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

Momoko Takagi; Suzuna Nagai; Hironori Kaminaka; Kazuya Akimitsu; Ken Shirasu; Kazuya Ichimura

doi:10.1080/15592324.2022.2046412

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

Plant Signal Behav. 2022 Dec 31;17(1):2046412. doi: 10.1080/15592324.2022.2046412.

Authors

Momoko Takagi^{1

2}, Suzuna Nagai¹, Hironori Kaminaka², Kazuya Akimitsu¹, Ken Shirasu³, Kazuya Ichimura¹

Affiliations

¹ Faculty of Agriculture, Kagawa University, Kagawa, Japan.
² Faculty of Agriculture, Tottori University, Tottori, Japan.
³ Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science, Yokohama, Japan.

Abstract

Disruption of the Arabidopsis mitogen-activated protein kinase pathway, MEKK1-MKK1/MKK2-MPK4 (hereafter designated as MEKK1 pathway), leads to the activation of distinct NLRs (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.

Keywords: Arabidopsis thaliana; MAP kinase pathway; autoimmunity; cell death; dwarfism; mutant; nucleotide-binding and leucine-rich repeat receptor.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Arabidopsis Proteins* / genetics
Arabidopsis Proteins* / metabolism
Arabidopsis* / metabolism
Mitogen-Activated Protein Kinases / metabolism
Mutation / genetics
Phenotype

Substances

Arabidopsis Proteins
Mitogen-Activated Protein Kinases

Grants and funding

This work was supported by the JSPS KAKENHI grants to K.I. (No.s 19770045, 22780037, 25450060, and 19K06054), Next Generation Leading Research Fund for 2017 and 2018 of Kagawa University Research Promotion Program (KURPP) granted to K.I., and the Sasakawa Scientific Research Grant from The Japan Science Society to M.T.