Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability
- Author
- Jose Salguero-Linares, Laia Armengot, Joel Ayet, Nerea Ruiz-Solaní, Svenja C Saile, Marta Salas-Gómez, Esperanza Fernandez, Lode Denolf (UGent) , Fernando Navarrete, Jenna Krumbach, Markus Kaiser, Simon Stael (UGent) , Frank Van Breusegem (UGent) , Kris Gevaert (UGent) , Farnusch Kaschani, Morten Petersen, Farid El Kasmi, Marc Valls and Núria S Coll
- Organization
- 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.
- Keywords
- Autoimmunity, Autophagy, Condensates, Metacaspases, Proteostasis, PROGRAMMED CELL-DEATH, STRESS GRANULES, PLANT AUTOIMMUNITY, IMMUNE RECEPTORS, PROTEIN, METACASPASES, RECOGNITION, AUTOPHAGY, FAMILY, LEADS
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-01JQRB5R1Q70FPF0MM65NT4N1B
- MLA
- Salguero-Linares, Jose, et al. “Lack of AtMC1 Catalytic Activity Triggers Autoimmunity Dependent on NLR Stability.” EMBO REPORTS, vol. 26, no. 9, 2025, pp. 2378–412, doi:10.1038/s44319-025-00426-4.
- APA
- Salguero-Linares, J., Armengot, L., Ayet, J., Ruiz-Solaní, N., Saile, S. C., Salas-Gómez, M., … Coll, N. S. (2025). Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability. EMBO REPORTS, 26(9), 2378–2412. https://doi.org/10.1038/s44319-025-00426-4
- Chicago author-date
- Salguero-Linares, Jose, Laia Armengot, Joel Ayet, Nerea Ruiz-Solaní, Svenja C Saile, Marta Salas-Gómez, Esperanza Fernandez, et al. 2025. “Lack of AtMC1 Catalytic Activity Triggers Autoimmunity Dependent on NLR Stability.” EMBO REPORTS 26 (9): 2378–2412. https://doi.org/10.1038/s44319-025-00426-4.
- Chicago author-date (all authors)
- Salguero-Linares, Jose, Laia Armengot, Joel Ayet, Nerea Ruiz-Solaní, Svenja C Saile, Marta Salas-Gómez, Esperanza Fernandez, Lode Denolf, Fernando Navarrete, Jenna Krumbach, Markus Kaiser, Simon Stael, Frank Van Breusegem, Kris Gevaert, Farnusch Kaschani, Morten Petersen, Farid El Kasmi, Marc Valls, and Núria S Coll. 2025. “Lack of AtMC1 Catalytic Activity Triggers Autoimmunity Dependent on NLR Stability.” EMBO REPORTS 26 (9): 2378–2412. doi:10.1038/s44319-025-00426-4.
- Vancouver
- 1.Salguero-Linares J, Armengot L, Ayet J, Ruiz-Solaní N, Saile SC, Salas-Gómez M, et al. Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability. EMBO REPORTS. 2025;26(9):2378–412.
- IEEE
- [1]J. Salguero-Linares et al., “Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability,” EMBO REPORTS, vol. 26, no. 9, pp. 2378–2412, 2025.
@article{01JQRB5R1Q70FPF0MM65NT4N1B,
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.}},
author = {{Salguero-Linares, Jose and Armengot, Laia and Ayet, Joel and Ruiz-Solaní, Nerea and Saile, Svenja C and Salas-Gómez, Marta and Fernandez, Esperanza and Denolf, Lode and Navarrete, Fernando and Krumbach, Jenna and Kaiser, Markus and Stael, Simon and Van Breusegem, Frank and Gevaert, Kris and Kaschani, Farnusch and Petersen, Morten and El Kasmi, Farid and Valls, Marc and Coll, Núria S}},
issn = {{1469-221X}},
journal = {{EMBO REPORTS}},
keywords = {{Autoimmunity,Autophagy,Condensates,Metacaspases,Proteostasis,PROGRAMMED CELL-DEATH,STRESS GRANULES,PLANT AUTOIMMUNITY,IMMUNE RECEPTORS,PROTEIN,METACASPASES,RECOGNITION,AUTOPHAGY,FAMILY,LEADS}},
language = {{eng}},
number = {{9}},
pages = {{2378--2412}},
title = {{Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability}},
url = {{http://doi.org/10.1038/s44319-025-00426-4}},
volume = {{26}},
year = {{2025}},
}
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