Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development

Abstract Metabolic reprograming has been linked to epithelial-to-mesenchymal transition (EMT) in cancer cells, but how it influences EMT in normal cells remains largely unknown. Here we explored how metabolism impacts delamination and migration of avian trunk neural crest cells, an important progeni...

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Main Authors: Nioosha Nekooie Marnany, Alwyn Dady, Isabelle Duband-Goulet, Frédéric Relaix, Roberto Motterlini, Roberta Foresti, Sylvie Dufour, Jean-Loup Duband
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-58573-0
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author Nioosha Nekooie Marnany
Alwyn Dady
Isabelle Duband-Goulet
Frédéric Relaix
Roberto Motterlini
Roberta Foresti
Sylvie Dufour
Jean-Loup Duband
author_facet Nioosha Nekooie Marnany
Alwyn Dady
Isabelle Duband-Goulet
Frédéric Relaix
Roberto Motterlini
Roberta Foresti
Sylvie Dufour
Jean-Loup Duband
author_sort Nioosha Nekooie Marnany
collection DOAJ
description Abstract Metabolic reprograming has been linked to epithelial-to-mesenchymal transition (EMT) in cancer cells, but how it influences EMT in normal cells remains largely unknown. Here we explored how metabolism impacts delamination and migration of avian trunk neural crest cells, an important progenitor cell population of the vertebrate embryo. We report that delamination exhibits a quiescent metabolic phenotype whereas migration is characterized by OXPHOS-driven metabolism coupled to distinct expression of metabolic, EMT and developmental genes. While glucose and glutamine are required for delamination and migration, we uncover a specific role for glutamine and its catabolizing enzyme glutaminase in the unfolding of NCC delamination. Namely, glutamine is required for nuclear accumulation of glutaminase, which interacts and cooperates with Wnt signaling to regulate EMT gene expression and cell cycle during delamination. Our data indicate that similarly to cancer cells, embryonic cells engage metabolic enzymes for non-canonical signaling functions to connect metabolism with EMT.
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publishDate 2025-07-01
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series Nature Communications
spelling doaj-art-1c32e2d794e8430b99c9acd7fafad2762025-08-20T03:03:34ZengNature PortfolioNature Communications2041-17232025-07-0116112210.1038/s41467-025-58573-0Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest developmentNioosha Nekooie Marnany0Alwyn Dady1Isabelle Duband-Goulet2Frédéric Relaix3Roberto Motterlini4Roberta Foresti5Sylvie Dufour6Jean-Loup Duband7Institut Mondor de Recherches Biomédicales, Faculté de Santé, INSERM, Université Paris-Est CréteilLaboratoire Gly-CRRET, Université Paris-Est CréteilLaboratoire de Myologie Fondamentale et Translationnelle, CNRS, Université Paris CitéInstitut Mondor de Recherches Biomédicales, Faculté de Santé, INSERM, Université Paris-Est CréteilInstitut Mondor de Recherches Biomédicales, Faculté de Santé, INSERM, Université Paris-Est CréteilInstitut Mondor de Recherches Biomédicales, Faculté de Santé, INSERM, Université Paris-Est CréteilInstitut Mondor de Recherches Biomédicales, Faculté de Santé, INSERM, Université Paris-Est CréteilInstitut Mondor de Recherches Biomédicales, Faculté de Santé, INSERM, Université Paris-Est CréteilAbstract Metabolic reprograming has been linked to epithelial-to-mesenchymal transition (EMT) in cancer cells, but how it influences EMT in normal cells remains largely unknown. Here we explored how metabolism impacts delamination and migration of avian trunk neural crest cells, an important progenitor cell population of the vertebrate embryo. We report that delamination exhibits a quiescent metabolic phenotype whereas migration is characterized by OXPHOS-driven metabolism coupled to distinct expression of metabolic, EMT and developmental genes. While glucose and glutamine are required for delamination and migration, we uncover a specific role for glutamine and its catabolizing enzyme glutaminase in the unfolding of NCC delamination. Namely, glutamine is required for nuclear accumulation of glutaminase, which interacts and cooperates with Wnt signaling to regulate EMT gene expression and cell cycle during delamination. Our data indicate that similarly to cancer cells, embryonic cells engage metabolic enzymes for non-canonical signaling functions to connect metabolism with EMT.https://doi.org/10.1038/s41467-025-58573-0
spellingShingle Nioosha Nekooie Marnany
Alwyn Dady
Isabelle Duband-Goulet
Frédéric Relaix
Roberto Motterlini
Roberta Foresti
Sylvie Dufour
Jean-Loup Duband
Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development
Nature Communications
title Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development
title_full Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development
title_fullStr Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development
title_full_unstemmed Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development
title_short Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development
title_sort non canonical nuclear function of glutaminase cooperates with wnt signaling to drive emt during neural crest development
url https://doi.org/10.1038/s41467-025-58573-0
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