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Plant immunity triggered by engineered in vivo release of oligogalacturonides, damage-associated molecular patterns
Saturday, 2015/05/02 | 19:05:12

Manuel Benedetti, Daniela Pontiggia, Sara Raggi, Zhenyu Cheng, Flavio Scaloni, Simone Ferrari, Frederick M. Ausubel, Felice Cervone, and Giulia De Lorenzo


Damage-associated molecular patterns (DAMPs), released from host tissues as a consequence of pathogen attack, have been proposed as endogenous activators of immune responses in both animals and plants. Oligogalacturonides (OGs), oligomers of α-1,4–linked galacturonic acid generated in vitro by the partial hydrolysis of pectin, have been shown to function as potent elicitors of immunity when they are applied exogenously to plant tissues. However, there is no direct evidence that OGs can be produced in vivo or that they function as immune elicitors. This report provides the missing evidence that OGs can be generated in planta and can function as DAMPs in the activation of plant immunity.


Oligogalacturonides (OGs) are fragments of pectin that activate plant innate immunity by functioning as damage-associated molecular patterns (DAMPs). We set out to test the hypothesis that OGs are generated in planta by partial inhibition of pathogen-encoded polygalacturonases (PGs). A gene encoding a fungal PG was fused with a gene encoding a plant polygalacturonase-inhibiting protein (PGIP) and expressed in transgenic Arabidopsis plants. We show that expression of the PGIP–PG chimera results in the in vivo production of OGs that can be detected by mass spectrometric analysis. Transgenic plants expressing the chimera under control of a pathogen-inducible promoter are more resistant to the phytopathogens Botrytis cinerea, Pectobacterium carotovorum, and Pseudomonas syringae. These data provide strong evidence for the hypothesis that OGs released in vivo act as a DAMP signal to trigger plant immunity and suggest that controlled release of these molecules upon infection may be a valuable tool to protect plants against infectious diseases. On the other hand, elevated levels of expression of the chimera cause the accumulation of salicylic acid, reduced growth, and eventually lead to plant death, consistent with the current notion that trade-off occurs between growth and defense.


See: http://www.pnas.org/content/112/17/5533.abstract.html?etoc

PNAS April 28, 2015 vol. 112 no. 17 5533-5538


Fig. 2.

Fig. 2. Expression of the PGIP–PG chimera induces defense responses. (A) PGIP–PG chimera levels determined by immunoblot upon induction with 50 µM β-estradiol. (B) PG activity evaluated by agar diffusion assay in protein extracts of Arabidopsis nontreated (−) and treated (+) with 50 µM β-estradiol. (C) A representative PGIP–PG transgenic plant without treatment or after 170 h of induction. (D) Callose staining after 140 h of induction. Both images are at the same scale. (Magnification: 10×.) (E) Defense gene induction upon treatment with 50 µM β-estradiol. The photographs shown are representative of typical results.

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