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La movilización de HP1-beta promueve cambios en la cromatina que inician la respuesta al daño del ADN

Nabieh Ayoub¹, Anand D Jeyasekharan, Juan A Bernal

¹The Medical Research Council Cancer Cell Unit, Hutchison/MRC Research Centre, Hills Road, Cambridge CB2 0XZ, UK.

|April 29, 2008

Resumen

La respuesta al daño del ADN se inicia rápidamente a través de la movilización y fosforilación de HP1-beta, una nueva cascada de señalización que promueve la fosforilación H2AX y la reparación del ADN en las células de mamíferos.

Área de la Ciencia:

Biología celular Biología celular.
Biología Molecular Biología Molecular
Genética La genética.

Sus antecedentes:

La variante histona H2AX se fosforila rápidamente después del daño del ADN, sirviendo como un marcador temprano para las rupturas cromosómicas.
Esta fosforilación recluta moléculas de señalización, iniciando la respuesta al daño del ADN y las vías de reparación.

Objetivo del estudio:

Identificar los cambios dinámicos de la cromatina que facilitan la fosforilación H2AX después del daño del ADN.
Para aclarar el papel de la heterocromatina proteína 1 (HP1)-beta en las primeras etapas de la respuesta al daño del ADN.

Principales métodos:

Investigó la movilización de HP1-beta después de rupturas de ADN.
Se analizó la fosforilación HP1-beta en Thr 51 y su efecto sobre la unión de la cromatina.
Utilizó la inhibición de la caseína quinasa 2 (CK2) para evaluar su papel en la movilización HP1-beta y la fosforilación H2AX.
Empleó un mutante HP1-beta constitutivamente unido a la cromatina para estudiar su impacto en la fosforilación H2AX.

Principales resultados:

Las rupturas de ADN desencadenan una rápida movilización de HP1-beta, un factor de cromatina asociado con H3K9me.me.
La fosforilación de HP1-beta en Thr 51 interrumpe su interacción con H3K9me, liberándolo de la cromatina.
La inhibición de CK2 suprime la fosforilación y movilización de HP1-beta, reduciendo en consecuencia la fosforilación de H2AX.
La alteración de la unión a la cromatina HP1-beta afecta a la fosforilación H2AX, destacando su papel crítico.

Conclusiones:

Una nueva cascada de señalización que involucra la modificación de HP1-beta inicia la respuesta al daño del ADN.
Esta cascada altera la cromatina mediante la modificación de HP1-beta, un mediador del código de la histona, sin cambiar el propio código de la histona.
Estos hallazgos revelan un mecanismo no reconocido previamente en la respuesta celular temprana al daño del ADN.

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