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.
ASJC Scopus subject areas
- Plant Science