Characterization of NPR1 suppressors and their role in plant immunity.

摘要

Plants have evolved inducible immune responses to pathogen infection. Pathogen-induced, isochorismate synthase-dependent salicylic acid (SA) biosynthesis promotes immunity to biotrophic pathogens, which keep the host alive as a long-term food source, partially through NPR1 (non-expresser of pathogenesis-related (1) activation. NPR1 also prevents harmful SA hyperaccumulation and SA cytotoxicity through an unknown mechanism. In this study, mutation of three genes was found to restore SA tolerance to npr1. Overexpression of one of these genes, the transcription factor ANAC1, was associated with increased pathogen resistance, but this gene was not essential for immunity. The other two genes, ELP2 (Elongator subunit (2) and ELP3 (Elongator subunit 3), encode subunits of the histone acetyltransferase Elongator, which is conserved in eukaryotes and functions in RNA polymerase II-dependent transcription, as well as in tRNA modification, exocytosis, and tubulin modification. Mutation of human ELP1 (Elongator subunit 1), causes the neural disorder familial dysautonomia. This study shows Elongator functions both upstream and downstream of SA to positively regulate biotrophic pathogen resistance, and does so in an NPR1-independent manner. Plants lacking ELP2 were susceptible to avirulent pathogen infection, possibly due to the delayed induction of defense genes including ICS1. Plants lacking both ELP2 and NPR1 were highly susceptible to avirulent pathogen infection compared to the single mutants, suggesting ELP2 and NPR1 act synergistically in plant immunity. However, pre-activation of defense genes during systemic acquired resistance (SAR) restored pathogen resistance to elp2 plants. In light of these results, a model is proposed where Elongator promotes immunity through the acceleration of defense gene activation.