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Here, we report that overexpression of SlWRKY81 led to increased ABA accumulation, whereas silencing <jats:italic>SlWRKY81<\/jats:italic> reduced ABA levels in tomato plants. Further analysis revealed that SlWRKY81 directly binds the promoters of ABA biosynthesis genes <jats:italic>SlABA2<\/jats:italic> and <jats:italic>SlABA3<\/jats:italic>, thereby activating their expression.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Infection by tomato chlorosis virus (ToCV) inhibited ABA content significantly. Consistently, heterologous expression of ToCV\u2010encoded p22 pathogenicity protein in tomato resulted in an ABA\u2010deficient phenotype. Additionally, exogenous ABA application significantly improved antiviral defense against ToCV, whereas ABA\u2010deficient tomato mutant <jats:italic>sitiens<\/jats:italic> exhibited higher susceptibility to ToCV.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>While it has been demonstrated that ABA modulates virus accumulation via fine\u2010tuning immunity, viral counter\u2010mechanisms remain unclear. We demonstrate that p22 inhibited the\u00a0nuclear localization of SlWRKY81. Furthermore, p22 entered the nucleus and impaired\u00a0the DNA binding activity of SlWRKY81, simultaneously accelerating its degradation through the ubiquitin\u201026S proteasome pathway via an unknown mechanism.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Our findings uncover the positive role of SlWRKY81 in regulating ABA biosynthesis in tomato and reveal mechanisms by which a viral pathogenicity factor interferes with ABA\u2010mediated antiviral defenses.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p>","DOI":"10.1111\/nph.70267","type":"journal-article","created":{"date-parts":[[2025,6,23]],"date-time":"2025-06-23T02:23:25Z","timestamp":1750645405000},"page":"1837-1854","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Pathogenicity factor p22 of tomato chlorosis virus interferes with abscisic acid\u2010mediated antiviral defenses by disrupting the function of <scp>WRKY81<\/scp> in 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