The role of Fgf9 in mouse pancreas development [bulk RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA866274 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20851754_1.fastq.gz | Fastqsanger.gz | |||
| SRR20851754_2.fastq.gz | Fastqsanger.gz | |||
| SRR20851755_1.fastq.gz | Fastqsanger.gz | |||
| SRR20851755_2.fastq.gz | Fastqsanger.gz | |||
| SRR20851756_1.fastq.gz | Fastqsanger.gz |
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Project description:Temporally and spatially coordinated epithelial–mesenchymal interactions are central to the development of the primitive gut tube endoderm and are necessary to form functional organs of the gastrointestinal tract, including the pancreas. Here, we examined the functional role of the secreted factor Fgf9 in murine pancreatic development. Bulk RNA-sequencing was performed on embryonic day (E) 13.5 and 14.5 mouse pancreas from both wildtype and Fgf9 knockout embryos. Our data have identified specific transcriptional programs and signaling pathways perturbed in the context of loss of Fgf9 during pancreatic development.
2023-03-28 | GSE210574 | GEO
Project description:Temporally and spatially coordinated epithelial–mesenchymal interactions are central to the development of the primitive gut tube endoderm and are necessary to form functional organs of the gastrointestinal tract, including the pancreas. Here, we examined the functional role of the secreted factor Fgf9 in murine pancreatic development. Single-cell RNA-sequencing was performed on embryonic day (E) 14.5 mouse pancreas from both wildtype and Fgf9 knockout embryos. Our data reveal shifts in cellular populations upon loss of Fgf9. In addition, we have identified specific transcriptional programs and signaling pathways perturbed in the context of loss of Fgf9 during pancreatic development.
2023-03-28 | GSE210645 | GEO
Project description:The role of Fgf9 in mouse pancreas development [scRNA-seq]
| PRJNA866546 | ENA
Project description:Objectives: Fibroblast growth factor 9 (FGF9) is expressed by somatic cells in the seminiferous tubules, yet little information exists about its role in regulating spermatogonial stem cells (SSCs). Materials and Methods: Fgf9 overexpression lentivirus was injected into mouse testes, and PLZF immunostaining was performed to investigate the effect of FGF9 on spermatogonia in vivo. Effect of FGF9 on SSCs was detected by transplanting cultured germ cells into tubules of testes. RNA-seq of bulk RNA and single-cell was performed to explore FGF9 working mechanisms. SB203580 was used to disrupt p38 MAPK pathway. p38 MAPK protein expression was detected by western blot and qPCR was performed to determine different gene expression. Small interfering RNA (siRNA) was used to knock down Etv5 gene expression in germ cells. Results: Overexpression of Fgf9 in vivo resulted in arrested spermatogenesis and accumulation of undifferentiated spermatogonia. Exposure of germ cell cultures to FGF9 resulted in larger numbers of SSCs over time. Inhibition of p38 MAPK phosphorylation negated the SSC growth advantage provided by FGF9. Etv5 and Bcl6b gene expression was enhanced by FGF9 treatment. Gene knockdown of Etv5 disrupted the growth effect of FGF9 in cultured SSCs along with downstream expression of Bcl6b. Conclusions: Taken together, this data indicates that FGF9 is an important regulator of SSC proliferation, operating through p38 MAPK phosphorylation and upregulating Etv5 and Bcl6b in turn.
2020-10-26 | GSE160062 | GEO
Project description:The role of long noncoding RNAs during pancreas development
| PRJNA604580 | ENA
Project description:Objectives: Fibroblast growth factor 9 (FGF9) is expressed by somatic cells in the seminiferous tubules, yet little information exists about its role in regulating spermatogonial stem cells (SSCs). Materials and Methods: Fgf9 overexpression lentivirus was injected into mouse testes, and PLZF immunostaining was performed to investigate the effect of FGF9 on spermatogonia in vivo. Effect of FGF9 on SSCs was detected by transplanting cultured germ cells into tubules of testes. RNA-seq of bulk RNA and single-cell was performed to explore FGF9 working mechanisms. SB203580 was used to disrupt p38 MAPK pathway. p38 MAPK protein expression was detected by western blot and qPCR was performed to determine different gene expression. Small interfering RNA (siRNA) was used to knock down Etv5 gene expression in germ cells. Results: Overexpression of Fgf9 in vivo resulted in arrested spermatogenesis and accumulation of undifferentiated spermatogonia. Exposure of germ cell cultures to FGF9 resulted in larger numbers of SSCs over time. Inhibition of p38 MAPK phosphorylation negated the SSC growth advantage provided by FGF9. Etv5 and Bcl6b gene expression was enhanced by FGF9 treatment. Gene knockdown of Etv5 disrupted the growth effect of FGF9 in cultured SSCs along with downstream expression of Bcl6b. Conclusions: Taken together, this data indicates that FGF9 is an important regulator of SSC proliferation, operating through p38 MAPK phosphorylation and upregulating Etv5 and Bcl6b in turn.
2020-10-26 | GSE160061 | GEO
Project description:We have previously shown that FGF9 is overexpressed in hypoxia through the IRES located in the 5’UTR. To identify the protein that binds to FGF9 IRES and controls FGF9 protein synthesis in hypoxia, FGF9 IRES RNA was in vitro synthesized and used to pulled-down interacting proteins. The RNA-protein complexes were first visualized by sliver staining, followed by cutting specific bands for protein identification using matrix-assisted laser desorption/ionization time-of-flight mass spectrometer (MALDI-TOF MS).
2019-11-13 | PXD012892 | Pride
Project description:Pancreas study with 5 sub-studies: (i) 14 assays (7 done on Affymetrix MGU74Av2 and 7 on MOE430 2.0) looking at 7 different time points in pancreas development, (ii) 2 assays (done on Affymetrix MGU74Av2) looking at tumorgenic cell lines alphaTC and betaTC, (iii) 8 assays (6 done on Affymetrix MGU74Av2 and 2 done on MOE430 2.0) looking at Ngn3 mutant and wildtype pancreas at 3 different embryonic time points in pancreas development, (iv) 3 assays (done on Affymetrix MGU74Av2) looking at embryonic e12.5, newborn pancreas and adult islets, (v) 3 assays (done on Affymetrix MGU74Av2) looking at e11.5 separated pancreatic epithelium and mesenchyme or the intact e11.5 pancreas.
2014-09-11 | E-MTAB-2924 | 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
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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:LncRNAs are developmentally regulated and highly cell type-specific non-coding RNAs that have emerged as important regulators of cell fate commitment and maintenance. In this study, we dissected the role of lncRNAs in human pancreas development by classifying lncRNAs based on their dynamic regulation, subcellular localization, and engagement with ribosomes during the stepwise differentiation of human embryonic stem cells (hESCs) towards pancreatic fate. We then deleted 10 candidate lncRNAs in hESCs and characterized the knockout phenotypes of pancreatic developmental intermediates, prioritizing dynamically regulated lncRNAs with validated translation potential and proximity to developmental TFs. This small-scale loss-of-function screen revealed that most lncRNAs are dispensable for pancreatic development and the regulation of nearby genes. We identify LINC00261 as the first translated lncRNA involved in human endocrine cell development, and show that it regulates gene expression in pancreatic progenitor cells in trans rather than cis. Through systematic dissection of LINC00261's coding and noncoding functions, we can exclude a role for the produced micropeptides in this process. Instead, we posit that, over the course of pancreatic differentiation, the biological activity of multiple lncRNAs is controlled by a regulatory, translation machinery dependent mechanism that employs ribosome engagement and short open reading frame translation to dose lncRNA activity in the nucleus. It is conceivable that inadequate nuclear LINC00261 dosage during human pancreas development could predispose individuals to developing diabetes.
2020-08-03 | GSE144682 | GEO