Authors
Wang, J., Ni, Z., Chen, X., Zhang, Y., Qin, H., Wang, H., He, Y., Tang, J., Huang, S.
Abstract
Summary Bacterial leaf streak (BLS), caused by Xanthomonas oryzae pv. oryzicola (Xoc), is a major bacterial disease that poses a substantial threat to rice production. Although Xoc deploys a variety of non-transcription activator-like (non-TAL) effectors to subvert host defenses, the mechanistic basis of how these effectors modulate plant immune signaling remains largely unclear. Through yeast two-hybrid screening, we identified the rice scaffold protein OsRACK1B as a host target of Xoc effector XopN, and its potential role during Xoc infection was characterized by combining gene function with biochemical analyses. We demonstrate that XopN suppresses rice immune responses and physically interacts with the rice scaffold protein OsRACK1B. Notably, OsRACK1B expression is induced following Xoc infection in a type III secretion system (T3SS)-independent manner. Functional analyses indicate that OsRACK1B overexpression enhances Xoc resistance, whereas loss-of-function mutants exhibit heightened susceptibility. This increased susceptibility is characterized by compromised immunity, including reduced callose deposition, diminished reactive oxygen species (ROS) accumulation, and attenuated expression of defense-related genes such as OsPBZ1 and OsPAL1. Furthermore, XopN competes with OsRap2.6 for binding to OsRACK1B, thereby disrupting the formation of the OsRACK1B-OsRap2.6 immune complex. Our findings reveal a novel virulence strategy employed by Xoc, in which XopN targets and disrupts OsRACK1B-mediated immune signaling, thereby compromising host defense.
Preprint server:
bioRxiv
The authors list and abstract were imported from bioRxiv on 05 Nov 2025.
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