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Tbx2 es un regulador maestro de la diferenciación de las células ciliadas internas versus externas
Jaime García-Añoveros1,2,3,4, John C Clancy5, Chuan Zhi Foo5,6
1Department of Anesthesiology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA. anoveros@northwestern.edu.
Nature
|May 4, 2022
Resumen
El factor de transcripción Tbx2 es esencial para la diferenciación de las células ciliadas internas (IHC) y el mantenimiento de la identidad distinta de las células ciliadas internas frente a las células ciliadas externas (OHC) en la cóclea.
Área de la Ciencia:
- Biología del desarrollo
- Neurociencia auditiva
- La genética
Sus antecedentes:
- La cóclea contiene células ciliadas internas (IHC) para la transmisión sensorial y células ciliadas externas (OHC) para la amplificación.
- Mientras que la diferenciación OHC involucra factores de transcripción como el INSM1, los factores que regulan la diferenciación IHC eran desconocidos.
- INSM1 normalmente impide que los OHC se conviertan en IHC, y su ausencia conduce a que los OHC expresen genes IHC.
Objetivo del estudio:
- Identificar el regulador clave responsable de la diferenciación de las células ciliadas internas (CEI) frente a las células ciliadas externas (CEO).
- Investigar el papel de Tbx2 en el establecimiento y mantenimiento de la identidad de las células ciliadas en la cóclea.
- Determinar la relación entre Tbx2 y INSM1 en la determinación del destino de las células ciliadas.
Principales métodos:
- Ablación genética de Tbx2 en células ciliadas embrionarias y postnatales en ratones.
- Análisis de los patrones de expresión génica, incluidos los marcadores OHC e IHC.
- Expresión ectópica de Tbx2 en los OHC para evaluar su función funcional.
Principales resultados:
- La ablación de Tbx2 en IHCs embrionarios causó su transdiferenciación en OHCs, expresando marcadores de OHC.
- Tbx2 actúa epistáticamente en INSM1, lo que indica que es crucial tanto para la diferenciación normal de IHC como para prevenir la transdiferenciación de OHC a IHC.
- La ablación de Tbx2 en los IHC postnatales indujo su conversión directa en OHC maduros; el Tbx2 ectópico en los OHC los hizo convertirse en IHC.
Conclusiones:
- Tbx2 es un regulador maestro, necesario y suficiente, para especificar los IHC y distinguirlos de los OHC.
- Tbx2 juega un papel crítico a lo largo del desarrollo en el mantenimiento de la identidad de las células ciliadas.
- La comprensión de la función de Tbx2 proporciona información sobre los mecanismos moleculares de la diferenciación celular sensorial auditiva.
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