Negative regulation of resistance protein-mediated immunity by master transcription factors SARD1 and CBP60g.

Abstract

Salicylic acid (SA) is an essential defence hormone in plants. Upon pathogen infection, induced biosynthesis of SA is mediated by Isochorismate synthase 1 (ICS1), whose gene transcription is controlled mainly through two redundant transcription factors, SAR Deficient 1 (SARD1) and Calmodulin-binding protein 60-like g (CBP60g). Although these master transcription factors regulate not only positive, but also negative regulators of immunity, how they control signaling events downstream of different immune receptors is unclear. Using autoimmune mutants activating immunity mediated by different receptors we show that, although the sard1 cbp60g double mutant almost fully suppresses the activation of defence mediated by suppressor of npr1-1, constitutive 2 (snc2), it strikingly enhances snc1, which carries a gain-of-function mutation in an intracellular nucleotide-binding leucine-rich repeat (NLR) immune receptor. This negative regulation of immunity is achieved through the transcriptional regulation of negative regulators, such as Nudix hydrolase homolog 6 (NUDT6). Our study highlights the diverse roles, especially the negative ones, in the regulation of plant immunity by the two master immune transcription factors SARD1 and CBP60g.