Leif R. Neitzel , Zachary T. Spencer , Anmada Nayak , Christopher S. Cselenyi , Hassina Benchabane , CheyAnne Q. Youngblood , Alya Zouaoui , Victoria Ng , Leah Stephens , Trevor Hann , James G. Patton , David Robbins , Yashi Ahmed , Ethan Lee
{"title":"Nagk和UDP-GlcNAc挽救通路对Wnt信号的发育调控","authors":"Leif R. Neitzel , Zachary T. Spencer , Anmada Nayak , Christopher S. Cselenyi , Hassina Benchabane , CheyAnne Q. Youngblood , Alya Zouaoui , Victoria Ng , Leah Stephens , Trevor Hann , James G. Patton , David Robbins , Yashi Ahmed , Ethan Lee","doi":"10.1016/j.mod.2019.03.002","DOIUrl":null,"url":null,"abstract":"<div><p>In a screen for human kinases that regulate <em>Xenopus laevis</em> embryogenesis, we identified Nagk and other components of the UDP-GlcNAc glycosylation salvage pathway as regulators of anteroposterior patterning and Wnt signaling. We find that the salvage pathway does not affect other major embryonic signaling pathways (Fgf, TGFβ, Notch, or Shh), thereby demonstrating specificity for Wnt signaling. We show that the role of the salvage pathway in Wnt signaling is evolutionarily conserved in zebrafish and <em>Drosophila</em>. Finally, we show that GlcNAc is essential for the growth of intestinal enteroids, which are highly dependent on Wnt signaling for growth and maintenance. We propose that the Wnt pathway is sensitive to alterations in the glycosylation state of a cell and acts as a nutritional sensor in order to couple growth/proliferation with its metabolic status. We also propose that the clinical manifestations observed in congenital disorders of glycosylation (CDG) in humans may be due, in part, to their effects on Wnt signaling during development.</p></div>","PeriodicalId":49844,"journal":{"name":"Mechanisms of Development","volume":"156 ","pages":"Pages 20-31"},"PeriodicalIF":2.6000,"publicationDate":"2019-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mod.2019.03.002","citationCount":"15","resultStr":"{\"title\":\"Developmental regulation of Wnt signaling by Nagk and the UDP-GlcNAc salvage pathway\",\"authors\":\"Leif R. Neitzel , Zachary T. Spencer , Anmada Nayak , Christopher S. Cselenyi , Hassina Benchabane , CheyAnne Q. Youngblood , Alya Zouaoui , Victoria Ng , Leah Stephens , Trevor Hann , James G. Patton , David Robbins , Yashi Ahmed , Ethan Lee\",\"doi\":\"10.1016/j.mod.2019.03.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>In a screen for human kinases that regulate <em>Xenopus laevis</em> embryogenesis, we identified Nagk and other components of the UDP-GlcNAc glycosylation salvage pathway as regulators of anteroposterior patterning and Wnt signaling. We find that the salvage pathway does not affect other major embryonic signaling pathways (Fgf, TGFβ, Notch, or Shh), thereby demonstrating specificity for Wnt signaling. We show that the role of the salvage pathway in Wnt signaling is evolutionarily conserved in zebrafish and <em>Drosophila</em>. Finally, we show that GlcNAc is essential for the growth of intestinal enteroids, which are highly dependent on Wnt signaling for growth and maintenance. We propose that the Wnt pathway is sensitive to alterations in the glycosylation state of a cell and acts as a nutritional sensor in order to couple growth/proliferation with its metabolic status. We also propose that the clinical manifestations observed in congenital disorders of glycosylation (CDG) in humans may be due, in part, to their effects on Wnt signaling during development.</p></div>\",\"PeriodicalId\":49844,\"journal\":{\"name\":\"Mechanisms of Development\",\"volume\":\"156 \",\"pages\":\"Pages 20-31\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2019-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.mod.2019.03.002\",\"citationCount\":\"15\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Mechanisms of Development\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0925477319300723\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mechanisms of Development","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0925477319300723","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
Developmental regulation of Wnt signaling by Nagk and the UDP-GlcNAc salvage pathway
In a screen for human kinases that regulate Xenopus laevis embryogenesis, we identified Nagk and other components of the UDP-GlcNAc glycosylation salvage pathway as regulators of anteroposterior patterning and Wnt signaling. We find that the salvage pathway does not affect other major embryonic signaling pathways (Fgf, TGFβ, Notch, or Shh), thereby demonstrating specificity for Wnt signaling. We show that the role of the salvage pathway in Wnt signaling is evolutionarily conserved in zebrafish and Drosophila. Finally, we show that GlcNAc is essential for the growth of intestinal enteroids, which are highly dependent on Wnt signaling for growth and maintenance. We propose that the Wnt pathway is sensitive to alterations in the glycosylation state of a cell and acts as a nutritional sensor in order to couple growth/proliferation with its metabolic status. We also propose that the clinical manifestations observed in congenital disorders of glycosylation (CDG) in humans may be due, in part, to their effects on Wnt signaling during development.
期刊介绍:
Mechanisms of Development is an international journal covering the areas of cell biology and developmental biology. In addition to publishing work at the interphase of these two disciplines, we also publish work that is purely cell biology as well as classical developmental biology.
Mechanisms of Development will consider papers in any area of cell biology or developmental biology, in any model system like animals and plants, using a variety of approaches, such as cellular, biomechanical, molecular, quantitative, computational and theoretical biology.
Areas of particular interest include:
Cell and tissue morphogenesis
Cell adhesion and migration
Cell shape and polarity
Biomechanics
Theoretical modelling of cell and developmental biology
Quantitative biology
Stem cell biology
Cell differentiation
Cell proliferation and cell death
Evo-Devo
Membrane traffic
Metabolic regulation
Organ and organoid development
Regeneration
Mechanisms of Development does not publish descriptive studies of gene expression patterns and molecular screens; for submission of such studies see Gene Expression Patterns.