A Rho GTPase-activating protein plays a positive role in tobacco resistance against chili veinal mottle virus.

Chili veinal mottle virus (ChiVMV) causes severe yield losses in solanaceous crops across Asia, making the exploration of host resistance imperative. Although GTPase-activating proteins (GAPs) are known to modulate host-pathogen interactions and participate in plant defense against bacterial and fungal pathogens, their role in antiviral immunity remains largely unexplored. Here, we demonstrate that NtRhoGAP1, a RhoGAP protein from Nicotiana tabacum, confers resistance to ChiVMV by potentiating salicylic acid (SA) defense signaling. SA binding protein 3 (SABP3) as a key regulatory hub integrating NtRhoGAP1-mediated immunity into SA signaling. NtRhoGAP1 interacts with NtSABP3 and modulates its expression and subcellular localization. Importantly, NtRhoGAP1 and NtSABP3 exert antagonistic effects on SA signaling during ChiVMV infection, highlighting their opposing roles in modulating plant immunity. Furthermore, we find that ChiVMV nuclear inclusion protease a (NIa-Pro) specifically binds to NtSABP3. NtSABP3 fails to compromise plant immunity against ChiVMV when it cannot interact with NIa-Pro. These findings unveil that NtRhoGAP1 positively regulates plant immunity by engaging the SA signaling pathway, representing a novel arms race between plants and pathogens.