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El acoplamiento molecular de la regulación de Tsix y la pluripotencia
Pablo Navarro1, Andrew Oldfield, Julie Legoupi
1Unité de Génétique Moléculaire Murine, URA 2578, Institut Pasteur, 75724 Paris Cedex 15, France. pablo.navarro@ed.ac.uk
Nature
|November 19, 2010
Resumen
Los factores de pluripotencia Nanog, Oct4 y Sox2 reprimen Xist, mientras que Klf4, c-Myc y Rex1 activan Tsix, coordinando la reprogramación de la inactivación del cromosoma X y la pluripotencia en las células madre embrionarias.
Área de la Ciencia:
- La epigenética es la epigenética.
- Genética La genética.
- Biología del desarrollo Biología del desarrollo.
Sus antecedentes:
- La reprogramación de la inactivación del cromosoma X (XCI) es crucial para la adquisición de pluripotencia.
- La represión xista y el aumento de la regulación de Tsix acompañan la reprogramación de XCI.
- Los factores de pluripotencia Nanog, Oct4 y Sox2 reprimen la transcripción de Xist.
Objetivo del estudio:
- Para aclarar la relación entre los factores de transcripción de pluripotencia y la regulación de Tsix.
- Identificar los factores involucrados en la regulación al alza de Tsix durante la diferenciación de células madre embrionarias.
Principales métodos:
- Eliminación de la región de minisatélites DXPas34.
- Los experimentos de knockdown para evaluar la importancia de los factores.
- Análisis del reclutamiento de factores de transcripción y la maquinaria de transcripción.
Principales resultados:
- La regulación ascendente de Tsix en las células madre embrionarias requiere el reclutamiento de Rex1, Klf4 y c-Myc por el minisatélite DXPas34.
- La eliminación de DXPas34 anula la vinculación del factor y perjudica el reclutamiento de promotores de Tsix.
- Rex1 es crítico para el alargamiento eficiente de la transcripción de Tsix.
Conclusiones:
- Distintos complejos específicos de células madre embrionarias vinculan la reprogramación XCI y la pluripotencia.
- Nanog, Oct4 y Sox2 reprimen el Xist, facilitando la reactivación del X inactivo.
- Klf4, c-Myc y Rex1 activan Tsix, asegurando la inactivación aleatoria de X tras la diferenciación.
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