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The C4 Protein from Tomato Yellow Leaf Curl Virus Can Broadly Interact with Plant Receptor-Like Kinases

Plant receptor-like kinases (RLKs) exert an essential function in the transduction of signals from the cell exterior to the cell interior, acting as important regulators of plant development and responses to environmental conditions. A growing body of evidence suggests that RLKs may play relevant ro...

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Detalles Bibliográficos
Autores principales: Garnelo Gómez, Borja, Zhang, Dan, Rosas-Díaz, Tábata, Wei, Yali, Macho, Alberto P., Lozano-Durán, Rosa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893482/
https://www.ncbi.nlm.nih.gov/pubmed/31683645
http://dx.doi.org/10.3390/v11111009
Descripción
Sumario:Plant receptor-like kinases (RLKs) exert an essential function in the transduction of signals from the cell exterior to the cell interior, acting as important regulators of plant development and responses to environmental conditions. A growing body of evidence suggests that RLKs may play relevant roles in plant-virus interactions, although the details and diversity of effects and underlying mechanisms remain elusive. The C4 protein from different geminiviruses has been found to interact with RLKs in the CLAVATA 1 (CLV1) clade. However, whether C4 can interact with RLKs in other subfamilies and, if so, what the biological impact of such interactions might be, is currently unknown. In this work, we explore the interaction landscape of C4 from the geminivirus Tomato yellow leaf curl virus within the Arabidopsis RLK family. Our results show that C4 can interact with RLKs from different subfamilies including, but not restricted to, members of the CLV1 clade. Functional analyses of the interaction of C4 with two well-characterized RLKs, FLAGELLIN SENSING 2 (FLS2) and BRASSINOSTEROID INSENSITIVE 1 (BRI1), indicate that C4 might affect some, but not all, RLK-derived outputs. The results presented here offer novel insight on the interface between RLK signaling and the infection by geminiviruses, and point at C4 as a potential broad manipulator of RLK-mediated signaling.