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La transcripción no codificante instruye el plegamiento y la compartimentación de la cromatina para dictar la
Takeshi Isoda1, Amanda J Moore1, Zhaoren He1
1Department of Molecular Biology, University of California, San Diego, La Jolla, CA 92093, USA.
Cell
|September 23, 2017
Resumen
Un nuevo ARN no codificante, ThymoD, guía el desarrollo de las células T mediante el reposicionamiento del potenciador Bcl11b. La deficiencia de ThymoD bloquea la maduración de las células T y conduce a tumores linfoides malignos, destacando su papel en la supresión tumoral.
Área de la Ciencia:
- Inmunología
- Biología molecular
- La epigenética
Sus antecedentes:
- Bcl11b es un factor de transcripción clave que determina el compromiso del linaje de células T.
- La organización nuclear juega un papel crítico en la regulación genética durante el desarrollo.
Objetivo del estudio:
- Identificar los factores involucrados en el reposicionamiento nuclear del potenciador Bcl11b.
- Aclarar el papel de los ARN no codificantes en la orquestación del desarrollo de células T y la supresión tumoral.
Principales métodos:
- Análisis de modelos de ratón con deficiencia de ThymoD.
- Las técnicas de captura de la conformación de la cromatina.
- Análisis de las marcas epigenéticas.
- Estudios de arquitectura nuclear.
Principales resultados:
- Se identificó un ARN no codificante, ThymoD, como un factor que reubica el potenciador de Bcl11b.
- La deficiencia de ThymoD causó un bloqueo del desarrollo de las células T y tumores linfoides malignos.
- La transcripción de ThymoD indujo la desmetilación en los sitios CTCF, promoviendo el bucle dependiente de la cohesión del potenciador y promotor de Bcl11b.
- Este reposicionamiento creó un dominio de bucle asociado con la activación de marcas epigenéticas y facilitó la separación de fases.
Conclusiones:
- La transcripción no codificante, ejemplificada por ThymoD, es crucial para orquestar el plegamiento y la compartimentación de la cromatina a gran escala durante el desarrollo.
- La comunicación precisa entre potenciador y promotor, regulada por la arquitectura nuclear, es esencial para la progresión del desarrollo y la supresión del tumor.
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