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Los cambios reversibles y persistentes en la estructura de la cromatina acompañan la activación de un elemento
Cell
|August 1, 1984
Resumen
Las hormonas glucocorticoides estimulan la transcripción del ADN del virus del tumor mamario del ratón (MTV) al alterar la estructura de la cromatina. La unión específica al receptor crea una región hipersensible, que actúa como un potenciador dependiente de las hormonas.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Genética La genética.
- Endocrinología Endocrinología.
Sus antecedentes:
- Los derivados de ADN del virus del tumor mamario del ratón (MTV) pueden ser diseñados para estudios de expresión génica.
- La regulación hormonal de la transcripción génica es un proceso clave en la función celular.
Objetivo del estudio:
- Investigar los efectos de las hormonas glucocorticoides en la estructura de la cromatina y la transcripción de un elemento de ADN MTV diseñado (LTL).
- Identificar los mecanismos moleculares subyacentes a la activación transcripcional inducida por las hormonas.
Principales métodos:
- Construcción in vitro e introducción de ADN LTL en células L de ratón.
- El tratamiento con dexametasona (una hormona glucocorticoide) y la abstinencia hormonal.
- Análisis de la sensibilidad de la DNAasa I y las regiones hipersensibles en la cromatina LTL.
- Ensayos de unión in vitro con el receptor de glucocorticoides purificado.
- Ensayos funcionales in vivo para la actividad del potenciador.
Principales resultados:
- El tratamiento con dexametasona aumentó la sensibilidad global a la DNAasa I de la cromatina LTL, un efecto que persistió después de la retirada de la hormona.
- Una región específica hipersensible a la DNAasa I fue inducida tras el tratamiento hormonal, en correlación con el aumento de la transcripción de LTL.
- Esta región hipersensible se mapeó a la repetición terminal larga de MTV (LTR) y se unió al receptor de glucocorticoides.
- El segmento MTV LTR funcionó como un potenciador dependiente de las hormonas in vivo.
Conclusiones:
- La unión específica del receptor glucocorticoide al MTV LTR altera la configuración de la cromatina cerca del sitio de unión.
- Estas alteraciones crean un potenciador dependiente de la hormona, lo que lleva a un aumento de la transcripción de LTL.
- Este estudio aclara un mecanismo para el control transcripcional mediado por hormonas que implica la remodelación de la cromatina.
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