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Adgrg6/Gpr126 es necesario para la integridad de la pared compacta y el establecimiento de la identidad trabecular

Swati Srivastava^1,2, Felix Gunawan^3,4,5, Silvia Vergarajauregui^1,6

¹Department of Nephropathology, Institute of Pathology, Experimental Renal and Cardiovascular Research, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany.

Nature communications

|February 7, 2026

Resumen

Los receptores acoplados a proteína G de adhesión (aGPCR) controlan el desarrollo del corazón. Gpr126

Área de la Ciencia:

Biología Cardiovascular
Biología del Desarrollo
Biología Celular

Sus antecedentes:

Los receptores acoplados a proteína G de adhesión (aGPCR) desempeñan roles cruciales en el desarrollo, pero sus funciones precisas siguen siendo en gran medida desconocidas.
El aGPCR Gpr126 está implicado en la trabeculación cardíaca, un proceso vital para la función cardíaca.
Los defectos en la trabeculación cardíaca pueden provocar miocardiopatías y disfunción cardíaca.

Objetivo del estudio:

Elucidar los roles distintos de los dominios de Gpr126 en la regulación del desarrollo de los cardiomiocitos y la trabeculación cardíaca.
Comprender cómo los cardiomiocitos adquieren la identidad trabecular durante el desarrollo cardíaco.

Principales métodos:

Se utilizaron mutantes maternos-cigóticos (MZ) gpr126^stl47 y gpr126^st49 con deleciones de dominios específicos.
Se analizó la localización de N-cadherina y la polarización de los cardiomiocitos en modelos mutantes.
Se investigó el impacto de la expresión del fragmento C-terminal (CTF) de Gpr126 endocárdico en la trabeculación.

Principales resultados:

Los mutantes MZ gpr126^stl47 mostraron hipotrabeculación con distribución aleatoria de N-cadherina en los cardiomiocitos de la capa compacta.
Los mutantes que expresan un fragmento N-terminal de Gpr126 que carece del motivo GPS (NTF^ΔGPS) mostraron una pared ventricular multicapa con localización normal de N-cadherina y aumento de la actividad Notch.
La expresión del CTF de Gpr126 endocárdico rescató los defectos de trabeculación en los mutantes gpr126^st49.

Conclusiones:

El fragmento N-terminal (NTF) de Gpr126 es esencial para mantener la integridad de la pared compacta y la adhesión célula-célula.
El fragmento C-terminal (CTF) de Gpr126 es fundamental para establecer la identidad trabecular de los cardiomiocitos.
Los dominios distintos de Gpr126 desempeñan roles específicos y no redundantes en la regulación del desarrollo cardíaco y la trabeculación.

Palabras clave:

Gpr126 Adgrg6 trabeculación cardíaca cardiomiocitos desarrollo cardíaco integridad de la pared compacta identidad trabecular fragmento N-terminal fragmento C-terminal N-cadherina actividad Notch

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