Figure 1.

Model for the action of γb protein in the SA signaling pathway. In uninfected cells with a low level of SA, most NPR1 forms inactive oligomers via intramolecular disulfide bonds, a process promoted by S-nitrosothiol (SNO). Upon infection with BSMV, the h-type thioredoxin (TRX h) triggers monomerization of NPR1 by reducing disulfide bonds. NPR1 monomers then move to the nucleus and induce the expression of pathogen-responsive genes in a SA-dependent manner, thereby enhancing plant defense. The γb proteins of the BSMV interact with TRX h (N. benthamiana TRX h1 in this study) and inactivate its reducing activity, which ultimately compromises SA-mediated immune responses. Adapted from Tada et al. (2008) and Jiang et al. (2022).