SlRLK‐like is a malectin‐like domain protein affecting localization and abundance of LeEIX2 receptor resulting in suppression of EIX‐induced immune responses.

The first line of plant defense occurs when a plant pattern recognition receptor (PRR) recognizes microbe‐associated molecular patterns. Plant PRRs are either receptor‐like kinases (RLKs), which have an extracellular domain for ligand binding, a single‐pass transmembrane domain, and an intracellular kinase domain for activating downstream signaling, or receptor‐like proteins (RLPs), which share the same overall structure but lack an intracellular kinase domain. The tomato (Solanum lycopersicum) LeEIX2 is an RLP that binds ethylene‐inducing xylanase (EIX), a fungal elicitor. To identify LeEIX2 receptor interactors, we conducted a yeast two‐hybrid screen and found a tomato protein that we termed SlRLK‐like. The interaction of LeEIX2 with SlRLK‐like was verified using co‐immunoprecipitation and bimolecular fluorescence complementation assays. The defense responses induced by EIX were markedly reduced when SlRLK‐like was overexpressed in Nicotiana benthamiana or Nicotiana tabacum, and knockout of SlRLK‐like using the CRISPR/Cas9 system increased EIX‐induced ethylene production and 1‐aminocyclopropane‐1‐carboxylate synthase (SlACS2) gene expression in tomato. Co‐expression of SlRLK‐like with LeEIX2 led to a reduction in its abundance, apparently through an endoplasmic reticulum‐associated degradation process. Notably, truncation of SlRLK‐like protein revealed that the malectin‐like domain is sufficient and essential for its function. Moreover, SlRLK‐like associated with the RLK FLS2, resulting in its degradation and concomitantly a reduction of the flagellin 22 (flg22)‐induced burst of reactive oxygen species. In addition, SlRLK‐like co‐expression with other RLPs, Ve1 and AtRLP23, also led to a reduction in their abundance. Our findings suggest that SlRLK‐like leads to a decreased stability of various PRRs, leading to a reduction in their abundance and resulting in attenuation of defense responses. [ABSTRACT FROM AUTHOR]