Simultaneous mutations in SMN1 and SUMM2 fully suppress the dwarf and autoimmune phenotypes of Arabidopsis mpk4 mutant

Disruption of the Arabidopsis mitogen-activated protein kinase pathway, MEKK1-MKK1/MKK2-MPK4 (hereafter designated as MEKK1 pathway), leads to the activation of distinct NLRB (nucleotide-binding and leucine-rich repeat receptors), TNL (TIR-type NLR) SMN1, and CNL (CC-type NLR) SUMM2, resulting in dwarf and autoimmune phenotypes. Unlike mekk1 and mkk1mkk2 mutants, the dwarf and autoimmune phenotypes of mpk4 are only partially suppressed by the summ2 mutation, suggesting a significant contribution of SMN1 to the mpk4 phenotypes. However, full suppression of mpk4 by the smn1summ2 double mutation remains to be elucidated. To address this key question, we generated a mpk4smn1summ2 triple mutant and analyzed the dwarf and constitutive cell death phenotypes. The mpk4smn1summ2 triple mutant showed restoration of plant size with no detectable cell death, indicating full suppression of the dwarf and autoimmune phenotypes. These results suggest that SMN1 and SUMM2 constitute a robust surveillance system for the MEKK1 pathway against pathogen infection.

Automated summary

Disruption of the MEKK1 pathway in Arabidopsis leads to dwarf and autoimmune phenotypes, and activates NLRB, TNL SMN1, and CNL SUMM2. The mpk4smn1summ2 triple mutant shows full suppression of the dwarf and autoimmune phenotypes, indicating that SMN1 and SUMM2 constitute a robust surveillance system against pathogen infection.