Pseudomonas syringae activates ZAT18 to inhibit salicylic acid accumulation by repressing EDS1 transcription for bacterial infection.

Abstract

Phytopathogens can manipulate plant hormone signaling to counteract immune responses; however, the underlying mechanism is mostly unclear. Here, we report that Pseudomonas syringae pv tomato (Pst) DC3000 induces expression of C2H2 zinc finger transcription factor ZAT18 in a jasmonic acid (JA)-signaling-dependent manner. Biochemical assays further confirmed that ZAT18 is a direct target of MYC2, which is a very important regulator in JA signaling. CRISPR/Cas9-generated zat18-cr mutants exhibited enhanced resistance to Pst DC3000, while overexpression of ZAT18 resulted in impaired disease resistance. Genetic characterization of ZAT18 mutants demonstrated that ZAT18 represses defense responses by inhibiting the accumulation of the key plant immune signaling molecule salicylic acid (SA), which is dependent on its EAR motif. ZAT18 exerted this inhibitory effect by directly repressing the transcription of Enhanced Disease Susceptibility 1 (EDS1), which is the key signaling component of pathogen-induced SA accumulation. Overexpression of ZAT18 resulted in decreased SA content, while loss of function of ZAT18 showed enhanced SA accumulation upon pathogen infection. Furthermore, enhanced resistance and SA content in zat18-cr mutants was abolished by the mutation in EDS1. Our data indicate that pathogens induce ZAT18 expression to repress the transcription of EDS1, further antagonising SA accumulation for bacterial infection.