Nagk和UDP-GlcNAc挽救通路对Wnt信号的发育调控

IF 2.6 Q2 Medicine Mechanisms of Development Pub Date : 2019-04-01 DOI:10.1016/j.mod.2019.03.002
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 ,&nbsp;Zachary T. Spencer ,&nbsp;Anmada Nayak ,&nbsp;Christopher S. Cselenyi ,&nbsp;Hassina Benchabane ,&nbsp;CheyAnne Q. Youngblood ,&nbsp;Alya Zouaoui ,&nbsp;Victoria Ng ,&nbsp;Leah Stephens ,&nbsp;Trevor Hann ,&nbsp;James G. Patton ,&nbsp;David Robbins ,&nbsp;Yashi Ahmed ,&nbsp;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 ,&nbsp;Zachary T. Spencer ,&nbsp;Anmada Nayak ,&nbsp;Christopher S. Cselenyi ,&nbsp;Hassina Benchabane ,&nbsp;CheyAnne Q. Youngblood ,&nbsp;Alya Zouaoui ,&nbsp;Victoria Ng ,&nbsp;Leah Stephens ,&nbsp;Trevor Hann ,&nbsp;James G. Patton ,&nbsp;David Robbins ,&nbsp;Yashi Ahmed ,&nbsp;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}
引用次数: 15

摘要

在筛选调节非洲爪蟾胚胎发生的人类激酶时,我们确定了Nagk和其他UDP-GlcNAc糖基化挽救途径的组分作为前后模式和Wnt信号的调节剂。我们发现挽救通路不影响其他主要的胚胎信号通路(Fgf、TGFβ、Notch或Shh),从而证明了Wnt信号通路的特异性。我们发现打捞通路在Wnt信号传导中的作用在斑马鱼和果蝇中是进化保守的。最后,我们发现GlcNAc对肠样细胞的生长至关重要,而肠样细胞的生长和维持高度依赖于Wnt信号。我们提出Wnt通路对细胞糖基化状态的改变很敏感,并作为营养传感器将生长/增殖与其代谢状态结合起来。我们还提出,在人类先天性糖基化障碍(CDG)中观察到的临床表现可能部分归因于它们在发育过程中对Wnt信号的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

摘要图片

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Mechanisms of Development
Mechanisms of Development 生物-发育生物学
CiteScore
3.60
自引率
0.00%
发文量
0
审稿时长
12.4 weeks
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.
期刊最新文献
Editorial Board Publisher's note Outside Front Cover Regulatory functions of gga-miR-218 in spermatogonial stem cells meiosis by targeting Stra8 Improved early development potence of in vitro fertilization embryos by treatment with tubacin increasing acetylated tubulin of matured porcine oocytes
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1