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Identification of Post-translational Modifications of Plant Protein Complexes
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Estructura del resistosoma ROQ1 activado que reconoce directamente el efector patógeno XopQ
Raoul Martin1,2, Tiancong Qi3,4, Haibo Zhang3
1Biophysics Graduate Group, University of California, Berkeley, CA 94720, USA.
Science (New York, N.Y.)
|December 4, 2020
Resumen
Los receptores inmunes de las plantas, los receptores de repetición ricos en leucina (NLR) que se unen a los nucleótidos, reconocen directamente los efectores bacterianos. Esta unión desencadena la oligomerización del NLR y la activación de las vías de señalización inmunológica de la planta.
Área de la Ciencia:
- Inmunidad vegetal
- Biología molecular
- Biología estructural
Sus antecedentes:
- Las plantas y los animales utilizan receptores de repetición ricos en leucina que se unen a los nucleótidos intracelulares (NLR) para detectar la infección por patógenos.
- Los mecanismos precisos por los cuales los NLR detectan efectores patógenos e inician respuestas inmunes no se comprenden completamente.
Objetivo del estudio:
- Aclarar la base estructural del reconocimiento del efector y la activación del NLR.
- Describir la estructura del NLR ROQ1 activado unido al efector Xanthomonas euvesicatoria XopQ.
Principales métodos:
- Microscopía cryoelectrónica (cryo-EM) con una resolución de 3,8 angstroms.
- Análisis estructural del complejo NLR-efector.
Principales resultados:
- La estructura revela la unión directa de ROQ1 tanto al sitio activo como a los residuos superficiales del efector XopQ.
- El ROQ1 activado forma un resistosoma tetramérico, que reúne los dominios del receptor de interleucina tipo Toll (TIR) para la señalización.
- Esto sugiere un mecanismo de reconocimiento de efector directo que conduce a la oligomerización y activación de NLR.
Conclusiones:
- El reconocimiento directo de los efectores patógenos por los NLR es un mecanismo clave para iniciar la inmunidad de las plantas.
- La activación dependiente de la oligomerización de los resistosomas vegetales por parte de los NLR facilita la señalización inmune posterior a través de los dominios TIR.
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