ArticlePloS one2011
Delta1 expression, cell cycle exit, and commitment to a specific secretory fate coincide within a few hours in the mouse intestinal stem cell system.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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Who cites it
48 citing papers in PubMed, 85 citations in OpenAlex.
- Therapeutic targeting of the NOTCH1 and neddylation pathways in T cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- H3K36 methylation regulates cell plasticity and regeneration in the intestinal epithelium.Nature cell biology · 2025Article
- Cbl and Cbl-b ubiquitin ligases are essential for intestinal epithelial stem cell maintenance.iScience · 2024Article
- Review
- Homeostasis, injury, and recovery dynamics at multiple scales in a self-organizing mouse intestinal crypt.eLife · 2023Article
- Organoid cell fate dynamics in space and time.Science advances · 2023Article
- From birth to death: The hardworking life of Paneth cell in the small intestine.Frontiers in immunology · 2023Review
- NF-κB determines Paneth versus goblet cell fate decision in the small intestine.Development (Cambridge, England) · 2021Article
- The Notch signaling pathway involvement in innate lymphoid cell biology.Biomedical journal · 2021Review
- Transit-Amplifying Cells Coordinate Changes in Intestinal Epithelial Cell-Type Composition.Developmental cell · 2021Article
- Transcriptional programmes underlying cellular identity and microbial responsiveness in the intestinal epithelium.Nature reviews. Gastroenterology & hepatology · 2021Review
- The Transcription Co-Repressors MTG8 and MTG16 Regulate Exit of Intestinal Stem Cells From Their Niche and Differentiation Into Enterocyte vs Secretory Lineages.Gastroenterology · 2020Article
- Review
- Stem Cell Signaling Pathways in the Small Intestine.International journal of molecular sciences · 2020Review
- Regulation of membrane phospholipid asymmetry by Notch-mediated flippase expression controls the number of intraepithelial TCRαβ+CD8αα+ T cells.PLoS biology · 2019Article
- Preservation of reserve intestinal epithelial stem cells following severe ischemic injury.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Unraveling the Control of Cell Cycle Periods during Intestinal Stem Cell Differentiation.Biophysical journal · 2018Article
- Stem Cells in Repair of Gastrointestinal Epithelia.Physiology (Bethesda, Md.) · 2017Review
- Kaiso differentially regulates components of the Notch signaling pathway in intestinal cells.Cell communication and signaling : CCS · 2017Article
- Alternative direct stem cell derivatives defined by stem cell location and graded Wnt signalling.Nature cell biology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The stem cells of the small intestine are multipotent: they give rise, via transit-amplifying cell divisions, to large numbers of columnar absorptive cells mixed with much smaller numbers of three different classes of secretory cells--mucus-secreting goblet cells, hormone-secreting enteroendocrine cells, and bactericide-secreting Paneth cells. Notch signaling is known to control commitment to a secretory fate, but why are the secretory cells such a small fraction of the population, and how does the diversity of secretory cell types arise? Using the mouse as our model organism, we find that secretory cells, and only secretory cells, pass through a phase of strong expression of the Notch ligand Delta1 (Dll1). Onset of this Dll1 expression coincides with a block to further cell division and is followed in much less than a cell cycle time by expression of Neurog3--a marker of enteroendocrine fate--or Gfi1--a marker of goblet or Paneth cell fate. By conditional knock-out of Dll1, we confirm that Delta-Notch signaling controls secretory commitment through lateral inhibition. We infer that cells stop dividing as they become committed to a secretory fate, while their neighbors continue dividing, explaining the final excess of absorptive over secretory cells. Our data rule out schemes in which cells first become committed to be secretory, and then diversify through subsequent cell divisions. A simple mathematical model shows how, instead, Notch signaling may simultaneously govern the commitment to be secretory and the choice between alternative modes of secretory differentiation.
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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.