Targeted degradation of NPR3 confers broad-spectrum resistance in wheat.

The plant immune system relies on a precisely balanced interplay between activation and repression to effectively combat pathogens without incurring self-damage. The salicylic acid (SA) signaling pathway, a cornerstone of this system, is currently experiencing a research renaissance. Landmark studies have recently elucidated the complete enzymatic pathways for SA biosynthesis from both chorismate and phenylalanine (Liu et al., 2025; Wang et al., 2025; Zhu et al., 2025), while advances in structural biology have resolved the atomic-level architecture of key signaling components (Kumar et al., 2022). Central to this network is the NPR proteins encoded by the NONEXPRESSER OF PATHOGENESIS-RELATED genes. In this family, NPR1 functions as a master transcriptional co-activator of defense genes. Conversely, its paralogs, NPR3 and NPR4, act as transcriptional co-repressors that attenuate the response, preventing aberrant immune activation and associated resource allocation (Ding et al., 2018). The dynamic turnover of these regulatory proteins is fundamental to immune homeostasis, yet the dedicated mechanisms that govern degradation of the repressors have remained partially elusive.