The tyrosine‐sulfated peptide receptors PSKR1 and PSY1R modify the immunity of Arabidopsis to biotrophic and necrotrophic pathogens in an antagonistic manner

Abstract

SUMMARYThe tyrosine-sulfated peptides PSKa and PSY1 bind to specific leucine-rich repeat surface receptor kinases and control cell proliferation in plants. In a reverse genetic screen, we identified the phytosulfokine (PSK) receptor PSKR1 as an important component of plant defense. Multiple independent loss-of-function mutants in PSKR1 are more resistant to biotrophic bacteria, show enhanced pathogen-associated molecular pattern responses and less lesion formation after infection with the bacterial pathogen Pseudomonas syringae pv. tomato DC3000. By contrast, pskr1 mutants are more susceptible to necrotrophic fungal infection with Alternaria brassicicola, show more lesion formation and fungal growth which is not observed on wildtype plants. The antagonistic effect on biotrophic and necrotrophic pathogen resistance is reflected by enhanced salicylate and reduced jasmonate responses in the mutants, suggesting that PSKR1 suppresses salicylate-dependent defense responses. Detailed analysis of single and multiple mutations in the three paralogous genes PSKR1, -2 and PSY1-receptor (PSY1R) determined that PSKR1 and PSY1R, but not PSKR2, have a partially redundant effect on plant immunity. In animals and plants, peptide sulfation is catalyzed by a tyrosylprotein sulfotransferase (TPST). Mutants lacking TPST show increased resistance to bacterial infection and increased susceptibility to fungal infection, mimicking the triple receptor mutant phenotypes. Feeding experiments with PSKa in tpst-1 mutants partially restore the defense-related phenotypes, indicating that perception of the PSKa peptide has a direct effect on plant defense. These results suggest that the PSKR subfamily integrates growth-promoting and defense signals mediated by sulfated peptides and modulates cellular plasticity to allow flexible adjustment to environmental changes.

Phytosulfokine Regulates Growth in Arabidopsis through a Response Module at the Plasma Membrane That Includes CYCLIC NUCLEOTIDE-GATED CHANNEL17, H+-ATPase, and BAK1

“…CNGCs may thus be general targets of LRR-RLKs that possess GC activity. Recent studies showed that PSK not only regulates growth but also modulates immune responses through PSKR1 (Igarashi et al, 2012;Mosher et al, 2013). It is tempting to speculate that CNGC17 may not only play a role in growth regulation but also in immunity.…”

The Arabidopsis Leucine-Rich Repeat Receptor Kinase BIR3 Negatively Regulates BAK1 Receptor Complex Formation and Stabilizes BAK1

“…by Mosher et al (2012). Alternaria brassicicola infection assays were carried out as 521 described by Kemmerling et al (2007).…”

“…Transcript levels were analyzed by standard or quantitative RT-PCR (qRT-PCR) 543 using SYBR-green as a dye as described by Mosher et al (2012) with primers listed 544 in Supplemental Table 2. 545 546…”

Receptor Kinases in Plant-Pathogen Interactions: More Than Pattern Recognition

“…Similar to fer mutants, Arabidopsis mutants lacking PSKR1 or TYROSINE PROTEIN SULFOTRANSFERASE (TPSP), the latter of which is required for sulfation of PSKs, exhibit enhanced defense gene expression in response to elf18 and flg22 and increased disease resistance to P. syringae, indicating a negative role of PSKR1 in pattern-triggered immunity (Igarashi et al, 2012). Similarly, PSKR1 and PSY1R play an additive role in the negative regulation of disease resistance to the fungal pathogen Alternaria brassicicola in addition to P. syringae (Mosher et al, 2013). The pskr1 pskr2 psy1r triple mutant is strongly enhanced in flg22-induced defense gene expression.…”