Carregant...
Fitxers
Tipus de document
ArticleVersió
Versió publicadaData de publicació
Llicència de publicació
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/227203
Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability
Títol de la revista
Director/Tutor
ISSN de la revista
Títol del volum
Recurs relacionat
Resum
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.
Matèries
Matèries (anglès)
Citació
Citació
SALGUERO-LINARES, Jose, ARMENGOT, Laia, AYET, Joel, RUIZ-SOLANÍ, Neus, SAILE, Svenja c., SALAS-GÓMEZ, Marta, FERNANDEZ, Esperanza, DENOLF, Lode, NAVARRETE, Fernando, KRUMBACH, Jenna, KAISER, Markus, STAEL, Simon, VAN BREUSEGEM, Frank, GEVAERT, Kris, KASCHANI, Farnusch, PETERSEN, Morten, EL KASMI, Farid, VALLS MATHEU, Marc, COLL, Núria s.. Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability. _EMBO Reports_. 2025. Vol. 26, núm. 9, pàgs. 2378-2412. [consulta: 1 de març de 2026]. ISSN: 1469-221X. [Disponible a: https://hdl.handle.net/2445/227203]