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Chk1 es una histona H3 treonina 11 quinasa que regula la represión transcripcional inducida por daño al ADN
Midori Shimada1, Hiroyuki Niida, Doaa H Zineldeen
1Department of Cell Biology and Biochemistry, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.
Cell
|February 5, 2008
Resumen
El daño al ADN disminuye rápidamente la fosforilación de la histona H3 Treonina 11, reprimiendo genes como la ciclina B1. Esto implica la disociación de Chk1 de la cromatina, reduciendo la acetilación de histonas y la transcripción génica.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Biología celular Biología celular.
- La epigenética es la epigenética.
Sus antecedentes:
- El daño al ADN desencadena cambios complejos en la expresión génica, incluida la activación y supresión transcripcional.
- Los mecanismos subyacentes a la supresión transcripcional inducida por daño al ADN siguen siendo poco conocidos en comparación con las vías de activación.
Objetivo del estudio:
- Para investigar el papel de las modificaciones histónicas en la represión transcripcional inducida por daño al ADN.
- Para dilucidar la participación de la quinasa Chk1 en la regulación de la expresión génica después del daño del ADN.
Principales métodos:
- Análisis de la dinámica de fosforilación de la histona H3 Treonina 11 (H3-T11) después del daño del ADN.
- Evaluación de la actividad de la quinasa Chk1 y la asociación de cromatina.
- Inmunoprecipitación de cromatina para evaluar la acetilación de histonas y la unión del factor de transcripción a los promotores de genes diana.
Principales resultados:
- El daño en el ADN reduce rápidamente la fosforilación H3-T11, lo que se correlaciona con la represión de genes como la ciclina B1 y cdk1.
- La fosforilación H3-T11 es dependiente del ciclo celular y está regulada por Chk1.
- Chk1 se disocia de la cromatina al dañar el ADN, lo que lleva a una disminución de la fosforilación H3-T11 y una reducción de la unión de la histona acetiltransferasa GCN5.
- La pérdida de la fosforilación H3-T11 está relacionada con la disminución de la acetilación H3-K9 en los promotores de genes diana.
Conclusiones:
- Chk1 actúa como una histona quinasa, mediando la represión transcripcional inducida por el daño al ADN.
- El mecanismo implica la fosforilación H3-T11 dependiente de Chk1 y la subsiguiente pérdida de la acetilación de la histona.
- Este estudio revela una nueva vía para la regulación epigenética de la expresión génica en respuesta al daño del ADN.
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