β-1,3 Glucan Sulfate, but Not β-1,3 Glucan, Induces the Salicylic Acid Signaling Pathway in Tobacco and Arabidopsis

Abstract

Sulfate substituents naturally occurring in biomolecules, such as oligosaccharides and polysaccharides, can play a critical role in major physiological functions in plants and animals. We show that laminarin, a b-1,3 glucan with elicitor activity in tobacco (Nicotiana tabacum), becomes, after chemical sulfation, an inducer of the salicylic acid (SA) signaling pathway in tobacco and Arabidopsis thaliana. In tobacco cell suspensions, the oxidative burst induced by the laminarin sulfate PS3 was Ca 2þ dependent but partially kinase independent, whereas laminarin triggered a strickly kinase-dependent oxidative burst. Cells treated with PS3 or laminarin remained fully responsive to a second application of laminarin or PS3, respectively, suggesting two distinct perception systems. In tobacco leaves, PS3, but not laminarin, caused electrolyte leakage and triggered scopoletin and SA accumulation. Expression of different families of Pathogenesis-Related (PR) proteins was analyzed in wild-type and mutant tobacco as well as in Arabidopsis. Laminarin induced expression of ethylene-dependent PR proteins, whereas PS3 triggered expression of ethylene-and SA-dependent PR proteins. In Arabidopsis, PS3-induced PR1 expression was also NPR1 (for nonexpressor of PR genes1) dependent. Structure-activity analysis revealed that (1) a minimum chain length is essential for biological activity of unsulfated as well as sulfated laminarin, (2) the sulfate residues are essential and cannot be replaced by other anionic groups, and (3) moderately sulfated b-1,3 glucans are active. In tobacco, PS3 and curdlan sulfate induced immunity against Tobacco mosaic virus infection, whereas laminarin induced only a weak resistance. The results open new routes to work out new molecules suitable for crop protection.

The novel elicitor AsES triggers a defense response against Botrytis cinerea in Arabidopsis thaliana

“…Other studies have reported that basic defenses of A. thaliana to B. cinerea depend mostly on JA and ET [16,17,39]. Nevertheless, SA-induced plant defenses were also reported to be involved against necrotrophs in A. thaliana [39][40][41] and tobacco [42]. Perhaps a difference with the studies cited above and our results is that we have tested the hormone dependence of elicitor-triggered defenses in contrast to hormone-dependence of basal resistance without elicitor pretreatment.…”

Algal polysaccharides as source of plant resistance inducers

“…For example, Ménard et al (2004) demonstrated that laminaran, with eliciting activity in tobacco and A. thaliana, after its sulfation, becomes an inducer of the salicylic acid (SA) pathway.…”

“…This water-soluble molecule is composed by glucose units with linkages β(1→3) and β(1→6) in a ratio of 11:1. Laminaran has an average polymerization degree of 25 glucose units and three simple ramifications of β-glucose at the C-6 position (Read et al, 1996;Ménard et al, 2004).…”

Rhamnolipids Elicit Defense Responses and Induce Disease Resistance against Biotrophic, Hemibiotrophic, and Necrotrophic Pathogens That Require Different Signaling Pathways in Arabidopsis and Highlight a Central Role for Salicylic Acid

“…Arabidopsis plants expressing the nahG gene and infected with B. cinerea show larger lesions compared with wild-type plants (Govrin and Levine, 2002). In tobacco (Nicotiana tabacum), acidic isoforms of PR3 and PR5 gene that are specifically induced by SA (Ménard et al, 2004) are up-regulated after challenge by B. cinerea (El Oirdi et al, 2010). Resistance to some necrotrophs like Fusarium graminearum involves both SA and JA signaling pathways (Makandar et al, 2010).…”

“…In these experiments, we chose NahG plants that totally degrade SA to be sure that no remaining traces of SA would be detected after RLs treatment and before protection assays (Heck et al, 2003;Ménard et al, 2004;Ferrari et al, 2007). We also used sid2 plants that are impaired in SA synthesis (Nawrath and Métraux, 1999;Wildermuth et al, 2001), npr1 that is insensitive to SA (Cao et al, 1994), and ein2 mutants that are insensitive to ET (Guzmán and Ecker, 1990).…”