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CNF1 explota la maquinaria ubiquitina-proteasoma para restringir la activación de la Rho GTPasa para la invasión
Anne Doye1, Amel Mettouchi, Guillaume Bossis
1INSERM U452, IFR 50, Faculté de Médecine, 28 avenue de Valombrose, 06107, Nice, France.
Cell
|November 20, 2002
Resumen
La toxina CNF1 de E. coli activa transitoriamente las Rho GTPasas en las células de la vejiga. Esta activación conduce a la degradación de Rac, lo que permite la invasión bacteriana y la motilidad de las células huésped.
Área de la Ciencia:
- Microbiología Microbiología.
- Biología celular Biología celular.
- La bioquímica es la bioquímica.
Sus antecedentes:
- La toxina CNF1 de la E. coli uropatógena es un factor de virulencia.
- CNF1 activa las Rho GTPasas (RhoA, Rac, Cdc42) desamidando un residuo clave de glutamina, lo que lleva a una actividad constitutiva.
Objetivo del estudio:
- Para investigar la dinámica de la activación de la Rho GTPasa por CNF1 en las células de la vejiga.
- Para dilucidar el mecanismo subyacente a la activación transitoria y la posterior desactivación de las Rho GTPasas.
Principales métodos:
- Medición de la activación de la Rho GTPasa en las células de la vejiga tratadas con CNF1.
- Análisis de la ubicuidad de Rac y la degradación proteasomal.
- Evaluación de la motilidad celular del huésped y la invasión bacteriana.
Principales resultados:
- CNF1 indujo una activación transitoria de las Rho GTPasas, en particular de Rac.
- La desactivación de Rac se relacionó con su mayor susceptibilidad a la degradación mediada por ubiquitina / proteosoma.
- La degradación del Rac activado facilitó la motilidad celular del huésped y la invasión bacteriana.
Conclusiones:
- La toxicidad del CNF1 surge de una activación controlada de las Rho GTPasas.
- La maquinaria proteasoma de la célula huésped es secuestrada por CNF1 para regular la actividad de la GTPasa.
- Este mecanismo permite la patogénesis bacteriana mediante la manipulación de las funciones de las células huésped.
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