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Un papel para la exonucleasa Dis3l2 del síndrome de Perlman en la vía Lin28-let-7

Hao-Ming Chang¹, Robinson Triboulet, James E Thornton

¹Stem Cell Program, Boston Children's Hospital, Massachusetts 02115, USA.

|April 19, 2013

Resumen

El factor de pluripotencia Lin28 inhibe la producción de microARN let-7. Los investigadores identificaron a Dis3l2 como la enzima que degrada el uridilado pre-let-7, descubriendo una nueva vía de desintegración del ARN crucial para el desarrollo y el cáncer.

Área de la Ciencia:

Biología Molecular Biología Molecular
Biología del desarrollo Biología del desarrollo.
Biología del cáncer Biología del cáncer.

Sus antecedentes:

Lin28 es un factor de pluripotencia que inhibe la expresión de let-7 microARN (miRNA) en células no diferenciadas.
Lin28 actúa como un oncogén en ciertos tipos de cáncer al bloquear la biogénesis del miRNA let-7.
Lin28 recluta uridylyl transferases a los ARN pre-let-7, lo que lleva a su degradación por una RNase. desconocida.

Objetivo del estudio:

Para identificar la RNasa específica responsable de la degradación del pre-let-7 uridilado.
Para dilucidar el papel de la oligouridilación 3' como señal de desintegración del ARN.
Investigar la relevancia fisiológica de esta vía en el desarrollo y la enfermedad.

Principales métodos:

Ensayos de reconstitución bioquímica utilizando proteínas purificadas y ARN.
Knockdown de las RNasas candidatas en células madre embrionarias de ratón.
Análisis de la estabilidad y el procesamiento del ARN pre-let-7.

Principales resultados:

Dis3l2, una exonucleasa de 3'-5', fue identificada como la enzima que degrada el uridilado pre-let-7.
Se demostró que la oligouridilación 3' estimula la actividad de Dis3l2 in vitro.
La eliminación de Dis3l2 en células madre embrionarias de ratón dio lugar a la estabilización pre-let-7.

Conclusiones:

Dis3l2 es la nucleasa primaria responsable de la desintegración de la uridinación pre-let-7.
La oligouridilación 3 'sirve como una señal de desintegración específica para Dis3l2.
Esta vía es crítica para regular los niveles de miARN let-7 y tiene implicaciones para el síndrome de Perlman y el tumor de Wilms.

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