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Múltiples mecanismos que limitan la ubicuidad de la ARN polimerasa II a las polimerasas sometidas a detención
Baggavalli P Somesh1, James Reid, Wei-Feng Liu
1Cancer Research UK London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms, Herts EN6 3LD, United Kingdom.
Cell
|June 18, 2005
Resumen
La ubicuidad y degradación de la ARN polimerasa II (RNAPII) están reguladas por la detención de la transcripción. Los complejos de alargamiento detenidos, que no inician formas, están ubicuos, apuntando al RNAPII para la degradación.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Regulación de la expresión génica Regulación de la expresión génica
- La degradación de las proteínas.
Sus antecedentes:
- La ARN polimerasa II (RNAPII) controla la transcripción de los genes.
- La ubicuidad y degradación del RNAPII son procesos reguladores cruciales.
- Comprender estos mecanismos es clave para comprender el control de la expresión génica.
Objetivo del estudio:
- Investigar los mecanismos y la regulación de la ubicuidad y degradación del RNAPII.
- Para identificar las formas específicas de RNAPII dirigidas a la ubicuidad.
- Para aclarar el papel de Def1 y la fosforilación de CTD en este proceso.
Principales métodos:
- Reconstitución in vitro de la ubicuidad del RNAPII utilizando factores purificados.
- Análisis de la ubicuidad del RNAPII in vivo bajo diversas condiciones.
- Mutagenesis dirigida al sitio de los sitios de fosforilación de CTD y las fosfatasas.
Principales resultados:
- Los complejos de elongación RNAPII detenidos son sustratos preferidos para la ubicuidad.
- Tanto la detención de la transcripción dependiente del daño del ADN como la independiente desencadenan la ubicuidad del RNAPII.
- Def1 estimula la ubicuidad específicamente en complejos de elongación.
- La ubiquitilación depende del dominio C-terminal del RNAPII (CTD) y es inhibida por la fosforilación de la serina 5.
- El RNAPII ubiquitulado es hipofosforilado en la serina 5, y la mutación SSU72 dificulta la degradación.
Conclusiones:
- La ubicuidad de RNAPII está dirigida principalmente a los complejos de alargamiento detenidos.
- El estado de fosforilación de la CTD, particularmente la serina 5, dicta la ubicuidad.
- Estos hallazgos revelan mecanismos que aseguran que la ubicuidad y degradación de RNAPII ocurran durante la detención de la transcripción.
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