Redox status regulates subcelluar localization of PpTGA1 associated with a BABA-induced priming defence againstRhizopus rot in peach fruit.

Abstract

This study attempted to characterize the involvement of a change in the redox status and subcellular localization in the BABA-induced priming resistance of peach fruit against Rhizopus rot. Specifically, 50mM BABA primed the peaches for the enhanced disease resistance against R. stolonifer, as demonstrated by suppression of the disease development upon pathogen challenge accompanied by the clearly elevated level of TGA transcription factor (PpTGA1) and NPR1 gene (PpNPR1). In addition, the BABA elicitation enhanced the activities of a series of critical enzymes in the PPP and AsA-GSH cycle, and eventually promoted the NADPH and GSH pools, which altered the intracellular redox state towards a highly reductive condition. Additionally, PpTGA1-GFP was localized in the cytoplasm in the absence of BABA treatment or R. stolonifer inoculation, while BABA elicitation plus R. stolonifer inoculation caused PpTGA1-GFP to specifically translocate to the nucleus, where it interacted with PpNPR1 and regulated the positive expression of PR genes. Therefore, the observations implied that BABA could promote the reduction of the redox state, resulting in the translocation of PpTGA1 to the nucleus, which was a prerequisite for the induction of a priming defence against Rhizopus rot in peach.