Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability

Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. During plant development and especially during aging, fine-tuning the homeostasis of these recept...

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Detalles Bibliográficos
Autores: Salguero-Linares, José Manuel, Armengot, Laia, Ayet, Joel, Ruiz-Solani, Nerea, Saile, Svenja C., Salas-Gómez, Marta, Denolf, Lode, Navarrete, Fernando, Krumbach, Jenna, Kaiser, Markus, Stael, Simon, Breusegem, Frank Van, Gevaert, Kris, Kaschani, Farnusch, Petersen, Morten, El Kasmi, Farid, Valls, Marc, Coll, Núria S., Fernandez, Esperanza
Tipo de recurso: conjunto de datos
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/391556
Acceso en línea:http://hdl.handle.net/10261/391556
Access Level:acceso abierto
Palabra clave:Autoimmunity
Proteostasis
Plant immunity
Autophagy
Metacaspases
Condensates
NLRs
autoimmunity
Descripción
Sumario:Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. During plant development and especially during aging, fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Although individual mutations in NLRs, PRRs or other immune-related components that interact with catalytically inactive AtMC1 do not rescue the autoimmune phenotype, overexpression of SNIPER1, a master regulator of NLR homeostasis, fully attenuates the phenotype, inferring that a broad defect in NLR turnover may underlie the severe autoimmunity observed. As opposed to Wt AtMC1 which exhibits a nucleocytoplasmic localization, catalytically inactive AtMC1 localizes to puncta structures that are degraded through autophagy. We infer that the phenotypes observed in plants overexpressing catalytically inactive AtMC1 may represent an additive phenotype to the relatively milder autoimmunity observed in atmc1 mutants. Altogether and considering previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels as plants approach adulthood, thus preventing autoimmunity.

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