Rpi-blb2-mediated late blight resistance in Nicotiana benthamiana requires SGT1 and salicylic acid-mediated signaling but not RAR1 or HSP90

• AVRblb2 is a modulator that triggers an Rpi-blb2-dependent HR in N. benthamiana.
• Rpi-blb2-mediated HR to P. infestans AVRblb2 requires SGT1 but not RAR1 or HSP90.
• Rpi-blb2-mediated resistance to late blight also requires SGT1-mediated signaling.
• SA is required for Rpi-blb2-mediated resistance to P. infestans but not for HR.
• The Rpi-blb2-mediated HR to Avrblb2 is associated with H2O2 accumulation.

The Rpi-blb2 recognizes the presence of the Phytophthora infestans AVRblb2 and initiates effector-triggered immunity (ETI). We performed gain-of-function and loss-of-function studies in Nicotiana benthamiana to elucidate Rpi-blb2-mediated resistance to P. infestans. Rpi-blb2 triggered a hypersensitive response through SGT1-mediated, but not RAR-mediated or HSP90-mediated, pathways. NbSGT1 was also required for basal and ETI-mediated by Rpi-blb2 in N. benthamiana. Moreover, salicylic acid (SA) affected basal defense and Rpi-blb2-mediated resistance against P. infestans. The increased susceptibility of Rpi-blb2-transgenic plants in the NahG-background correlated with reduced levels of SA. These findings provide evidence for the roles of SGT1- and SA-signaling in Rpi-blb2-mediated resistance against P. infestans.