ArticleDevelopment (Cambridge, England)2012
Ptf1a-mediated control of Dll1 reveals an alternative to the lateral inhibition mechanism.
Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 71 citations in OpenAlex.
- Extracellular matrix-driven metabolic control of pancreatic endocrine lineage allocation.EMBO reports · 2025Article
- Oscillatory control of embryonic development.Development (Cambridge, England) · 2024Review
- Notch pathway mutants do not equivalently perturb mouse embryonic retinal development.PLoS genetics · 2023Article
- Jag1-Notch cis-interaction determines cell fate segregation in pancreatic development.Nature communications · 2023Article
- Pancreas agenesis mutations disrupt a lead enhancer controlling a developmental enhancer cluster.Developmental cell · 2022Article
- Deregulation of Transcription Factor Networks Driving Cell Plasticity and Metastasis in Pancreatic Cancer.Frontiers in cell and developmental biology · 2021Review
- A Yap-Myc-Sox2-p53 Regulatory Network Dictates Metabolic Homeostasis and Differentiation in Kras-Driven Pancreatic Ductal Adenocarcinomas.Developmental cell · 2019Article
- LATS1/2 suppress NFκB and aberrant EMT initiation to permit pancreatic progenitor differentiation.PLoS biology · 2019Article
- Transcription factor Ptf1a in development, diseases and reprogramming.Cellular and molecular life sciences : CMLS · 2019Review
- Notch Signaling-Induced Oscillatory Gene Expression May Drive Neurogenesis in the Developing Retina.Frontiers in molecular neuroscience · 2019Article
- Inflammation and de-differentiation in pancreatic carcinogenesis.World journal of clinical cases · 2018Review
- Deterministic fate assignment of Müller glia cells in the zebrafish retina suggests a clonal backbone during development.The European journal of neuroscience · 2018Article
- Direct reprogramming of fibroblasts into neural stem cells by single non-neural progenitor transcription factor Ptf1a.Nature communications · 2018Article
- Induced PTF1a expression in pancreatic ductal adenocarcinoma cells activates acinar gene networks, reduces tumorigenic properties, and sensitizes cells to gemcitabine treatment.Molecular oncology · 2018Article
- GLIS1-3: emerging roles in reprogramming, stem and progenitor cell differentiation and maintenance.Stem cell investigation · 2017Review
- An insulin signaling feedback loop regulates pancreas progenitor cell differentiation during islet development and regeneration.Developmental biology · 2016Article
- Transcription factor regulation of pancreatic organogenesis, differentiation and maturation.Islets · 2016Review
- Notch Signaling in Pancreatic Development.International journal of molecular sciences · 2015Review
- A Gene Regulatory Network Cooperatively Controlled by Pdx1 and Sox9 Governs Lineage Allocation of Foregut Progenitor Cells.Cell reports · 2015Article
- Hnf1b controls pancreas morphogenesis and the generation of Ngn3+ endocrine progenitors.Development (Cambridge, England) · 2015Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Neurog3-induced Dll1 expression in pancreatic endocrine progenitors ostensibly activates Hes1 expression via Notch and thereby represses Neurog3 and endocrine differentiation in neighboring cells by lateral inhibition. Here we show in mouse that Dll1 and Hes1 expression deviate during regionalization of early endoderm, and later during early pancreas morphogenesis. At that time, Ptf1a activates Dll1 in multipotent pancreatic progenitor cells (MPCs), and Hes1 expression becomes Dll1 dependent over a brief time window. Moreover, Dll1, Hes1 and Dll1/Hes1 mutant phenotypes diverge during organ regionalization, become congruent at early bud stages, and then diverge again at late bud stages. Persistent pancreatic hypoplasia in Dll1 mutants after eliminating Neurog3 expression and endocrine development, together with reduced proliferation of MPCs in both Dll1 and Hes1 mutants, reveals that the hypoplasia is caused by a growth defect rather than by progenitor depletion. Unexpectedly, we find that Hes1 is required to sustain Ptf1a expression, and in turn Dll1 expression in early MPCs. Our results show that Ptf1a-induced Dll1 expression stimulates MPC proliferation and pancreatic growth by maintaining Hes1 expression and Ptf1a protein levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.