Calmodulin-binding transcription activator AtSR1/CAMTA3 fine-tunes plant
immune response by transcriptional regulation of the salicylate receptor
NPR1
Abstract
Calcium signaling regulates salicylic acid (SA)-mediated immune response
through calmodulin-meditated transcriptional activators, AtSRs/CAMTAs,
but its mechanism is not fully understood. Here, we report an
AtSR1/CAMTA3-mediated regulatory mechanism involving the expression of
the SA receptor, NPR1. Transcriptional expression of NPR1 increased in
knockout mutant, atsr1, independently of SA biosynthesis. AtSR1 directly
bound to a CGCG box in the NPR1 promotor. The atsr1 mutant exhibited
resistance to the virulent strain of Pseudomonas syringae pv. tomato
(Pst), however it was susceptible to an avirulent Pst strain carrying
avrRpt2, due to the failure of the induction of hypersensitive
responses. These resistant/susceptible phenotypes in the atsr1 mutant
were reversed in the npr1 mutant background, suggesting that AtSR1
regulates NPR1 as a downstream target during plant immune response. The
virulent Pst strain triggered a transient elevation in intracellular
Ca2+ concentration, whereas the avirulent Pst strain triggered a
prolonged change. The distinct Ca2+ signatures were decoded into the
regulation of NPR1 expression through AtSR1’s IQ motif binding to
calcium-free-CaM2, while AtSR1’s calmodulin-binding domain binding to
calcium-bound-CaM2. These observations reveal a role for AtSR1 as a
Ca2+-mediated transcription regulator for controlling the NPR1-mediated
plant immune response.