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mTOR controla la función oxidativa mitocondrial a través de un complejo transcripcional YY1-PGC-1alpha.

John T Cunningham1, Joseph T Rodgers, Daniel H Arlow

  • 1Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Resumen

El objetivo mamífero de la rapamicina (mTOR) es esencial para la función oxidativa mitocondrial. mTOR regula la expresión génica mitocondrial y el consumo de oxígeno a través del factor de transcripción YY1, impactando la homeostasis energética.

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Área de la Ciencia:

  • El metabolismo celular es el metabolismo celular.
  • Biología mitocondrial Biología mitocondrial
  • Endocrinología Molecular La Endocrinología Molecular

Sus antecedentes:

  • Peroxisome-proliferator-activated receptor coactivator (PGC) - 1alpha regula la función oxidativa mitocondrial y la homeostasis de la energía.
  • El objetivo de la rapamicina en mamíferos (mTOR) es una quinasa clave en las vías de nutrientes y energía, que controla el crecimiento y la supervivencia celular.
  • El papel preciso de mTOR en la regulación de la actividad oxidativa mitocondrial sigue sin estar claro.

Objetivo del estudio:

  • Para investigar si y cómo mTOR controla las actividades oxidativas mitocondriales.
  • Para dilucidar los mecanismos moleculares que vinculan la señalización mTOR a la función mitocondrial.
  • Identificar posibles dianas terapéuticas para enfermedades metabólicas y cáncer.

Principales métodos:

  • Utilizó la inhibición de mTOR con rapamicina en tejidos y células del músculo esquelético.
  • Expresión génica evaluada de los reguladores transcripcionales mitocondriales (PGC-1alpha, receptor alfa relacionado con el estrógeno, factores respiratorios nucleares).
  • Empleó genómica computacional para identificar objetivos de factores de transcripción, seguido de estudios de knockdown genético y ensayos de interacción proteína-proteína.

Principales resultados:

  • La inhibición de mTOR disminuyó la expresión de PGC-1alfa, el receptor alfa relacionado con el estrógeno y los factores respiratorios nucleares, reduciendo la expresión génica mitocondrial y el consumo de oxígeno.
  • Identificó el yin-yang 1 (YY1) como un objetivo transcripcional común de mTOR y PGC-1alpha.
  • El knockdown de YY1 disminuyó significativamente la expresión génica y la respiración mitocondriales; YY1 era necesario para la represión génica inducida por la inhibición de mTOR. mTOR y raptor interactuaron con YY1, y la inhibición de mTOR interrumpió la interacción y la coactivación de YY1-PGC-1alpha.

Conclusiones:

  • mTOR es crucial para mantener la función oxidativa mitocondrial.
  • Un nuevo mecanismo revela que la señalización mTOR regula la función oxidativa mitocondrial a través del control transcripcional de YY1 y PGC-1alpha.
  • Esta vía es vital para equilibrar el metabolismo energético y tiene implicaciones para las enfermedades metabólicas y el cáncer.