A recessive mutation in the Arabidopsis SSI2 gene confers SA‐ and NPR1‐independent expression of PR genes and resistance against bacterial and oomycete pathogens

Abstract

SummaryThe Arabidopsis thaliana NPR1 gene is required for salicylic acid (SA)-induced expression of pathogenesis-related (PR) genes and systemic acquired resistance. However, loss-of-function mutations in NPR1 do not confer complete loss of PR gene expression or disease resistance. Thus these responses also can be activated via an NPR1-independent pathway that currently remain to be elucidated. The ssi2-1 mutant, identi®ed in a genetic screen for suppressors of npr1-5, affects signaling through the NPR1-independent defense pathway(s). In comparison with the wild-type (SSI2 NPR1) plants and the npr1-5 mutant (SSI2 npr1-5), the ssi2-1 npr1-5 double mutant and the ssi2-1 NPR1 single mutant constitutively express PR genes [PR-1, BGL2 (PR-2) and PR-5]; accumulate elevated levels of SA; spontaneously develop lesions; and possess enhanced resistance to a virulent strain of Peronospora parasitica. The ssi2-1 mutation also confers enhanced resistance to Pseudomonas syringae pv. tomato (Pst); however, this is accomplished primarily via an NPR1-dependent pathway. Analysis of ssi2-1 NPR1 nahG and ssi2-1 npr1-5 nahG plants revealed that elevated SA levels were not essential for the ssi2-1-conferred phenotypes. However, expression of the nahG transgene did reduce the intensity of some ssi2-1-conferred phenotypes, including PR-1 expression, and disease resistance. Based on these results, SSI2 or an SSI2-generated signal appears to modulate signaling of an SA-dependent, NPR1-independent defense pathway, or an SA-and NPR1-independent defense pathway.

Salicylic acid mediates the reduced growth of lignin down-regulated plants

“…3 A and D). These results are consistent with the fact that PR genes can be regulated by an alternative NPR1-independent pathway (25,26); for example, constitutive PR gene expression in the cpr6-1 dominant mutation in Arabidopsis requires elevated SA levels but not NPR1 function (25).…”

HLM1, an Essential Signaling Component in the Hypersensitive Response, Is a Member of the Cyclic Nucleotide–Gated Channel Ion Channel Family[W]

“…Thus, among the different lesion-mimic mutants identified to date, some of them present a normal HR (all of the lsd mutants except lsd1, acd5, cpr22, and dll1) (Dietrich et al, 1994;Greenberg et al, 2000;Yoshioka et al, 2001;Pilloff et al, 2002), one of them exhibits an accelerated HR (cpn1) (Jambunathan et al, 2001), some of them show runaway cell death (lsd1 and acd2) (Dietrich et al, 1994;Greenberg et al, 1994), and some others show a suppressed HR phenotype (dnd1, acd6, agd2, and hrl1) (Yu et al, 1998;Rate et al, 1999;Rate and Greenberg, 2001;Devadas and Raina, 2002). Among these mutants, lesion formation can be either nahG and/or NPR dependent or nahG and/or NPR independent (lsd2, lsd4, cpr5, and ssi2) (Bowling et al, 1997;Hunt et al, 1997;Shah et al, 2001). Such studies highlight the complexity involved in the regulation of the defense responses in plants, about which relatively little is known.…”

A Gain-of-Function Mutation in an Arabidopsis Toll Interleukin1 Receptor–Nucleotide Binding Site–Leucine-Rich Repeat Type R Gene Triggers Defense Responses and Results in Enhanced Disease Resistance

“…Because the ssi4 mutation was isolated in the npr1-5 background, all of these SA-dependent defenses must be activated via an NPR1-independent pathway. Analyses of several other Arabidopsis mutants also have revealed an SA-dependent, NPR1-independent pathway(s) that mediates PR gene expression and/or disease resistance (Bowling et al, 1997;Clarke et al, 1998;Li et al, 1999Li et al, , 2001Rate et al, 1999;Shah et al, 1999Shah et al, , 2001Kachroo et al, 2001;Yoshioka et al, 2001). Because SA alone does not induce PR expression or enhanced resistance in npr1 plants, the activation of the SA-dependent, NPR1-independent pathway(s) is thought to require a second signal that works in conjunction with SA.…”