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La quinasa de señalización AMPK activa la transcripción promovida por el estrés a través de la fosforilación de la
David Bungard1, Benjamin J Fuerth, Ping-Yao Zeng
1Department of Cellular and Developmental Biology, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA.
Science (New York, N.Y.)
|July 22, 2010
Resumen
La proteína quinasa activada por monofosfato de adenosina (AMPK) regula la energía celular. Este estudio revela que AMPK fosforila directamente la histona H2B en la serina 36, activando la transcripción génica para la adaptación al estrés.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- La proteína quinasa activada por monofosfato de adenosina (AMPK) es un regulador clave de la homeostasis de la energía celular.
- Los mecanismos precisos por los cuales AMPK controla las respuestas celulares al estrés metabólico no se comprenden completamente.
Objetivo del estudio:
- Para aclarar el papel de la AMPK en la regulación de la transcripción génica durante el estrés metabólico.
- Investigar la interacción directa de AMPK con la cromatina y su impacto en las modificaciones de histona.
Principales métodos:
- Pruebas de inmunoprecipitación de cromatina para evaluar la unión de AMPK y la fosforilación de histonas.
- Mutagénesis dirigida al sitio de la histona H2B para estudiar el significado funcional de la fosforilación de la serina 36.
- Análisis de la expresión génica y la asociación de ARN polimerasa II en respuesta a la activación de AMPK y la modificación de la histona H2B.
Principales resultados:
- AMPK se asocia directamente con la cromatina y fosforila la histona H2B en la serina 36 (H2B Ser36).
- El reclutamiento de AMPK y la fosforilación de H2B Ser36 se observaron en promotores y regiones transcritas de genes activados por AMPK.
- La mutación de H2B Ser36 a alanina alteró la transcripción génica, redujo la asociación de ARN polimerasa II y disminuyó la supervivencia celular bajo estrés.
Conclusiones:
- La fosforilación H2B Ser36 dependiente de AMPK es un mecanismo crítico para regular la transcripción génica.
- Esta vía juega un papel directo en la regulación de la cromatina y la adaptación celular al estrés metabólico.
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