Abstract
The Xanthomonas campestris pv vesicatoria (Xcv) effector AvrBsT induces a hypersensitive cell death in pepper (Capsicum annuum). However, the molecular mechanisms underlying AvrBsT-triggered cell death are not fully understood. Here, we identified pepper arginine decarboxylase (CaADC1) as an AvrBsT-interacting protein, which is early and strongly induced in incompatible pepper-Xcv interactions. Bimolecular fluorescence complementation and coimmunoprecipitation assays showed that the CaADC1-AvrBsT complex was localized to the cytoplasm. Transient coexpression of CaADC1 with avrBsT in Nicotiana benthamiana leaves specifically enhanced AvrBsT-triggered cell death, accompanied by an accumulation of polyamines, nitric oxide (NO), and hydrogen peroxide (H₂O₂) bursts. Among the polyamines, spermine application strongly induced NO and H₂O₂ bursts, ultimately leading to cell death. CaADC1 silencing in pepper leaves significantly compromised NO and H₂O₂ accumulation and cell death induction, leading to the enhanced avirulent Xcv growth during infection. The levels of salicylic acid, polyamines, and γ-aminobutyric acid (GABA), and the expression of defense response genes during avirulent Xcv infection, were distinctly lower in CaADC1-silenced plants than those in the empty vector control plants. GABA application significantly inhibited avirulent Xcv growth in CaADC1-silenced leaves and the empty vector control plants. Together, these results suggest that CaADC1 may act as a key defense and cell death regulator via mediation of polyamine and GABA metabolism.