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Terminación de la autofagia y reformación de los lisosomas regulados por mTOR
Li Yu1, Christina K McPhee, Lixin Zheng
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Nature
|June 8, 2010
Resumen
La autofagia recicla los componentes celulares durante la inanición. Este estudio revela un ciclo en el que la detección de nutrientes a través de la reactivación de mTOR restaura los lisosomas, manteniendo la función celular.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- Fisiología Fisiología Fisiología.
Sus antecedentes:
- La autofagia es un proceso celular conservado para la degradación de los componentes citoplasmáticos.
- El objetivo de la quinasa sensible a los nutrientes de la señalización de la rapamicina (TOR) inhibe la autofagia durante la abundancia de nutrientes.
- La regulación de la autofagia y el destino de los lisosomas durante la inanición no se entiende completamente.
Objetivo del estudio:
- Investigar la regulación de la autofagia y la señalización mTOR durante la inanición prolongada.
- Para aclarar el papel de la homeostasis del lisosoma en la detección de nutrientes y la autofagia.
Principales métodos:
- Se utilizaron células renales de rata para estudiar la autofagia y la señalización mTOR.
- Se ha investigado la reactivación mTOR dependiente de la autofagia.
- Examinó la biogénesis del lisosoma y la homeostasis durante la inanición.
Principales resultados:
- La señalización mTOR, inicialmente inhibida durante el inicio de la autofagia, se reactiva durante la inanición prolongada.
- La reactivación de mTOR depende de la degradación de los productos autolisómicos.
- Este proceso genera nuevos lisosomas, restaurando el complemento lisosómico en las células de todas las especies.
Conclusiones:
- Un ciclo de autofagia conservado vincula la detección de nutrientes con la homeostasis del lisosoma durante el hambre.
- La reactivación de la señalización mTOR atenúa la autofagia y promueve la regeneración del lisosoma.
- Este mecanismo asegura el suministro celular de nutrientes y la función de los lisosomas durante la privación de nutrientes.
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