ArticleBiology open2013
Gastrointestinal defects of the Gas1 mutant involve dysregulated Hedgehog and Ret signaling.
Article in Biology open, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Gas1 regulates embryonic tongue muscle proliferation, differentiation and maturation via alternative pathways to Hedgehog signaling.Development (Cambridge, England) · 2025Article
- IGSF10 is a RET antagonist regulating Ewing sarcoma growth and GnRH neuron migration.Cell reports · 2025Article
- Hedgehog-dependent and hedgehog-independent roles for growth arrest specific 1 in mammalian kidney morphogenesis.Development (Cambridge, England) · 2024Article
- Differences in enteric neuronal density in the NSE-Noggin mouse model across institutes.Scientific reports · 2024Article
- Article
- Self-Renewal and Cancers of the Gastric Epithelium: An Update and the Role of the Lectin TFF1 as an Antral Tumor Suppressor.International journal of molecular sciences · 2022Review
- Hedgehog Signaling in Intestinal Development and Homeostasis.Annual review of physiology · 2021Review
- TALPID3/KIAA0586 Regulates Multiple Aspects of Neuromuscular Patterning During Gastrointestinal Development in Animal Models and Human.Frontiers in molecular neuroscience · 2021Article
- Rno_circ_0005139 regulates apoptosis by targetingWorld journal of gastroenterology · 2020Article
- Ptch2/Gas1 and Ptch1/Boc differentially regulate Hedgehog signalling in murine primordial germ cell migration.Nature communications · 2020Article
- Enteric nervous system development: what could possibly go wrong?Nature reviews. Neuroscience · 2018Review
- Expression of Gas1 in Mouse Brain: Release and Role in Neuronal Differentiation.Cellular and molecular neurobiology · 2018Article
- Mouse models of Hirschsprung disease and other developmental disorders of the enteric nervous system: Old and new players.Developmental biology · 2016Review
- Growth Arrest Specific-1 (GAS1) Is a C/EBP Target Gene That Functions in Ovulation and Corpus Luteum Formation in Mice.Biology of reproduction · 2016Article
- Sonic hedgehog controls enteric nervous system development by patterning the extracellular matrix.Development (Cambridge, England) · 2016Article
- Mesenchymal-epithelial interactions during digestive tract development and epithelial stem cell regeneration.Cellular and molecular life sciences : CMLS · 2015Review
- Gas1 is a receptor for sonic hedgehog to repel enteric axons.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Growth arrest specific 1 (GAS1) is abundantly expressed in the adult mouse central nervous system.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013Article
- Analysis of duodenojejunal flexure formation in mice: implications for understanding the genetic basis for gastrointestinal morphology in mammals.Journal of anatomy · 2013Article
- Associations of anorectal malformations and related syndromes.Pediatric surgery international · 2013Review
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Authors and funding
3 authors.
Funding
Abstract
The gastrointestinal (GI) tract defines the digestive system and is composed of the stomach, intestine and colon. Among the major cell types lining radially along the GI tract are the epithelium, mucosa, smooth muscles and enteric neurons. The Hedgehog (Hh) pathway has been implicated in directing various aspects of the developing GI tract, notably the mucosa and smooth muscle growth, and enteric neuron patterning, while the Ret signaling pathway is selectively required for enteric neuron migration, proliferation, and differentiation. The growth arrest specific gene 1 (Gas1) encodes a GPI-anchored membrane protein known to bind to Sonic Hh (Shh), Indian Hh (Ihh), and Ret. However, its role in the GI tract has not been examined. Here we show that the Gas1 mutant GI tract, compared to the control, is shorter, has thinner smooth muscles, and contains more enteric progenitors that are abnormally distributed. These phenotypes are similar to those of the Shh mutant, supporting that Gas1 mediates most of the Shh activity in the GI tract. Because Gas1 has been shown to inhibit Ret signaling elicited by Glial cell line-derived neurotrophic factor (Gdnf), we explored whether Gas1 mutant enteric neurons displayed any alteration of Ret signaling levels. Indeed, isolated mutant enteric progenitors not only showed increased levels of phospho-Ret and its downstream effectors, phospho-Akt and phospho-Erk, but also displayed altered responses to Gdnf and Shh. We therefore conclude that phenotypes observed in the Gas1 mutant are due to a combination of reduced Hh signaling and increased Ret signaling.
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