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El TFEB vincula la autofagia con la biogénesis lisosomal
Carmine Settembre1, Chiara Di Malta, Vinicia Assunta Polito
1Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131 Naples, Italy.
Science (New York, N.Y.)
|May 28, 2011
Resumen
La inanición desencadena un proceso celular llamado autofagia, que mejora la degradación mediante la coordinación de los autofagosomas y lisosomas. Esto está controlado por el factor de transcripción EB (TFEB) y una vía de quinasa sensible a los nutrientes.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- La autofagia es un proceso catabólico celular fundamental que involucra a los autofagosomas y los lisosomas.
- El hambre celular aumenta la degradación mediante la expansión de estos orgánulos.
- Los mecanismos moleculares precisos que regulan esta respuesta coordinada están bajo investigación.
Objetivo del estudio:
- Para dilucidar el programa de transcripción activado por el hambre que controla la autofagia.
- Para identificar el regulador clave que coordina la función de los autofagosomas y lisosomas durante la inanición.
- Para investigar la vía de señalización que controla la actividad de este regulador clave.
Principales métodos:
- Perfiles de transcripción para identificar genes inducidos por el hambre.
- Análisis de la expresión génica lisosomal y autofágica.
- Western blotting y inmunofluorescencia para evaluar la localización de proteínas y la fosforilación.
- Inhibición farmacológica y manipulación genética de las vías de señalización.
Principales resultados:
- El hambre activa un programa transcripcional que gobierna la formación de los autofagosomas, la fusión lisosoma-autofagosoma y la degradación del sustrato.
- El factor de transcripción EB (TFEB), un regulador maestro de la biogénesis lisosomal, coordina este programa.
- La quinasa regulada por la señal extracelular 2 (ERK2) fosforila TFEB, regulando su localización y actividad nuclear.
- La actividad de ERK2 está modulada por los niveles de nutrientes extracelulares, vinculando la detección de nutrientes a la autofagia.
Conclusiones:
- Una vía dependiente de la proteína quinasa activada por mitógeno (MAPK) regula la autofagia.
- Esta vía controla tanto la biogénesis de lisosomas y autofagosomas y su asociación funcional.
- TFEB actúa como un coordinador central, integrando las vías lisosomal y autofágica en respuesta a la disponibilidad de nutrientes.
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