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Biochemical assays further confirmed that <jats:italic>ZAT18<\/jats:italic> is a direct target of MYC2, which is a very important regulator in JA signaling. CRISPR\/Cas9\u2010generated <jats:italic>zat18\u2010cr<\/jats:italic> mutants exhibited enhanced resistance to <jats:italic>Pst<\/jats:italic> DC3000, while overexpression of <jats:italic>ZAT18<\/jats:italic> resulted in impaired disease resistance.<\/jats:p><\/jats:list-item>\n\n<jats:list-item><jats:p>Genetic characterization of <jats:italic>ZAT18<\/jats:italic> 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 <jats:italic>Enhanced Disease Susceptibility 1<\/jats:italic> (<jats:italic>EDS1<\/jats:italic>), which is the key signaling component of pathogen\u2010induced SA accumulation. Overexpression of <jats:italic>ZAT18<\/jats:italic> resulted in decreased SA content, while loss of function of <jats:italic>ZAT18<\/jats:italic> showed enhanced SA accumulation upon pathogen infection. Furthermore, enhanced resistance and SA content in <jats:italic>zat18\u2010cr<\/jats:italic> mutants was abolished by the mutation in <jats:italic>EDS1<\/jats:italic>.<\/jats:p><\/jats:list-item>\n\n<jats:list-item><jats:p>Our data indicate that pathogens induce <jats:italic>ZAT18<\/jats:italic> expression to repress the transcription of <jats:italic>EDS1<\/jats:italic>, further antagonising SA accumulation for bacterial infection.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p>","DOI":"10.1111\/nph.17870","type":"journal-article","created":{"date-parts":[[2021,11,19]],"date-time":"2021-11-19T15:30:18Z","timestamp":1637335818000},"page":"1274-1288","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["<i>Pseudomonas syringae<\/i> activates <i>ZAT18<\/i> to inhibit salicylic acid accumulation by repressing <i>EDS1<\/i> transcription for bacterial 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