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La clasificación de la nexina 5 media la autofagia inducida por el virus y la inmunidad
Xiaonan Dong1, Yuting Yang1, Zhongju Zou1,2
1Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Nature
|December 17, 2020
Resumen
La clasificación de la nexina 5 (SNX5) es crucial para iniciar la autofagia durante las infecciones virales, mejorando la defensa del huésped. SNX5 activa un complejo de enzimas clave en los endosomas, impulsando la célula
Área de la Ciencia:
- Inmunología y biología celular
- Mecanismos moleculares de la autofagia y la defensa viral
Sus antecedentes:
- La autofagia, un proceso de degradación celular, juega un papel vital en la inmunidad y la defensa del huésped contra los patógenos.
- Los mecanismos precisos que inician la autofagia en respuesta a las infecciones virales siguen siendo incompletamente entendidos.
Objetivo del estudio:
- Identificar los factores del huésped esenciales para iniciar la autofagia durante la infección viral.
- Para aclarar el mecanismo molecular por el cual los virus desencadenan la autofagia.
Principales métodos:
- Las pantallas de ARN corto de interferencia (siRNA) de todo el genoma para identificar genes esenciales.
- Ensayos de infección viral in vitro y estudios in vivo con ratones knockout de Snx5.
- Análisis bioquímicos de las interacciones proteicas, la actividad enzimática y la producción de lípidos.
Principales resultados:
- La clasificación de la nexina 5 (SNX5) se identifica como esencial para la autofagia inducida por el virus, pero no para la autofagia basal o inducida por el estrés.
- La deficiencia de SNX5 aumenta la susceptibilidad celular a la infección viral y aumenta la letalidad en ratones.
- SNX5 interactúa con el complejo PI3KC3-C1, aumentando su actividad y promoviendo la generación de PtdIns ((3) P en los endosomas para el aclaramiento viral.
Conclusiones:
- SNX5 actúa como un mediador crítico para iniciar la autofagia específicamente durante las infecciones virales.
- La activación dependiente de SNX5 de PI3KC3-C1 en los endosomas representa un nuevo mecanismo para la defensa del huésped contra los virus.
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