Stael, Simon
- Department of Molecular Sciences, Swedish University of Agricultural Sciences
- Flanders Institute for Biotechnology (VIB)
- Ghent University
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
Published in
EMBO Reports
2025, volume: 26, number: 9, pages: 2378 - 2412
Publisher: SPRINGERNATURE
SLU Authors
UKÄ Subject classification
Biochemistry
Molecular Biology
Publication identifier
- DOI: https://doi.org/10.1038/s44319-025-00426-4
Permanent link to this page (URI)
https://res.slu.se/id/publ/141733