ArticleNature communications2025
Steroid hormone-induced wingless ligands tune female intestinal size in Drosophila.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Systematic generation ofFly · 2026Article
- Beyond the mouse: 3R-guided alternative animal models transforming cancer research.Molecular cancer · 2026Review
- Frazzled/DCC directs spatial progenitor integration ensuring steady-state intestinal turnover.Nature communications · 2026Article
- Mating regulates growth, metabolism, and digestive efficiency in the femaleProceedings of the National Academy of Sciences of the United States of America · 2026Article
- A pro-inflammatory neutrophil subpopulation drives intestinal ischemia-reperfusion injury via the ATF4-mediated endoplasmic reticulum stress pathway.Scientific reports · 2026Article
- Gut hormone signaling drives sex differences in metabolism and behavior.Molecular metabolism · 2026Article
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Female reproduction comes at great expense to energy metabolism compensated by extensive organ adaptations including intestinal size. Upon mating, endocrine signals orchestrate a 30% net increase of absorptive epithelium. Mating increases production of the steroid hormone Ecdysone released by the Drosophila ovaries that stimulates intestinal stem cell (ISC) divisions. Here, we uncover the transcription factor crooked legs (crol) as an intraepithelial coordinator of Ecdysone-induced ISC mitosis. For the precise investigation of non-autonomous factors on ISC behaviour, we establish Rapport, a spatiotemporally-controlled dual expression and tracing system for the analysis of paracrine genetic manipulation while tracing ISC behaviour. Rapport tracing reveals that Ecdysone-induced Crol controls mitogenic Wnt/Wg-ligand expression from epithelial enterocytes activating ISC mitosis. Paracrine Wg stimulation is counterbalanced by Crol-repression of string/CDC25 and CyclinB autonomously in ISC. Rapport-based ISC tumours confirm paracrine stimulation through the Ecdysone-Crol-Wg axis on mitotic behaviour, whereas the autonomous anti-proliferative role of Crol in ISC is conserved in models of colorectal cancer. Finally, mathematical modelling corroborates increasing enterocyte numbers and Wnt/Wg-degradation to set a stable post-mating intestinal size. Together, our findings provide insights into the complex endocrine growth control mechanisms during mating-induced adaptations and might help untangling pleiotropic hormonal effects observed in gastrointestinal tumorigenesis.
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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 Socratic graph.