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Los mecanismos dependientes de la metilación de histonas imponen dependencia de ligandos para la activación de genes
Ivan Garcia-Bassets1, Young-Soo Kwon2, Francesca Telese1
1Howard Hughes Medical Institute, Department of Molecular Medicine, University of California, San Diego, School of Medicine 9500 Gilman Drive, La Jolla, CA 92093-0648.
Cell
|February 10, 2007
Resumen
Las histonas metiltransferasas específicas (HMTs) actúan como guardianes, impidiendo que los receptores nucleares no ligados activen los genes. Este código histónico dependiente de la HMT requiere desmetilasas histónicas para la activación genética adecuada, vinculando la metilación a la expresión genética regulada.
Área de la Ciencia:
- La epigenética es la epigenética.
- Biología Molecular Biología Molecular
- Regulación genética Reglamento genético.
Sus antecedentes:
- Los receptores nucleares requieren la unión de ligandos para los cambios conformacionales, lo que permite el intercambio de corepressor-coactivador.
- El papel de las marcas epigenéticas en la aplicación de la dependencia de ligandos para la activación de genes mediada por receptores nucleares no se entiende completamente.
Objetivo del estudio:
- Investigar el requisito de hitos epigenéticos específicos para imponer la dependencia de ligandos para la activación de genes mediada por receptores nucleares.
- Aclarar el mecanismo por el cual las funciones gatekeeper específicas del gen previenen la activación del gen constitutivo por factores de transcripción no ligados.
Principales métodos:
- Investigó el papel de las histona metiltransferasas (HMTs) en la regulación de la unión del factor de transcripción a los promotores de genes diana.
- Examinó la participación de un código de histona inhibidora dependiente de HMT en el control de la expresión génica.
- Evaluó el requisito de las histonas desmetilasas, como la LSD1, en la activación de genes dependientes de ligandos y señales.
Principales resultados:
- Identificó una estrategia general que involucra cohortes específicas de HMT que funcionan como guardianes genéticos específicos.
- Se demostró que estos HMT impiden que los receptores nucleares no ligados y otros factores de transcripción se unan a los promotores en ausencia de señales.
- Se demostró que un código de histona inhibidora dependiente de la HMT requiere demetilasas de histona específicas para la activación de genes regulados.
Conclusiones:
- Un código de histona inhibidora dependiente de HMT impone una función de guardián, impidiendo la activación del gen constitutivo por factores de transcripción no ligados.
- Se requieren demetilasas de histonas específicas para eliminar esta marca inhibidora, lo que permite la expresión génica dependiente de ligandos y señales.
- Este mecanismo vincula la metilación inhibidora de la histona con una estrategia conservada para prevenir la inducción de genes patológicos por factores de transcripción regulados.
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