Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability
Salguero Linares, Jose (Centre de Recerca en Agrigenòmica)
Armengot, Laia (Centre de Recerca en Agrigenòmica)
Ayet, Joel (Centre de Recerca en Agrigenòmica)
Ruiz Solaní, Nerea (Centre de Recerca en Agrigenòmica)
Saile, Svenja (Center for Plant Molecular Biology)
Salas Gómez, Marta (Centre de Recerca en Agrigenòmica)
Fernandez, Esperanza (VIB UGent Centrum voor Medische Biotechnologie)
Denolf, Lode (VIB UGent Centrum voor Medische Biotechnologie)
Navarrete, Fernando (Centre de Recerca en Agrigenòmica)
Krumbach, Jenna (Centre de Recerca en Agrigenòmica)
Kaiser, Markus (University of Duisburg-Essen. Center of Medical Biotechnology)
Stael, Simon (Ghent University. Department of Plant Biotechnology and Bioinformatics)
Van Breusegem, Frank (Center for Plant Systems Biology)
Gevaert, Kris (Ghent University. Department of Biomolecular Medicine)
Kaschani, Farnusch (University of Duisburg-Essen. Center of Medical Biotechnology)
Petersen, Morten (Copenhagen University. Department of Biology)
El Kasmi, Farid (Center for Plant Molecular Biology)
Valls, Marc (Centre de Recerca en Agrigenòmica)
Sánchez Coll, Núria (Centre de Recerca en Agrigenòmica)

Date:	2025
Abstract:	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. 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 a catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Overexpression of the E3 ligase SNIPER1, a master regulator of NLR homeostasis, fully reverts the AtMC1-dependent autoimmunity phenotype, inferring that a broad defect in NLR turnover may underlie the severe phenotype observed. Catalytically inactive AtMC1 localizes to punctate structures that are degraded through autophagy. Considering also previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels, thereby preventing autoimmunity.
Grants:	Agencia Estatal de Investigación PID2022-136922NB-I00 Agencia Estatal de Investigación PID2019-108595RB-I00 Agencia Estatal de Investigación TED2021-131457B-I00 Agencia Estatal de Investigación BES-2017-080210 Agencia Estatal de Investigación PREP2022-000557 Agencia Estatal de Investigación FJC2021-046667-I European Commission 945043 European Commission 101081581 European Commission 101068121 Agencia Estatal de Investigación CEX2019-000902-S
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; recerca ; Versió publicada
Subject:	Autoimmunity ; Autophagy ; Condensates ; Metacaspases ; Proteostasis
Published in:	EMBO reports, Vol. 26, Issue 9 (March 2025) , p. 2378-2412, ISSN 1469-3178

DOI: 10.1038/s44319-025-00426-4
PMID: 40113992

35 p, 16.4 MB

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Research literature > UAB research groups literature > Research Centres and Groups (research output) > Experimental sciences > CRAG (Centre for Research in Agricultural Genomics)
Articles > Research articles
Articles > Published articles