Gene expression analysis of E13.5 Prox1-deficient mouse embryonic pancreas
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA737506 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14808705.fastq.gz | Fastqsanger.gz | |||
| SRR14808706.fastq.gz | Fastqsanger.gz | |||
| SRR14808707.fastq.gz | Fastqsanger.gz | |||
| SRR14808708.fastq.gz | Fastqsanger.gz | |||
| SRR14808709.fastq.gz | Fastqsanger.gz |
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Project description:RNA sequencing was used to identify gene expression changes in the pancreas of E13.5 Prox1-nullyzygous mouse embryos.
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Project description:By using His6-tagged recombinant human secretagogin in the presence of Ca2+ (100 µM), we isolated its putative interacting partners from mouse embryonic (E13.5) pancreata and identified their amino acid sequences by mass spectrometry. Next to previously described interacting partners (participating in vesicle-mediated transport, cytoskeletal organization and members of chaperonin-containing complex), we found a substantial group of proteins involved in proteasomal catabolic process including 15 different subunits of the 26S proteasome. Our data support that secretagogin protects Pdx1 from proteasomal degradation to control a transcriptional program required for β cell specification.
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Project description:Oncogenic mutations in Kras initiate neoplastic transformation in the pancreas through a process that hijacks the activity of developmental regulators and induces an inflammatory microenvironment. We report that the homeodomain transcription factor Prox1 is a novel component of a progenitor signature that is activated in acinar cells undergoing dedifferentiation and ductal metaplasia conversion. Also, the conditional deletion of a single Prox1 allele markedly accelerates early transformation and significantly enhances features of inflammation in pancreatic tissues carrying a Kras oncogene. By using in vitro and in silico approaches, we demonstrate that Prox1 negatively regulates the expression of proinflammatory genes and genes implicated in malignant transformation in pancreatic cells. Microrrays were used to identify gene expression profiles and pathways that are differentially activated after enforced expression of PROX1 in the PROX1-negative human pancreatic ductal adenocarcinoma (PDAC) cell line Capan1. MSCV retroviral transduction was used to generate Capan1 cells that ectopically express PROX1 and selected for puromycin resistance. Three independent transductions with control virus (MSCV_puro) and 3 independent transductions with Prox1-cDNA virus (MSCV_PROX1_puro) were conducted for these experiments.
2016-02-11 | E-GEOD-58547 | biostudies-arrayexpress
Project description:Oncogenic mutations in Kras initiate neoplastic transformation in the pancreas through a process that hijacks the activity of developmental regulators and induces an inflammatory microenvironment. We report that the homeodomain transcription factor Prox1 is a novel component of a progenitor signature that is activated in acinar cells undergoing dedifferentiation and ductal metaplasia conversion. Also, the conditional deletion of a single Prox1 allele markedly accelerates early transformation and significantly enhances features of inflammation in pancreatic tissues carrying a Kras oncogene. By using in vitro and in silico approaches, we demonstrate that Prox1 negatively regulates the expression of proinflammatory genes and genes implicated in malignant transformation in pancreatic cells.
2016-02-11 | GSE58547 | GEO
Project description:Oncogenic mutations in Kras initiate neoplastic transformation in the pancreas through a process that hijacks the activity of developmental regulators and induces an inflammatory microenvironment. We report that the homeodomain transcription factor Prox1 is a novel component of a progenitor signature that is activated in acinar cells undergoing dedifferentiation and ductal metaplasia conversion. Also, the conditional deletion of a single Prox1 allele markedly accelerates early transformation and significantly enhances features of inflammation in pancreatic tissues carrying a Kras oncogene. By using in vitro and in silico approaches, we demonstrate that Prox1 negatively regulates the expression of proinflammatory genes and genes implicated in malignant transformation in pancreatic cells.
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Project description:Control or A2V+CD40 treated Prox1-proficient (AP) and Prox1-deficient (APP) tumors
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Project description:Bicaudal C1 KO embryonic pancreas develops cysts and has less endocrine progenitors after E14.5 (14.5 days after fertilization), while no defect is observed at E13.5. Bicaudal C1 is an RNA-binding protein. To understand the molecular mechanisms leading to both phenotypes, the mRNA expression profile of E13.5 WT vs. Bicaudal C1 dorsal pancreas was studied by high-throughput sequencing using the Illumina HiSeq 2000 platform. This time point was selected as a time point where no phenotypic modification was detected. 3 replicates for each condition were sequenced and each replicate consisted of 3 E13.5 dorsal pancreas of the same genotype. There were only few differences between both transcriptomes. Pkd2 was 1.9-fold reduced in Bicaudal C1 KO. Pkd2 inactivation causes renal and pancreatic cyst. Some genes having immune/inflammatory functions were up or downregulated highlighting the early immune cell infiltration observed in Bicaudal C1 KO pancreas. No hit could explain the endocrine progenitor decrease. It may be due to the ability of Bicaudal C1 to regulate mRNA translation without affecting the mRNAs themselves. Comparison of mRNA profiles of E13.5 WT vs. Bicaudal C1 KO dorsal pancreas using the Illumina HiSeq 2000 platform (platform ID SN865), 3 replicates per condition.
2015-04-07 | E-GEOD-58833 | biostudies-arrayexpress
Project description:Gene expression analysis of mouse pancreas carrying Prox1 ectopic acinar expression
| PRJNA737507 | ENA
Project description:Bicaudal C1 KO embryonic pancreas develops cysts and has less endocrine progenitors after E14.5 (14.5 days after fertilization), while no defect is observed at E13.5. Bicaudal C1 is an RNA-binding protein. To understand the molecular mechanisms leading to both phenotypes, the mRNA expression profile of E13.5 WT vs. Bicaudal C1 dorsal pancreas was studied by high-throughput sequencing using the Illumina HiSeq 2000 platform. This time point was selected as a time point where no phenotypic modification was detected. 3 replicates for each condition were sequenced and each replicate consisted of 3 E13.5 dorsal pancreas of the same genotype. There were only few differences between both transcriptomes. Pkd2 was 1.9-fold reduced in Bicaudal C1 KO. Pkd2 inactivation causes renal and pancreatic cyst. Some genes having immune/inflammatory functions were up or downregulated highlighting the early immune cell infiltration observed in Bicaudal C1 KO pancreas. No hit could explain the endocrine progenitor decrease. It may be due to the ability of Bicaudal C1 to regulate mRNA translation without affecting the mRNAs themselves.
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Project description:The homeobox transcription factor Prox1 is critical for organogenesis including brain, retina, liver and pancreas and lymphatic system. Prox1 is transiently expressed in mouse cochlear hair cells (HCs) and supporting cells (SCs), however, it remains elusive about its in vivo DNA binding site and roles during cochlear development. Here, by using fresh cochlear tissues and Prox1 antibody, we firstly mapped out the genome-wide binding sites of Prox1 via Cleavage Under Targets and Release Using Nuclease (CUT&RUN). Gene function enrichment analysis suggests several potential functions of Prox1, one of which is regulating cell cycle progression. Secondly, to validate our CUT&RUN data, we further performed in vivo prox1 gain-of-function studies through genetic approaches. Onset of ectopic Prox1 at early embryonic otocyst leads to shorter cochlea with density of HCs and SCs distribution, suggesting a precocious cell cycle exit of cochlear sensory progenitor cells. These findings highlight the power of CUT&RUN in mapping DNA binding sites even in tissues (i.e. cochlea) with rare cells, as well as providing the first genetic evidence to support roles of Prox1 in regulating progenitor pools of cochlear progenitors.
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