Vitamin B1-Induced Priming Is Dependent on Hydrogen Peroxide and theNPR1Gene in Arabidopsis

Abstract

Thiamine confers systemic acquired resistance (SAR) on susceptible plants through priming, leading to rapid counterattack against pathogen invasion and perturbation of disease progress. Priming reduces the metabolic cost required for constitutive expression of acquired resistance. To investigate the effects of priming by thiamine on defense-related responses, Arabidopsis (Arabidopsis thaliana) was treated with thiamine and effects of pathogen challenge on the production of active oxygen species, callose deposition, hypersensitive cell death, and pathogenesis-related 1 (PR1)/Phe ammonia-lyase 1 (PAL1) gene expression was analyzed. Thiamine did not induce cellular and molecular defense responses except for transient expression of PR1 per se; however, subsequent Pseudomonas syringae pv tomato challenge triggered pronounced cellular defense responses and advanced activation of PR1/PAL1 gene transcription. Thiamine treatment and subsequent pathogen invasion triggered hydrogen peroxide accumulation, callose induction, and PR1/PAL1 transcription activation in Arabidopsis mutants insensitive to jasmonic acid (jar1), ethylene (etr1), or abscisic acid (abi3-3), but not in plants expressing bacterial NahG and lacking regulation of SAR (npr1 [nonexpressor of PR genes 1]). Moreover, removal of hydrogen peroxide by catalase almost completely nullified cellular and molecular defense responses as well as SAR abolishing bacterial propagation within plants. Our results indicated that priming is an important cellular mechanism in SAR by thiamine and requires hydrogen peroxide and intact NPR1.Plants have developed an effective immanent surveillance mechanism and pathogen invasions often induce ubiquitous plant defense responses that activate biochemical and structural changes within plant cells. A specific plant's resistance (R) gene product functions as a signaling receptor for the corresponding avirulence (Avr) gene product from the pathogen. The key differences between the compatible (susceptible) and incompatible (resistant) interactions are the early recognition of pathogen attack and the timely expression of defense responses (Yang et al

Nitric Oxide-Mediated Maintenance of Redox Homeostasis Contributes to NPR1-Dependent Plant Innate Immunity Triggered by Lipopolysaccharides

“…PR1 gene expression and callose deposition are indicators of defense-related responses (van Loon and van Strein, 1999;Ton and Mauch-Mani, 2004). Some biological agents and synthetic compounds cannot induce PR1 expression and callose deposition per se until pathogen infection; these induced reactions are based on primed accumulation (Ton and Mauch-Mani, 2004;van Hulten et al, 2006;Ahn et al, 2007). However, a number of elicitors can induce direct callose accumulation (Gómez-Gómez et al, 1999;Galletti et al, 2008;Millet et al, 2010).…”

“…NPR1 plays an important role in defense gene activation (Zhang et al, 1999;Ahn et al, 2007). During pathogen or SA induction, NPR1 regulates the high transcript accumulation of the callose synthase genes CalS1 and CalS12 (Dong et al, 2008).…”

Rice Blast Fungus (Magnaporthe oryzae) Infects Arabidopsis via a Mechanism Distinct from That Required for the Infection of Rice

“…Cell death, indicated by a loss of plasma membrane integrity, was detected by staining the infected cells with Evans blue solution (0.25% [w/v] in 0.1 mM CaCl 2 , pH 5.6; Sigma) for 30 min. Evans blue was infiltrated into the leaves as a 0.25% aqueous solution 72 h after pathogen inoculation (Baker and Mock, 1994;Ahn et al, 2007). After at least 30 min of staining, the leaves were rinsed with water and observed with a light microscope.…”

Dissecting Phosphite-Induced Priming in Arabidopsis Infected withHyaloperonospora arabidopsidis

“…Similarly, treatments with natural or synthetic compounds enhance resistance responses only after pathogen challenge. Treatment of plants with SA, riboflavin (vitamin B2), thiamine (vitamin B1), menadione, 2,6-dichloroisonicotinic acid, benzo(1,2,3,)thiadiazole-7-carbothioc acid S-methyl ester (BTH), the nonprotein amino acid b-aminobutyric acid (BABA), or phosphite (Phi) has been shown to prime defenses for augmented responses to pathogens (Kauss et al, 1992;Kauss and Jeblick, 1995;Katz et al, 1998;Zimmerli et al, 2000;Ahn et al, 2007;Borges et al, 2009;Zhang et al, 2009;Eshraghi et al, 2011). Numerous studies have attempted to decipher the molecular components of defense priming (Zimmerli et al, 2000;Kohler et al, 2002;Ton et al, 2005;Zhang et al, 2009).…”