Salicylic acid-mediated innate immunity in Arabidopsis is regulated by SIZ1 SUMO

E3 ligase

SIZ1-mediated SUMOylation represses autoimmunity to ensure proper plant development under non-

pathogenic conditions. this work reveals that siz1 mutant plants exhibited constitutive systemic-acquired
resistance characterized by hyperaccumulation of SA, constitutive expression of pathogenesis-related
genes, and increased resistance to bacteria pathogen Pseudomonas syringae pv. Tomato DC3000. Because
pad4 is epistatic tosiz1, SIZ1 negatively controls PAD4-mediated TIR-NBS-LRR-type R gene signaling.
However, SIZ1 is not involved in jasmonic acid signaling or defense against Botrytis cinerea. The loss-of-
function siz1 mutants and the sum1-1 amiR-SUM2 double mutant accumulate higher levels of salicylic acid
(SA) and exhibit increased resistance to the bacterial pathogen Pseudomonas syringae pv. tomato (P.s.t.)
DC3000 compared with the wild type.

The siz1-2 and siz1-3 Arabidopsis loss-of-function mutants exhibit autoimmunity, as characterized by the

hyperaccumulation of SA, constitutive activation of defense-related gene expression, and a dwarf
phenotype.

Since SA plays a role in the positive feedback regulation of SNC1 expression, and siz1-2 accumulates higher

levels of SA than the wild type.

The expression of nahG (a bacterial salicylate hydroxylase) or a mutation

in ARABIDOPSIS PHYTOALEXIN DEFICIENT 4 (PAD4, an important positive regulator of SA signaling)
substantially suppresses autoimmunity in siz1-2. The tpr1 mutation significantly suppressed the dwarf
phenotype of siz1-2. Moreover, the upregulated expression of PR1, PR2, and ICS1. The autoimmunity-
related phenotypes of siz1-2, including dwarfism, upregulated PR1, PR2, and ICS1 expression,
downregulated DND1 and DND2 expression, and higher SA levels were strongly, but not completely,
suppressed in the siz1-2 tpr1 tpl tpr4 quadruple mutant. The siz1 mutant exhibits enhanced resistance
to P.s.t. DC3000 and P.s.t. DC3000 AvrRps4 (recognized by the TIR-NB-LRR type R protein), but not DC3000
AvrRpm1 (recognized by the CC-NB-LRR type R protein).