Developmental regulation of Wnt signaling by Nagk and the UDP-GlcNAc salvage pathway.
Animals
Body Patterning
/ genetics
Drosophila
/ genetics
Embryonic Development
/ genetics
Evolution, Molecular
Gene Expression Regulation, Developmental
Glycosylation
Humans
Phosphotransferases (Alcohol Group Acceptor)
/ genetics
Wnt Signaling Pathway
/ genetics
Xenopus laevis
/ genetics
Zebrafish
/ genetics
Development
Nagk
UDP-GlcNAc salvage pathway
Wnt signaling
Journal
Mechanisms of development
ISSN: 1872-6356
Titre abrégé: Mech Dev
Pays: Ireland
ID NLM: 9101218
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
19
02
2019
revised:
15
03
2019
accepted:
18
03
2019
pubmed:
25
3
2019
medline:
23
8
2019
entrez:
25
3
2019
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 30904594
pii: S0925-4773(19)30072-3
doi: 10.1016/j.mod.2019.03.002
pmc: PMC6574174
mid: NIHMS1526497
pii:
doi:
Substances chimiques
Phosphotransferases (Alcohol Group Acceptor)
EC 2.7.1.-
N-acetylglucosamine kinase
EC 2.7.1.59
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
20-31Subventions
Organisme : NCI NIH HHS
ID : R01 CA105038
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM122516
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM121421
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA219189
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY024354
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM122222
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000445
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.
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