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Los sitios de entrada de ribosomas internos similares al virus de la hepatitis C desplazan a eIF3 para obtener acceso

Yaser Hashem¹, Amedee des Georges, Vidya Dhote

¹1] Howard Hughes Medical Institute (HHMI), Department of Biochemistry and Molecular Biophysics, Columbia University, New York City, New York 10032, USA [2] Department of Biochemistry and Molecular Biophysics, Columbia University, New York City, New York 10032, USA.

|November 5, 2013

Resumen

El virus de la hepatitis C (HCV) y el virus de la peste porcina clásica (CSFV) utilizan los sitios de entrada de ribosomas internos (IRES) para la traducción. Este estudio revela cómo la interacción de eIF3 con el CSFV IRES impide su unión a la subunidad 40S, favoreciendo la traducción del ARNm viral.

Área de la Ciencia:

Biología Molecular Biología Molecular
Virología Virología.
Biología Estructural Biología estructural.

Sus antecedentes:

El virus de la hepatitis C (HCV) y el virus de la peste porcina clásica (CSFV) utilizan los sitios de entrada de ribosomas internos (IRES) para la iniciación de la traducción independiente de la capa.
Estos IRES requieren un subconjunto de factores de iniciación eucariota (eIF) e interactúan con la subunidad ribosómica 40S para formar complejos de iniciación.
El papel específico de la interacción de eIF3 con los IRES similares al VHC en la iniciación de la traducción seguía siendo en gran medida desconocido.

Objetivo del estudio:

Para aclarar la función de la interacción de eIF3 con IRES similares al VHC durante la iniciación de la traducción.
Investigar la base estructural de la unión de eIF3 al IRES CSFV y su impacto en la formación de complejos ribosómicos.

Principales métodos:

Se empleó microscopía criolectrónica (cryo-EM) para determinar la estructura de un complejo ribosómico 40S que contiene eIF3 y el IRES.
Análisis de las posiciones ribosómicas e interacciones de IRES y eIF3 dentro del complejo.

Principales resultados:

El IRES CSFV se une a la subunidad 40S de manera similar al IRES HCV.
eIF3 se desplaza de su sitio de enlace canónico en la subunidad 40S e interactúa directamente con la región apical del dominio III de IRES.
Esta interacción impide la asociación de eIF3 con la subunidad 40S, evitando así la competencia por los sitios de enlace.

Conclusiones:

La interacción específica entre los IRES similares al VHC y el eIF3 juega un papel crucial en la regulación de la iniciación de la traducción.
El desplazamiento de eIF3 alivia la competencia para la unión de subunidades 40S y reduce la formación de complejos de preiniciación 43S.
Este mecanismo favorece la traducción de los ARNm virales sobre los ARNm celulares.

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