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Spatial and Temporal Analysis of Active ERK in the C. elegans Germline
Published on: November 29, 2016
La señalización a través de la proteína quinasa activada por mitógeno (MEK1) es necesaria para la fragmentación de
U Acharya1, A Mallabiabarrena, J K Acharya
1Department of Biology, University of California, San Diego, La Jolla 92093-0347, USA.
Cell
|February 11, 1998
Resumen
La fragmentación de Golgi durante la mitosis es impulsada por la proteína quinasa activada por mitógeno 1 (MEK1), no por p34cdc2.2. Un ERK específico asociado a Golgi es identificado como el probable objetivo, crucial para este proceso.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- El complejo de Golgi sufre cambios estructurales significativos durante la división celular.
- Comprender los mecanismos moleculares que regulan la fragmentación de Golgi en la mitosis es crucial para la biología celular.
Objetivo del estudio:
- Para investigar los actores moleculares involucrados en la fragmentación del complejo de Golgi durante la mitosis.
- Para identificar las quinasas específicas y sus sustratos responsables de la fragmentación de Golgi.
Principales métodos:
- Desarrollo de un ensayo utilizando células permeabilizadas de riñón normal de rata (NRK).
- Incubación de células permeabilizadas con extractos mitóticos para inducir la fragmentación de Golgi.
- Análisis del papel de la p34cdc2, la proteína kinasa activada por mitógeno kinasa 1 (MEK1) y las quinasas reguladas por señales extracelulares (ERK1/2).
Principales resultados:
- Las pilas de Golgi en las células NRK de interfase se fragmentan extensamente después de la incubación con extractos mitóticos.
- p34cdc2 no es necesario para la fragmentación de Golgi.
- La proteína quinasa activada por mitógeno quinasa 1 (MEK1) es esencial para la fragmentación de Golgi, pero sus conocidos sustratos citoplasmáticos ERK1 y ERK2 no lo son.
- Se identificó una nueva ERK asociada a Golgi y se propuso como el probable objetivo de MEK1.
Conclusiones:
- La fragmentación de Golgi durante la mitosis está regulada por MEK1, independiente de p34cdc2.2.
- Una ERK asociada a Golgi, en lugar de una ERK1/2 citoplasmática, es el objetivo probable de MEK1 en este proceso.
- Este estudio revela una nueva vía reguladora para la dinámica de Golgi en la división celular.
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