Targeting of the Hybrid Bamboo BDDnaJ by Pathogen Effector ApcE12 Regulates the Unfolded Protein Response.

Abstract

The shoot blight disease of Bambusa pervariabilis × Dendrocalamopsis grandis, caused by Arthrinium phaeospermum, threatens bamboo's ecological and economic value. This study explores the pathogenic effector ApcE12's role in modulating plant immunity through interactions with the host proteins BDClp and BDDnaJ. ApcE12 directly interacts with BDDnaJ, a vital regulator of the unfolded protein response (UPR), as validated through yeast two-hybrid, bimolecular fluorescence complementation, and GST pull-down assays. Functional analyses demonstrated that silencing BDDnaJ reduces UPR, activating programmed cell death (PCD) and blocking further pathogen infection to enhance plant resistance. BDDnaJ was found to regulate BDBiP protein stability by interacting with BDBiP, and it is this mechanism by which the pathogenic effector ApcE12 regulates BDDnaJ expression, enhances UPR signalling, and inhibits PCD, thereby promoting infection. These findings deepen our understanding of how fungal effectors manipulate UPR and PCD to overcome plant defences, providing novel insights for developing resistance strategies in bamboo species.