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A peninsular structure coordinates asynchronous differentiation with morphogenesis to generate pancreatic islets

ABSTRACT: A peninsular structure coordinates asynchronous differentiation with morphogenesis to generate pancreatic islets

PROVIDER: PRJNA497287 | ENA |

REPOSITORIES: ENA

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A peninsular structure coordinates asynchronous differentiation with morphogenesis to generate pancreatic islets [bulk vs buds]

Project description:A peninsular structure coordinates asynchronous differentiation with morphogenesis to generate pancreatic islets [bulk vs buds]

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A peninsular structure coordinates asynchronous differentiation with morphogenesis to generate pancreatic islets [bulk vs buds]

Project description:This RNA-seq data is an integral part of a manuscript with the above title. To better characterize the buds appearing on the surface of the spheroidal clusters during the directed differentiation of HUES8 human embryonic stem cells to pancreatic endocrine cells, we performed bulk RNA-sequencing of the buds versus the bulks. Our results indicate that the buds indeed consist of pancreatic endocrine cells, illustrating our ability to recapitulate in vitro our in vivo observations of pancreatic islets forming via peninsular intermediates. See manuscript for more information.

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A Peninsular Structure Coordinates Asynchronous Differentiation with Morphogenesis to Generate Pancreatic Islets.

Project description: Not available

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A peninsular structure coordinates asynchronous differentiation with morphogenesis to generate pancreatic islets

Project description:This scRNA-seq data is an integral part of a manuscript with the above title. Using computational methods, we were able to reconstruct a detailed branched trajectory reflecting pancreatic endocrine differentiation in the mouse embryo. Analysis of the transcriptional changes occuring during the differentiation suggested that epithelial-to-mesenchymal transition likely plays no role in this process, contrary to the prevailing dogma. Our findings were corroborated with high-resolution imaging of the developing pancreas, revealing how differentiating endocrine progenitors migrate in cohesion, forming bud-like islet precursors, or "peninsulas", and that spatiotemporal collinearity during differentiation leads to the typical core-mantle architecture of the mature, spherical islet. This work led to a complete overhaul of our understanding of how pancreatic islets are developed, laying the ground for the generation of entire islets in vitro as a potential novel source of islet transplantation.

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Project description:The entire genome is divided into distinct 1-2 Mb zones that replicate in an ordered and coordinated manner during S phase. While most regions of the genome replicate both alleles in a synchronous manner, some loci have been found to replicate asynchronously, with one allele undergoing DNA synthesis early in S phase, with the other replicating during late S. Random asynchronous replication timing is characterized by cell heterogeneity with some cells. having the maternal allele early replicating while in others, the orientation is reversed, with the paternal allele being early. This type of asynchronous replication can only be studied in a clonal or single cell manner. We have used the repli-seq method to study pre-B clonal f1 mouse cells in order to identify and study asynchronous regions in a genome-wide manner.

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

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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

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