Pathogenicity factor p22 of tomato chlorosis virus interferes with abscisic acid-mediated antiviral defenses by disrupting the function of WRKY81 in tomato.

Abscisic acid (ABA) is essential for plant resistance to both biotic and abiotic stresses, but its regulation during virus infection and role in antiviral defense remain poorly understood. Here, we report that overexpression of SlWRKY81 led to increased ABA accumulation, whereas silencing SlWRKY81 reduced ABA levels in tomato plants. Further analysis revealed that SlWRKY81 directly binds the promoters of ABA biosynthesis genes SlABA2 and SlABA3, thereby activating their expression. Infection by tomato chlorosis virus (ToCV) inhibited ABA content significantly. Consistently, heterologous expression of ToCV-encoded p22 pathogenicity protein in tomato resulted in an ABA-deficient phenotype. Additionally, exogenous ABA application significantly improved antiviral defense against ToCV, whereas ABA-deficient tomato mutant sitiens exhibited higher susceptibility to ToCV. While it has been demonstrated that ABA modulates virus accumulation via fine-tuning immunity, viral counter-mechanisms remain unclear. We demonstrate that p22 inhibited the nuclear localization of SlWRKY81. Furthermore, p22 entered the nucleus and impaired the DNA binding activity of SlWRKY81, simultaneously accelerating its degradation through the ubiquitin-26S proteasome pathway via an unknown mechanism. 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-mediated antiviral defenses.