E-MTAB-1929
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-1929 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-1929-analysis-methods.tsv | Tabular | |||
| E-MTAB-1929-analytics.tsv | Tabular | |||
| E-MTAB-1929-analytics.tsv.undecorated | Tabular | |||
| E-MTAB-1929-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-MTAB-1929-analytics.tsv.unrounded | Tabular |
Items per page: 5 1 - 5 of 70 |
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Project description:Transcriptional regulation of endocrine cell differentiation by Insm1
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2019-05-14 | E-MTAB-3352 | ExpressionAtlas
Project description:The Insm1 gene encodes a zinc finger factor expressed in many endocrine organs. We show here that Insm1 is required for differentiation of all endocrine cell types in the pituitary. Thus, in Insm1 mutant mice, hormones characteristic of the different pituitary cell types (thyroid, follicle and melanocyte stimulating hormone, adrenocorticotrope hormone, growth hormone and prolactin) are absent or produced at markedly reduced levels. The differentiation deficit is accompanied by an up-regulated expression of components of the Notch signaling pathway. Further, skeletal muscle-specific genes are ectopically expressed, indicating that Insm1 blocks a muscle-specific expression program. Since Insm1 is also essential for differentiation of endocrine cells in the pancreas, intestine and adrenal gland, it is emerging as a transcription factor that acts in a pan-endocrine manner. The Insm1 factor contains a SNAG domain at its N-terminus, and we show here that the SNAG domain recruits histone modifying factors (Kdm1a, Hdac1/2 and Rcor1-3) and other proteins implicated in transcriptional regulation (Hmg20a/b and Gse1). Deletion of the SNAG domain in mice disrupted differentiation of pituitary endocrine cells, and resulted in an upregulated expression of components of the Notch signaling pathway and ectopic expression of skeletal muscle-specific genes. Our work demonstrates that Insm1 acts in the transcriptional network that controls differentiation of endocrine cells in the anterior pituitary gland, and requires the SNAG domain to exert this function in vivo. Analysis of genes regulated by Insm1 in embryonic day 17.5 pituitary gland. Total RNA from pituitary glands of E17.5 control embryos was compared to E17.5 Insm1 mutant embryos.
2013-10-20 | E-GEOD-46139 | biostudies-arrayexpress
Project description:deBack2012 - Lineage Specification in Pancreas Development
This model of two neighbouring pancreas precursor cells, describes the exocrine versus endocrine lineage specification process. To account for the tissue scale patterns, this couplet model has been extended to hundreds of coupled cells.
This model is described in the article:
On the role of lateral stabilization during early patterning in the pancreas
de Back W., Zhou JX, Brusch L
J. R. Soc. Interface 6 February 2013 vol. 10 no. 79 20120766
Abstract:
The cell fate decision of multi-potent pancreatic progenitor cells between the exocrine and endocrine lineages is regulated by Notch signalling, mediated by cell–cell interactions. However, canonical models of Notch-mediated lateral inhibition cannot explain the scattered spatial distribution of endocrine cells and the cell-type ratio in the developing pancreas. Based on evidence from acinar-to-islet cell transdifferentiation in vitro, we propose that lateral stabilization, i.e. positive feedback between adjacent progenitor cells, acts in parallel with lateral inhibition to regulate pattern formation in the pancreas. A simple mathematical model of transcriptional regulation and cell–cell interaction reveals the existence of multi-stability of spatial patterns whose simultaneous occurrence causes scattering of endocrine cells in the presence of noise. The scattering pattern allows for control of the endocrine-to-exocrine cell-type ratio by modulation of lateral stabilization strength. These theoretical results suggest a previously unrecognized role for lateral stabilization in lineage specification, spatial patterning and cell-type ratio control in organ development.
This model is hosted on BioModels Database
and identified by: MODEL1211010000
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
2024-09-02 | BIOMD0000000435 | BioModels
Project description:The Insm1 gene encodes a zinc finger factor expressed in many endocrine organs. We show here that Insm1 is required for differentiation of all endocrine cell types in the pituitary. Thus, in Insm1 mutant mice, hormones characteristic of the different pituitary cell types (thyroid, follicle and melanocyte stimulating hormone, adrenocorticotrope hormone, growth hormone and prolactin) are absent or produced at markedly reduced levels. The differentiation deficit is accompanied by an up-regulated expression of components of the Notch signaling pathway. Further, skeletal muscle-specific genes are ectopically expressed, indicating that Insm1 blocks a muscle-specific expression program. Since Insm1 is also essential for differentiation of endocrine cells in the pancreas, intestine and adrenal gland, it is emerging as a transcription factor that acts in a pan-endocrine manner. The Insm1 factor contains a SNAG domain at its N-terminus, and we show here that the SNAG domain recruits histone modifying factors (Kdm1a, Hdac1/2 and Rcor1-3) and other proteins implicated in transcriptional regulation (Hmg20a/b and Gse1). Deletion of the SNAG domain in mice disrupted differentiation of pituitary endocrine cells, and resulted in an upregulated expression of components of the Notch signaling pathway and ectopic expression of skeletal muscle-specific genes. Our work demonstrates that Insm1 acts in the transcriptional network that controls differentiation of endocrine cells in the anterior pituitary gland, and requires the SNAG domain to exert this function in vivo.
2013-10-20 | GSE46139 | GEO
Project description:MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. This analysis revealed miRNAs that increase in expression during endocrine cell differentiation. Employing gain-of-function experiments, we identified four miRNAs that can repress a large number of genes that are normally down-regulated during endocrine cell differentiation, including genes encoding transcription factors known to regulate endocrine cell development as well as cell cycle regulators. This knowledge about miRNA target genes in conjunction with HITS-CLIP data allowed us to construct an integrated miRNA-gene regulatory network of endocrine cell differentiation. Our integrated analysis indicates a key role for the identified miRNAs in establishing a transcriptional landscape that promotes the differentiation of pancreatic progenitor cells into endocrine cells. This study not only sheds light on the mechanisms that underlie human endocrine cell differentiation, but also has important implications for devising improved protocols for producing replacement beta cells for diabetes cell therapy.
2019-11-14 | GSE135197 | GEO
Project description:MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. This analysis revealed miRNAs that increase in expression during endocrine cell differentiation. Employing gain-of-function experiments, we identified four miRNAs that can repress a large number of genes that are normally down-regulated during endocrine cell differentiation, including genes encoding transcription factors known to regulate endocrine cell development as well as cell cycle regulators. This knowledge about miRNA target genes in conjunction with HITS-CLIP data allowed us to construct an integrated miRNA-gene regulatory network of endocrine cell differentiation. Our integrated analysis indicates a key role for the identified miRNAs in establishing a transcriptional landscape that promotes the differentiation of pancreatic progenitor cells into endocrine cells. This study not only sheds light on the mechanisms that underlie human endocrine cell differentiation, but also has important implications for devising improved protocols for producing replacement beta cells for diabetes cell therapy.
2019-11-14 | GSE140403 | GEO
Project description:MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. This analysis revealed miRNAs that increase in expression during endocrine cell differentiation. Employing gain-of-function experiments, we identified four miRNAs that can repress a large number of genes that are normally down-regulated during endocrine cell differentiation, including genes encoding transcription factors known to regulate endocrine cell development as well as cell cycle regulators. This knowledge about miRNA target genes in conjunction with HITS-CLIP data allowed us to construct an integrated miRNA-gene regulatory network of endocrine cell differentiation. Our integrated analysis indicates a key role for the identified miRNAs in establishing a transcriptional landscape that promotes the differentiation of pancreatic progenitor cells into endocrine cells. This study not only sheds light on the mechanisms that underlie human endocrine cell differentiation, but also has important implications for devising improved protocols for producing replacement beta cells for diabetes cell therapy.
2019-11-14 | GSE115312 | GEO
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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