AcNAC10, regulated by AcTGA07, enhances kiwifruit resistance to Pseudomonas syringae pv. actinidiae via inhibiting jasmonic acid pathway
Zhao, C (Zhao, Chao) [1] ; Liu, W (Liu, Wei) [1] ; Yao, CX (Yao, Chenxiao) [1] ; Zhang, YL (Zhang, Yali) [1] ; Du, XF (Du, Xiaofei) [1] ; Ma, C (Ma, Chao) [1] ; Li, R (Li, Rui) [1] ; Wang, H (Wang, Hua) [1] ; Huang, LL (Huang, Lili)
MOLECULAR HORTICULTURE
DOI：10.1186/s43897-024-00143-x
Abstract
Kiwifruit bacterial canker is a devastating disease caused by Pseudomonas syringae pv. actinidiae (Psa). NAC transcription factors play a significant role in host immunity. However, the potential molecular mechanism of resistance to semi-biotrophic Psa mediated by NAC transcription factors in kiwifruit remains unclear. In this study, we identified a typical NAC transcription factor, AcNAC10, which is involved in the jasmonic acid (JA) pathway and is highly expressed in resistant variety RH12 responsing to Psa. By overexpression and silencing of AcNAC10 in kiwifruit, it plays a positive role in enhancing kiwifruit resistance. Likewise, heterologous expression of AcNAC10 in transgenic Arabidopsis and tomato enhanced resistance to P. syringae. By directly binding to the promoter of AcLOX3, AcNAC10 inhibited its expression as a transcriptional suppressor. Using a yeast one-hybrid screening library, electrophoretic mobility shift assay (EMSA), and dual-luciferase reporter assays, it showed that AcTGA07 can activate the expression of AcNAC10. Moreover, we demonstrated that AcTGA07 decreased JA accumulation independently of the AcNAC10-AcLOX3 pathway. Our study elucidated the transcriptional cascade regulatory network of AcTGA07-AcNAC10-AcLOX3, which enhanced the disease resistance of kiwifruit to Psa by inhibiting JA synthesis.