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El complejo ATAC acetiltransferasa coordina las quinasas MAP para regular los genes diana del JNK
Tamaki Suganuma1, Arcady Mushegian, Selene K Swanson
1Stowers Institute for Medical Research, Kansas City, MO 64110, USA.
Cell
|September 4, 2010
Resumen
El complejo ATAC histona acetiltransferasa actúa como un cofactor para c-Jun, regulando la expresión génica y suprimiendo la señalización aguas arriba durante la respuesta celular al estrés.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- La señalización celular de las células.
- La epigenética es la epigenética.
Sus antecedentes:
- Las vías de transducción de señales, como Jun N-terminal kinase (JNK), activan factores de transcripción como c-Jun para regular la expresión génica en respuesta a estímulos extracelulares.
- Los complejos de histona acetiltransferasa (HAT) juegan un papel crucial en la modulación de la estructura de la cromatina e influyen en la transcripción génica.
Objetivo del estudio:
- Para investigar el papel del complejo de histona acetiltransferasa ATAC (Ada dos que contiene A) como un cofactor de transcripción para c-Jun.
- Para aclarar la función de ATAC en la regulación de los genes diana de JNK y su participación en la respuesta al estrés celular.
Principales métodos:
- Los ensayos de inmunoprecipitación de cromatina evalúan la ocupación de c-Jun y la acetilación de H4K16 en los genes objetivo.
- Microscopía de inmunofluorescencia para observar la colocalización de ATAC y c-Jun bajo estrés osmótico.
- Ensayos bioquímicos para analizar el reclutamiento de las quinasas y la supresión de la activación de la JNK.
Principales resultados:
- El complejo ATAC es esencial para la unión de c-Jun a los genes Jra y chickadee y para la acetilación de H4K16.
- ATAC se colocaliza con c-Jun durante el estrés osmótico, reclutando kinasas aguas arriba (Misshapen, MKK4, JNK) e inhibiendo una mayor activación de JNK.
- La subunidad CG10238 de ATAC es crítica para la reubicación de MAPK y la supresión de la vía JNK.
Conclusiones:
- El complejo ATAC funciona como un coactivador transcripcional para c-Jun en genes objetivo específicos.
- ATAC actúa como un regulador negativo de la señalización de la cinasa MAP aguas arriba, suprimiendo la activación de JNK durante el estrés.
- ATAC integra la regulación transcripcional y la modulación de la transducción de señales en respuesta a las señales celulares.
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