ArticleNature2017
Feedback regulation of steady-state epithelial turnover and organ size.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 168 citations in OpenAlex.
- A screen for adherens junction proteins regulating collective cell migration and testis morphogenesis reveals important roles for the Rab GAP RN-tre and the kinase Par-1.Molecular biology of the cell · 2026Article
- Effects of High-Dextrose Intake on the Structural and Functional Properties of the Small Intestine in Young-Maturing and Middle-Aged Rats.International journal of molecular sciences · 2026Article
- Heme acts as a metabolic brake on erebosis in the Drosophila gut.PLoS biology · 2026Article
- Article
- Psc and Su(z)2 safeguard intestinal stem cell identity and prevent chinmo-dependent tumorigenesis.EMBO reports · 2026Article
- Gut Metabolism Links Precision Nutrition, Exercise, and Healthspan in Drosophila melanogaster.Aging cell · 2026Article
- The signaling and regulatory functions of dying cells and cell corpses.Communications biology · 2026Review
- A screen for adherens junction proteins regulating collective cell migration and testis morphogenesis reveals important roles for the Rab GAP RN-tre and the kinase Par-1.bioRxiv : the preprint server for biology · 2026Article
- Natural Negative Feedback Loops Confer Indica-Japonica Differentiation for Grain Size Homeostasis in Rice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Frazzled/DCC directs spatial progenitor integration ensuring steady-state intestinal turnover.Nature communications · 2026Article
- Toll signalling controls intestinal regeneration in Drosophila.Development (Cambridge, England) · 2026Article
- Article
- Gut metabolism links precision nutrition, exercise, and healthspan inbioRxiv : the preprint server for biology · 2025Article
- Pvf1-Pvr-mediated crosstalk between trachea and gut guides intestinal stem cell migration to promote gut regeneration.Nature communications · 2025Article
- Microbes and diet reshape the intestine via distinct cellular dynamics.bioRxiv : the preprint server for biology · 2025Article
- Age mosaic of gut epithelial cells prevents aging.Nature communications · 2025Article
- Adherens junctions limit septate junction length in Drosophila midgut enterocytes but are not required for polarity.Journal of cell science · 2025Article
- Alternate Grainy head isoforms regulate Drosophila midgut intestinal stem cell differentiation.Cell death discovery · 2025Article
- Steroid hormone-induced wingless ligands tune female intestinal size in Drosophila.Nature communications · 2025Article
- Reduction of endocytosis and EGFR signaling is associated with the switch from isolated to clustered apoptosis during epithelial tissue remodeling in Drosophila.PLoS biology · 2024Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial organs undergo steady-state turnover throughout adult life, with old cells being continually replaced by the progeny of stem cell divisions. To avoid hyperplasia or atrophy, organ turnover demands strict equilibration of cell production and loss. However, the mechanistic basis of this equilibrium is unknown. Here we show that robustly precise turnover of the adult Drosophila intestine arises through a coupling mechanism in which enterocyte apoptosis breaks feedback inhibition of stem cell division. Healthy enterocytes inhibit stem cell division through E-cadherin, which prevents secretion of mitogenic epidermal growth factors (EGFs) by repressing transcription of the EGF maturation factor rhomboid. Individual apoptotic enterocytes promote divisions by loss of E-cadherin, which releases cadherin-associated β-catenin (Armadillo in Drosophila) and p120-catenin to induce rhomboid. Induction of rhomboid in the dying enterocyte triggers activation of the EGF receptor (Egfr) in stem cells within a discrete radius. When we blocked apoptosis, E-cadherin-controlled feedback suppressed divisions, and the organ retained the same number of cells. When we disrupted feedback, apoptosis and divisions were uncoupled, and the organ developed either hyperplasia or atrophy. Together, our results show that robust cellular balance hinges on the obligate coupling of divisions to apoptosis, which limits the proliferative potential of a stem cell to the precise time and place at which a replacement cell is needed. In this way, localized cell-cell communication gives rise to tissue-level homeostatic equilibrium and constant organ size.
Indexed as
Identifiers
What OpenQuestion holds
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.