Hua-Yu Ma, Yi-Jie Liu, Xiao-Xue Huan, Shu-Yu Liu, Xiu-Qi Mu, Li-Meng Zhang, Zhi-Long Bao, Yan-Ping Tian, Zhi-Yong Yan, Xiang-Dong Li

Abstract

Tomato brown rugose fruit virus (ToBRFV) overcomes Tm-22-mediated resistance, posing a serious threat to global tomato production. We previously identified that key residues in the movement protein (MP)-H67, N125, K129, A134, I147 and I168 are essential for ToBRFV evasion of Tm-22 resistance. However, the underlying mechanisms remain unclear. In Tm-22-transgenic Nicotiana benthamiana plants at later infection stages, MP mutations H67C, N125A, K129Q and A134N abolished ToBRFV-GFP cell-to-cell and systemic movement, whereas I168N abolished ToBRFV-GFP systemic but not cell-to-cell movement, and I147M partially impaired both. Correspondingly, the MPH67C, MPN125A, MPK129Q and MPA134N mutants elicited strong Tm-22-mediated hypersensitive response (HR), MPI168N elicited mild HR and MPI147M elicited none. Confocal microscopy revealed I147M reduced MP localisation at plasmodesmata in Tm-22-transgenic N. benthamiana leaves. The interaction with Tm-22 was weak for wild-type MP and I147M (slightly enhanced), but moderately or strongly enhanced for I168N and the other four mutants. Wild-type MP and MPI147M failed to induce Tm-22 self-association, MPI168N only weakly induced it, whereas the other four markedly induced it. Collectively, these findings demonstrate that ToBRFV evades Tm-22-mediated resistance by attenuating MP–Tm-22 interaction strength, thereby avoiding Tm-22 self-association and downstream immune activation.

Paper Linkage:https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/mpp.70243