LURP1, a SARD1-regulated protein, coordinates with the helper NLR ADR1 to promote plant immunity.

In Arabidopsis, loss of transcription factors Calmodulin-Binding Transcription Activators 1/2/3 (CAMTA1/2/3) results in enhanced defense responses with increased salicylic acid (SA) and N-hydroxy-pipecolic acid (NHP) biosynthesis. This is achieved through modulating the expression of master immune transcription factors SAR Deficient 1 (SARD1) and Calmodulin-Binding Protein 60-like g (CBP60g). SARD4 is an NHP biosynthesis enzyme, the camta2/3 sard4 triple mutant remains dwarfed and autoimmune. To identify positive immune regulators of the SA and NHP pathways, a forward genetic screen was performed using the camta2/3 sard4 mutant. Here, we report on a loss-of-function allele of Late Upregulated in Response to Hyaloperonospora parasitica 1 (lurp1) that suppresses the autoimmunity of camta2/3 sard4. LURP1 transcripts are strongly induced by pathogens. Chromatin immunoprecipitation and expression analyses revealed that LURP1 expression is directly controlled by SARD1. LURP1 belongs to a small gene family. Knocking out LURP1 and its three close homologs compromises both flg22- and nlp20-induced resistance and SA accumulation, supporting their redundant roles in promoting plant defense. Interestingly, LURP1 interacts with the helper nucleotide-binding leucine-rich repeat receptor (hNLR) Activated Disease Resistance 1 (ADR1) family, suggestive of a model where LURP1 boosts pattern-triggered immunity and SA-mediated defense signaling through the ADR1s.