{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Salguero-Linares J"],"funding":["Ministerio de Ciencia, Innovación y Universidades (MCIU)","Deutsche Forschungsgemeinschaft (DFG)","Reinhard-Frank Stiftung","Ministerio de Ciencia e Innovación (MCIN)","Centres de Recerca de Catalunya (CERCA)","EC | H2020 | PRIORITY 'Excellent science' | H2020 Marie Skłodowska-Curie Actions (MSCA)"],"pagination":["2378-2412"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12069761"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(9)"],"pubmed_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 N"],"journal":["EMBO reports"],"pubmed_title":["Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability."],"pmcid":["PMC12069761"],"funding_grant_id":["CEX2019-000902-S","GA#945043","PID2022-136922NB-I00,PID2019-108595RB-I00,TED2021-131457B-I00","945043","BES-2017-080210","MCIN/AEI/10.13039/501100011033","rePLANT-GA101081581","No grant number","FJC2021-046667","GA#101068121","FPU19/03778","CRC1101 D09","PREP2022-000557","helperless plant"],"pubmed_authors":["Petersen M","Denolf L","Krumbach J","Kaschani F","Stael S","Fernandez E","Salas-Gomez M","Navarrete F","Salguero-Linares J","Ayet J","Gevaert K","Van Breusegem F","Saile SC","El Kasmi F","Valls M","Coll NS","Armengot L","Ruiz-Solani N","Kaiser M"],"additional_accession":[]},"is_claimable":false,"name":"Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability.","description":"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 N","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-01T22:25:13.388Z","creation":"2026-05-22T03:08:23.307Z"},"accession":"S-EPMC12069761","cross_references":{"pubmed":["40113992"],"doi":["10.1038/s44319-025-00426-4"]}}