Dissection of Cell Death Induction by Arabidopsis thaliana CC-NBS-LRR Receptor SUT1 and Its Interacting Protein TOPP4 Mutant in Nicotiana benthamiana

TL;DR

This paper explores how a plant receptor and its interacting protein trigger cell death in a model plant species.

Contribution

The study reveals the role of specific amino acid sites in the localization and function of SUT1 in plant cell death.

Findings

Co-expression of SUT1 with TOPP4 mutant versions causes cell death in Nicotiana benthamiana.

Gly2, Cys4, and Ser6 are crucial for SUT1's plasma membrane localization and function.

Mutations in conserved residues affect SUT1's function and localization.

Abstract

Nucleotide-binding and leucine-rich repeat receptors (NLRs) play an important role in plant innate immunity. Previous reports indicate that SUT1 (SUPPRESSOR OF TOPP4 1) is required for the autoimmune response mediated by TYPE ONE PROTEIN PHOSPHATASE 4 (TOPP4) mutation topp4-1 (namely TOPP4T246M) in Arabidopsis. We observed that co-expression of SUT1 with TOPP4 mutant versions, instead of wild-type TOPP4, produced robust cell death in N. benthamiana. The YFP-labeled SUT1 was localized on the plasma membrane (PM), and Gly2, Cys4, and Ser6 are crucial amino acid sites for its PM localization and function. Further dissection proclaimed that the function and localization of SUT1 are influenced by mutations in conserved specific residues. These findings may provide a new perspective for elucidating the activation mechanism of SUT1.

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