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Una subunidad COPII actúa con un receptor de autofagia para dirigirse al retículo endoplasmático para la degradación
Yixian Cui1, Smriti Parashar1, Muhammad Zahoor2
1Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA.
Science (New York, N.Y.)
|July 6, 2019
Resumen
El complejo Lst1-Sec23 ayuda inesperadamente en la degradación del retículo endoplasmático (ER) (ER-fagia) al vincular los componentes de ER a los autofagosomas. Esta función conservada es vital para la salud celular y para prevenir la agregación de proteínas.
Área de la Ciencia:
- Biología celular
- Biología molecular
- La autofagia
Sus antecedentes:
- El retículo endoplasmático (ER) es crucial para la síntesis y el plegamiento de proteínas.
- La ER-fagia es una vía de autofagia selectiva para degradar los componentes de la ER.
- El complejo Lst1-Sec23 normalmente media el transporte de proteínas desde el ER hasta el Golgi.
Objetivo del estudio:
- Investigar el papel del complejo Lst1-Sec23 en la ER-fagia.
- Para determinar si Lst1-Sec23 tiene funciones más allá de la secreción de proteínas.
- Para explorar la conservación de Lst1-Sec23 en la ER-fagia.
Principales métodos:
- Genética de levaduras y técnicas de biología celular.
- Investigar las interacciones proteína-proteína entre los receptores Lst1-Sec23 y ER-fagia.
- Analizando el papel de Lst1 y su homólogo en mamíferos SEC24C en la degradación de ER.
Principales resultados:
- Lst1-Sec23 participa inesperadamente en la ER-fagia, independientemente de su función secretora.
- Lst1-Sec23 se asocia con el receptor de fagia ER Atg40 en sitios específicos de ER.
- La ER-fagia mediada por Lst1 es esencial para prevenir la acumulación de proteínas propensas a la agregación y mantener la homeostasis celular.
- El homólogo de mamíferos SEC24C también es necesario para la ER-fagia, lo que indica la conservación funcional.
Conclusiones:
- Lst1-Sec23 juega un papel novedoso y conservado en la ER-fagia.
- Esta función es crítica para la homeostasis celular y la prevención de la proteotoxicidad.
- Lst1-Sec23 actúa como puente entre los componentes de ER y la maquinaria autofágica durante la ER-fagia.
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