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Regulación del complejo Bub2/Bfa1 GAP por Cdc5 y puntos de control del ciclo celular
1Verna and Mars McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Cell
|December 6, 2001
Resumen
La cinasa Polo/Cdc5 antagoniza el Bfa1/Bub2 para promover la salida mitótica. Los puntos de control del ciclo celular regulan la fosforilación de Bfa1, asegurando la detención mitótica cuando se produce un daño en el ADN.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- Genética La genética.
Sus antecedentes:
- Tem1 La GTPasa inicia la salida mitótica a través de una vía de transducción de señales.
- El complejo Bfa1/Bub2 antagoniza la función Tem1 durante la mayor parte del ciclo celular.
- La regulación del complejo Bfa1/Bub2 no se entiende completamente.
Objetivo del estudio:
- Para investigar los reguladores aguas arriba del complejo Bfa1/Bub2.
- Para aclarar cómo Bfa1/Bub2 es controlado por los puntos de control del ciclo celular.
- Para entender el papel de la cinasa Polo/Cdc5 en la red de salida mitótica.
Principales métodos:
- Investigó la interacción entre la cinasa Polo/Cdc5 y el Bfa1/Bub2.2.
- Se analizó el efecto de Cdc5 en la fosforilación de Bfa1.
- Se examinó la regulación Bfa1 por ensamblaje de husillo y puntos de control de orientación de husillo.
- Estudió el impacto del daño del ADN en la modificación de Bfa1 a través de Rad53 y Dun1.
Principales resultados:
- La cinasa Polo/Cdc5 fosforila la Bfa1, antagonizando su función y promoviendo la salida mitótica.
- El ensamblaje del husillo y los puntos de control de orientación del husillo inhiben la fosforilación Bfa1.
- El daño al ADN induce una modificación Rad53- y Dun1-dependiente de Bfa1, independiente de la fosforilación inhibidora.
- La regulación de Bfa1 por Cdc5 y puntos de control es crucial para garantizar la detención mitótica.
Conclusiones:
- La cinasa Polo/Cdc5 es un regulador aguas arriba de Bfa1/Bub2 en la vía de salida mitótica.
- La fosforilación de Bfa1 está regulada diferencialmente por los puntos de control del ciclo celular y el daño al ADN.
- La modificación de Bfa1 por múltiples vías es un mecanismo clave para garantizar la detención mitótica adecuada.
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