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Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A

ABSTRACT: Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A

PROVIDER: PRJNA341322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4103530.fastq.gz	Fastqsanger.gz
	SRR4103531.fastq.gz	Fastqsanger.gz
	SRR4103512.fastq.gz	Fastqsanger.gz
	SRR4103532.fastq.gz	Fastqsanger.gz
	SRR4103513.fastq.gz	Fastqsanger.gz

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Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A [ChIP-Seq]

Project description:Genome-wide maps of Ptf1a-bound sites in adult pancrea acinar cells.

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Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A [6-day RNA-Seq]

Project description:RNA-seq analysis documented mRNA changes in total pancreatic RNA preparations 6 days after Ptf1a inactivation.

2016-09-01 | GSE86261 | GEO

Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation, and Homeostasis by PTF1A.

Project description:Maintenance of cell type identity is crucial for health, yet little is known of the regulation that sustains the long-term stability of differentiated phenotypes. To investigate the roles that key transcriptional regulators play in adult differentiated cells, we examined the effects of depletion of the developmental master regulator PTF1A on the specialized phenotype of the adult pancreatic acinar cell in vivo Transcriptome sequencing and chromatin immunoprecipitation sequencing results showed that PTF1A maintains the expression of genes for all cellular processes dedicated to the production of the secretory digestive enzymes, a highly attuned surveillance of unfolded proteins, and a heightened unfolded protein response (UPR). Control by PTF1A is direct on target genes and indirect through a ten-member transcription factor network. Depletion of PTF1A causes an imbalance that overwhelms the UPR, induces cellular injury, and provokes acinar metaplasia. Compromised cellular identity occurs by derepression of characteristic stomach genes, some of which are also associated with pancreatic ductal cells. The loss of acinar cell homeostasis, differentiation, and identity is directly relevant to the pathologies of pancreatitis and pancreatic adenocarcinoma.

| S-EPMC5126291 | biostudies-literature

Ptf1a promotes an inhibitory peptidergic identity in cortical pyramidal cells in vivo

Project description:Ptf1a has been shown to be necessary for determining an inhibitory interneuronal fate in many regions of the nervous system. In this study, we aim to investigate the sufficiency of Ptf1a to cell-autonomously promote a specific neuronal identity by misexpressing it in developing excitatory cortical pyramidal cells and studying its impact on pyramidal cell features, such as its gene expression profile. To accomplish this, we electroporate either a Ptf1a/GFP-misexpression construct or a GFP-only control construct into E12.5 mouse embryonic cortices, harvest the cortices at E15.5, and examine Ptf1a-induced changes to the pyramidal cell transcriptome, molecular expression pattern, neurotransmitter status, and morphology. We conclude that Ptf1a is sufficient to cell-autonomously promote an inhibitory peptidergic identity and alter neuronal morphology in developing cortical pyramidal cells. The results of this study provide insight into intrinsic transcriptional controls over neuronal identity, specifically implicate Ptf1a as a potent regulator of an inhibitory peptidergic identity, and may guide future studies of neuronal reprogramming for circuit repair after disease or injury.

2015-03-20 | GSE59481 | GEO

RNA-Seq of mouse genotypes Ptf1a^YFP/+ and Ptf1a^YFP/YFP

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Ptf1a^YFP/+ [het] FACS sorted cells at E11.5 (early pancreatic Multipotent Progenitor Cells) and E15.5 (nascent acinar cells) as well as in Ptf1a^YFP/YFP [null] at E11.5 (delayed early MPC). 376 selected genes identified as differentially expressed between early pancreatic MPC and nascent acinar cells or between early pancreatic and delayed early MPCs have then been examined by Taqman Low Density Arrays (TLDAs) with Real Time RT-PCR for each 1-day time point from E10.5 to E15. 5 in Ptf1a^YFP/+ [het] and for E10.5 and E11.5 in Ptf1aYFP/YFP [null] . Finally, 94 genes identified in the first phase of TLDAs (including 2 endogenous control, Gapdh and 18S) were analyzed in a second TLDA phase for each 1-day time point from E10.5 to -E18.5 in Ptf1a^YFP/+ [het] and for E11.5 in Ptf1aYFP/YFP [null] with biological replicates (n>=3) for each time point.

2014-11-15 | E-MTAB-449 | biostudies-arrayexpress

Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-09-01 | GSE86263 | GEO

Microarray data Ptf1a gain-of-function Xenopus pancreas development

Project description:The Ptf1a gene has essential functions during several stages of pancreas development. It is expressed in the naïve endoderm and required pancreas cell fate specification; it is also required later in the differentiation and maintenance of acinar cells. To identify the regulatory genetic program downstream of Ptf1a required for early pancreatic fate acquisition, we used microarrays to perform a comprehensive gene expression analysis of Ptf1a overexpressing endodermal tissue at NF32 and NF36. The results revealed an up-regulation on 1142 probe sets over 2-fold. Additional analyses, by in situ hybridizations, identified 9 genes that were endodermally expressed after the onset of endogenous Ptf1a; STXBP1, putative transmembrane protein TA-2, C25H, IGFBP1, IRF1, HALPN3, Hey1, sestrin 1, syndecan-4. These results provide insight into the regulatory network activated by Ptf1a during early pancreas development.

2012-11-01 | GSE34193 | GEO

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Project description:Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A [ChIP-Seq]

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c-Myc down-regulation is required for pre-acinar to acinar maturation in the pancreas (ChIP-Seq)

Project description:Multipotent pancreatic progenitors (MPC) are defined as Ptf1a+, Mychigh, Cpa+ cells. During the transition from MPC to unipotent acinar progenitors, c-Myc is down-regulated whereas Ptf1a is up-regulated, leading to the deployment of the acinar program. Here, we show that c-Myc and Ptf1a interact directly and c-Myc binds to, and represses, the transcriptional activity of the PTF1 complex in vitro and in vivo. Using Ela1-Myc mice, in which c-Myc is overexpressed in acinar cells starting at E14.5, we find that acinar cells fail to undergo normal maturation at P1 and this is followed by a massive subsequent repression of the acinar programme. Lineage tracing with Ptf1aCreERT2;Rosa26YFP and Ela1-Myc;Ptf1aCreERT2;Rosa26YFP mice receiving TMX at E15.5 and analyzed at E18.5 revealed that c-Myc overexpression is associated with activation of a hepatic programme but not with pancreatic lineage misspecification At 8 weeks, the silencing of the acinar program is associated with increased expression of the PRC2 complex in a c-Myc dependent manner. Genome wide studies show that Ptf1a and c-Myc display partially overlapping chromatin occupancy patterns and DNA binding competition. We conclude that c-Myc down-regulation during development is crucial for the maturation of pre-acinar to acinar cells. c-Myc overexpression may contribute to pancreatic carcinogenesis by restraining cell differentiation and rendering cells susceptible to transformation.

2017-12-11 | GSE77409 | GEO

c-Myc down-regulation is required for pre-acinar to acinar maturation in the pancreas (RNA-Seq)

2017-12-11 | GSE77410 | GEO