The Fusarium sacchari Effector FsP4H1 Targets the Transcription Factor DPb to Disrupt Catalase‐Mediated H ₂ O ₂ Homeostasis and Suppress Host Immunity

Pokkah boeng disease has been reported in nearly all countries where sugarcane is commercially cultivated. Historically, this disease was regarded as a minor concern; however, due to the impacts of climate change, it has now escalated into a significant issue. The causative agents of this disease are fungi, specifically belonging to the Fusarium fungal complex, with Fusarium sacchari being the predominant species in Guangxi Zhuang Autonomous Region, China. However, the pathogenic mechanism remains largely unknown. In this study, we have identified and characterized an effector protein designated as FsP4H1, which contains a prolyl‐4‐hydroxylase domain and is crucial for the virulence of F. sacchari . FsP4H1 localizes to the host cytoplasm and nucleus, and its nuclear localization is required for the immune suppression in the host. We demonstrate that FsP4H1 interacts with the transcription factor DPb, a positive regulator of plant immunity, and facilitates degradation of DPb via the 26S proteasome. This degradation leads to downregulation of catalase genes, ScCAT9 , ScCAT34 or NbCAT , which are direct transcriptional targets of DPb and play a crucial role in maintaining hydrogen peroxide (H 2 O 2 ) homeostasis. Consequently, in the interaction between F. sacchari and sugarcane, F. sacchari secretes FsP4H1 into the hosts' nuclei, resulting in the disruption of the DPb–CAT module to enhance host susceptibility. Our study reveals a novel virulence strategy in which a fungal effector hijacks a conserved plant transcriptional network to suppress antioxidant defences, providing potential targets for resistance breeding in sugarcane.