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Assay for Adhesion and Agar Invasion in S. cerevisiae
Published on: November 8, 2006
Control de retroalimentación de la fase S en la levadura en ciernes independiente de la fosforilación de la tirosina
1Department of Microbiology and Immunology, University of California, San Francisco 94143-0502.
Nature
|January 23, 1992
Resumen
En la levadura en ciernes, la división celular no depende de la fosforilación de la tirosina de p34cdc2 para los puntos de control de la replicación del ADN. Este estudio revela un mecanismo alternativo para la detención del ciclo celular, crucial para la reparación del ADN y la estabilidad genómica.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- Genética La genética.
Sus antecedentes:
- La progresión del ciclo celular, particularmente la entrada en mitosis, está estrictamente regulada por la finalización de la síntesis del ADN.
- Los controles de retroalimentación de la fase S aseguran que la división celular se detenga en presencia de ADN dañado o no replicado.
- En la levadura de fisión (Schizosaccharomyces pombe), las mutaciones que afectan a la fosforilación de p34cdc2 tirosina 15 (Y15) interrumpen la detención de G2, lo que sugiere una función reguladora conservada.
Objetivo del estudio:
- Investigar el papel de la fosforilación de la tirosina en los controles de retroalimentación de la fase S y la entrada mitótica en la levadura en ciernes (Saccharomyces cerevisiae).
- Para determinar si la fosforilación de la tirosina conservada de p34cdc2 es esencial para los puntos de control de replicación del ADN en Saccharomyces cerevisiae.
Principales métodos:
- El análisis genético de Saccharomyces cerevisiae.
- Mutagénesis dirigida al sitio del gen CDC28 para prevenir la fosforilación de tirosina.
- Análisis fenotípico de la progresión del ciclo celular y la respuesta al daño del ADN.
Principales resultados:
- El producto del gen CDC28, el homólogo de Saccharomyces cerevisiae de cdc2, se fosforila en la tirosina 19 (Y19) durante la fase S.
- Las mutaciones que impiden la fosforilación de la tirosina de CDC28 no causaron mitosis prematura.
- Estas mutaciones tampoco abolieron la detención del ciclo celular G2 en respuesta al ADN no replicado.
Conclusiones:
- La fosforilación por tirosina de p34cdc2 no es esencial para los controles de retroalimentación de la fase S o el inicio de la mitosis en Saccharomyces cerevisiae.
- La levadura de brote utiliza un mecanismo independiente de la fosforilación de la tirosina p34 para detener la división celular cuando el ADN no se replica o está dañado.
- Este mecanismo alternativo puede implicar la regulación de la actividad catalítica de p34 sin fosforilación de tirosina.
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