Effector Fg34 triggers TaHRC-R-mediated calcium signaling to bolster Fusarium head blight resistance in wheat.

Fusarium head blight, one of the most devastating diseases affecting wheat, is primarily caused by Fusarium graminearum. The TaHRC gene (also designated Fhb1), encoding a histidine-rich calcium-binding protein, exists as 2 allelic variants, TaHRC-R (resistant) and TaHRC-S (susceptible), which are widely present in wheat cultivars. However, the role of TaHRC in Fusarium head blight resistance remains controversial. Here, we demonstrated that TaHRC physically interacts with Fg34, a secreted effector protein of F. graminearum. This interaction induced a translocation of TaHRC-R from the nucleus to the cytoplasmic membrane, thereby enhancing Fusarium head blight resistance. In contrast, TaHRC-S retained nuclear localization and conferred susceptibility. We demonstrate that TaHRC physically interacts with Fg34, a secreted effector protein of F. graminearum. This interaction triggers the translocation of TaHRC-R from the nucleus to the plasma membrane, thereby enhancing resistance to Fusarium head blight. In contrast, TaHRC-S remains localized in the nucleus and confers susceptibility. Notably, this is the first report of a direct physical interaction between TaHRC and a Fusarium-derived effector. The TaHRC-R/Fg34 complex elevates intracellular Ca2+ levels, activating calcium signaling pathways that reinforce Fusarium head blight resistance. Furthermore, Fg34 also binds to TaCBL4, forming a ternary complex with TaCIPK5 that enhances TaCIPK5 kinase activity, leading to increased phosphorylation of TaRBOHB. Collectively, these findings elucidate a novel calcium-signal-dependent mechanism potentially mediated by TaHRC underlying Fusarium head blight resistance in wheat. These discoveries deepen the understanding of the molecular mechanisms of Fusarium head blight resistance and provide a theoretical foundation for developing breeding strategies for durable disease resistance.