levels in islet progenitors, including those cells that have not been committed to the endocrine fate and those having committed to it. At present, we will determine the gene expression changes in these progenitors.

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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.

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

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Transcriptional profiling of Ngn3-dependent pancreatic endocrine differentiation at E15.5

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Ngn3^GFP/+ [het] FACS sorted pancreatic cells at E15.5 (commited endocrine progenitor cells) and in Ngn3^GFP/GFP [null] at E15.5 (defective endocrine progenitor cells). This experiment is designed to understand the gene expression alteration in the endocrine lineage at different embryonic days. The aim is to understand both Ngn3 dependent and independent gene expression profiles so as to reveal the instructive signals that specfy the collective endocrine islet cell fate or specific islet cell type.

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

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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.

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Project description:During embryonic development, islet progenitors are specified from pancreatic duct cells by transient expression of Neurog3, a transcription factor necessary and sufficient for initiation of islet development. To understand the dynamics of Neurog3-dependent endocrine cell fate determination, in this study we used ATAC-Seq to identify accessible genomic regions of purified duct, endocrine progenitor, and endocrine cells isolated from mice with varying Neurog3 dosage

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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.

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