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Absence of Nodal signaling promotes precocious neural differentiation in the mouse embryo
Anne Camus1, Aitana Perea-Gomez, Anne Moreau
1Laboratoire de Développement des Vertébrés, Institut Jacques Monod UMR 7592 CNRS, Universités Paris 6 et 7, 2 place Jussieu, 75251 Paris, France. acamus@ijm.jussieu.fr
Abstract:
After implantation, mouse embryos deficient for the activity of the transforming growth factor-beta member Nodal fail to form both the mesoderm and the definitive endoderm. They also fail to specify the anterior visceral endoderm, a specialized signaling center which has been shown to be required for the establishment of anterior identity in the epiblast. Our study reveals that Nodal-/- epiblast cells nevertheless express prematurely and ectopically molecular markers specific of anterior fate. Our analysis shows that neural specification occurs and regional identities characteristic of the forebrain are established precociously in the Nodal-/- mutant with a sequential progression equivalent to that of wild-type embryo. When explanted and cultured in vitro, Nodal-/- epiblast cells readily differentiate into neurons. Genes normally transcribed in organizer-derived tissues, such as Gsc and Foxa2, are also expressed in Nodal-/- epiblast. The analysis of Nodal-/-;Gsc-/- compound mutant embryos shows that Gsc activity plays no critical role in the acquisition of forebrain characters by Nodal-deficient cells. This study suggests that the initial steps of neural specification and forebrain development may take place well before gastrulation in the mouse and highlights a possible role for Nodal, at pregastrula stages, in the inhibition of anterior and neural fate determination.
Insights
Mouse embryos lacking Nodal signaling fail to form mesoderm and endoderm but surprisingly develop anterior neural fates prematurely. This suggests Nodal normally inhibits early neural development before gastrulation.
Area of Science:
- Developmental biology
- Molecular biology
- Genetics
Background:
- Nodal signaling is crucial for mesoderm and endoderm formation in mouse embryos.
- Anterior visceral endoderm (AVE) specifies anterior identity, and Nodal is implicated in its formation.
Purpose of the Study:
- To investigate the role of Nodal in early mouse embryonic development, specifically focusing on anterior-posterior patterning and neural fate determination.
- To determine if Nodal deficiency impacts neural specification and forebrain development.
Main Methods:
- Analysis of Nodal knockout (Nodal-/-) mouse embryos.
- In vitro culture of Nodal-/- epiblast cells.
- Expression analysis of molecular markers for anterior fate, neural specification, and organizer-derived tissues.
- Analysis of compound Nodal-/-;Gsc-/- mutants.
Main Results:
- Nodal-/- embryos failed to form mesoderm and definitive endoderm, and lacked AVE.
- Despite these defects, Nodal-/- epiblast cells prematurely expressed anterior fate markers and underwent neural specification.
- Forebrain regional identities were established precociously in Nodal-/- mutants.
- Nodal-/- epiblast cells readily differentiated into neurons in vitro.
- Genes like Gsc and Foxa2 were ectopically expressed in Nodal-/- epiblast.
- Gsc deficiency did not affect forebrain character acquisition in Nodal-deficient cells.
Conclusions:
- Nodal signaling is not required for, and may actively inhibit, early neural specification and forebrain development in mouse embryos.
- Key steps in neural and forebrain development can occur prior to gastrulation.
- Nodal plays a role in suppressing anterior and neural fates at pregastrula stages.
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