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