Abstract
Salicylic acid (SA) is a key defense signal molecule against biotrophic and hemibiotrophic pathogens in plants, but how SA is synthesized in plant cells still remains elusive. Identification of new components involved in pathogen-induced SA accumulation would help address this question. To this end, we performed a large-scale genetic screen for mutants with altered SA accumulation during pathogen infection in Arabidopsis using a bacterial biosensor Acinetobacter sp. ADPWH_lux-based SA quantification method. A total of 35,000 M2 plants in the npr1-3 mutant background have been individually analyzed for the bacterial pathogen Pseudomonas syringae pv. maculicola (Psm) ES4326-induced SA accumulation. Among the mutants isolated, 19 had SA levels lower than npr1 (sln) and two exhibited increased SA accumulation in npr1 (isn). Complementation tests revealed that seven of the sln mutants are new alleles of eds5/sid1, two are sid2/eds16 alleles, one is allelic to pad4, and the remaining seven sln and two isn mutants are new non-allelic SA accumulation mutants. Interestingly, a large group of mutants (in the npr1-3 background), in which Psm ES4326-induced SA levels were similar to those in the wild-type Columbia plants, were identified, suggesting that the signaling network fine-tuning pathogen-induced SA accumulation is complex. We further characterized the sln1 single mutant and found that Psm ES4326-induced defense responses were compromised in this mutant. These defense response defects could be rescued by exogenous SA, suggesting that SLN1 functions upstream of SA. The sln1 mutation was mapped to a region on the north arm of chromosome I, which contains no known genes regulating pathogen-induced SA accumulation, indicating that SLN1 likely encodes a new regulator of SA biosynthesis. Thus, the new sln and isn mutants identified in this genetic screen are valuable for dissecting the molecular mechanisms underlying pathogen-induced SA accumulation in plants.
Highlights
As sessile organisms, plants are under constant attack from diverse microbes including bacteria, fungi, oomycetes, and viruses
In order to identify new components involved in pathogeninduced Salicylic acid (SA) accumulation, we took advantage of the SA biosensor-based method to screen for mutants with altered levels of pathogen-induced SA in Arabidopsis
The npr1-3 mutant was used as the starting material for the genetic screen, because it accumulates significantly higher levels of SA than wild type upon bacterial pathogen infection (Figures 1A,B; Cao et al, 1997; Ryals et al, 1997; Shah et al, 1997; Zhang et al, 2010)
Summary
Plants are under constant attack from diverse microbes including bacteria, fungi, oomycetes, and viruses. Plants activate their immune system to mount multiple defense responses, which are similar to animal innate immunity (Jones and Dangl, 2006). Recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors results in PAMP-triggered immunity (PTI). To achieve successful colonization, adapted pathogens can deliver effector molecules directly into the plant cells to suppress PTI, resulting in effector-triggered susceptibility (ETS) (Jones and Dangl, 2006). Plants have evolved resistance (R) proteins to detect the presence of certain pathogen effector molecules, inducing effector-triggered immunity (ETI). Activation of PTI or ETI leads to generation of mobile signals, which induce a long-lasting broad-spectrum immune response known as systemic acquired resistance (SAR) (Durrant and Dong, 2004)
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