Valsa canker, caused by Valsa mali (Cytospora mali) or V. pyri, is a destructive fungal disease affecting apple and pear production. NAC transcription factors have been shown to participate in multiple immune signaling pathways. However, the key members of this family involved in Valsa canker resistance remain largely unknown. In this study, we demonstrate that PbeNAC72, an NAC transcription factor responsive to Valsa canker signals in Pyrus betulifolia, positively regulates resistance in apple and pear fruits. In ‘Duli-G03’ (P. betulifolia) suspension cells, overexpression of PbeNAC72 significantly enhanced resistance to Valsa canker and induced reactive oxygen species bursts, as well as the expression of salicylic acid and jasmonic acid-related genes. Subsequent weighted gene co-expression network analysis revealed that PbeNAC72 is primarily linked to genes associated with “DNA replication” and “microtubule-based movement.” We therefore suggest that PbeNAC72 activates genes related to core signaling pathways and fundamental cellular processes, which further contribute to the positive regulation of Valsa canker resistance. Our results provide novel insights into the resistance mechanism and identify a candidate gene for future molecular breeding efforts.

Valsa canker, caused by Valsa pyri (Vp), severely threatens global pear production. The VAMP72 family modulates plant immunity, but its role in Valsa canker resistance remains unclear. In this study, it was found that PbeVAMP724, encoding a membrane-localized SNARE protein, was significantly induced by Vp infection and Abscisic acid (ABA), salicylic acid (SA), and jasmonic acid (JA) in the resistant pear rootstock Pyrus betulaefolia. Transient overexpression of PbeVAMP724 in ‘Huangguan’ fruits reduced Vp-induced lesions, and the lesion diameter was reduced by 23.1% at 48 h and 20.0% at 72 h compared to the empty vector control (pFGC-5941), whereas VIGS silencing compromised the resistance. Stable overexpression in suspension cells ‘Duli-G03’ (P. betulifolia) enhanced tolerance to Vp metabolites (VpM), alleviated cell death, and induced ROS bursts and defense responses. Weighted gene co-expression network analysis (WGCNA) revealed that phloem/xylem histogenesis-related genes (GWHGAAYT028948, GWHGAAYT039435) are co-expressed with PbeVAMP724. In conclusion, we demonstrate that PbeVAMP724 integrates hormone signaling, triggers ROS bursts, and activates defense responses to positively regulate resistance to Valsa canker in pear, representing a promising candidate for breeding Valsa canker-resistant pear varieties.

Valsa canker, a destructive necrotrophic disease caused by Valsa species (V. mali and V. pyri), threatens global apple and pear production. Resistance breeding has gained much attention because of its environmental friendliness and effectiveness, making it extremely critical to obtain key disease resistance genes. In this study, we identified that the expression of PbeSTOP2, a C2H2-type transcription factor in ‘Duli-G03’ (Pyrus betulifolia, rootstock of pear), was induced in response to signals from Vp and Vp metabolites (VpM). Transient expression in fruits and stable overexpression in suspension cells demonstrated that PbeSTOP2 enhances resistance to Vp. In overexpressing cells, genes associated with jasmonic acid (JA) and pattern-triggered immunity (PTI) signaling were upregulated, and endogenous JA and auxin (IAA) levels increased. These results revealed that JA signaling was involved in the enhanced Valsa canker resistance conferred by PbeSTOP2 overexpression. This finding on host disease resistance should facilitate the breeding efforts for Valsa canker resistance.