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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE86262 | GEO | 2016/09/01

SECONDARY ACCESSION(S): PRJNA341323

REPOSITORIES: GEO

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

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

| PRJNA341322 | ENA

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

Project description: Not available

| S-EPMC5126291 | biostudies-literature

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:This SuperSeries is composed of the SubSeries listed below.

2016-09-01 | GSE86263 | GEO

Induced MIST1 and PTF1a Expression in Pancreatic Ductal Adenocarcinoma Cells

Project description:Purpose: The goal of the study was to determine the effects of forced expression of the acinar transcription factors MIST1 and PTF1a in PDAC cells. Methods: Doxycycline inducible MIST1myc and PTF1amyc Panc-1 cells were generated using Clontech's Tetone System and subjected to RNA-Sequencing following doxycycline treatment. Results: 50 million sequence reads were mapped to the human genome. Data suggests acinar associated molecules were induced upon doxycyline treatment. Conclusions: MIST1 and PTF1a retain functional activity and can promote acinar gene expression in the context of pancreatic cancer cells.

2018-10-27 | GSE106290 | GEO

Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation and Homeostasis by PTF1A [E18.5 RNA-Seq]

Project description:RNA-seq analysis of RNA from embryonic day 18.5 pancreas

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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

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

Ptf1a-dependent gene expression during pancreas development (TLDA part)

Project description:We first 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): this is deposited with accession number E-MTAB-449. We then examined 376 selected genes identified as differentially expressed between early pancreatic MPC and nascent acinar cells or between early pancreatic and delayed early MPCs 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-2780 | biostudies-arrayexpress

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