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.plant immunity | DAMPs | polygalacturonase | PGIP | oligogalacturonides
The structure of the cell wall has a major impact on plant growth and development, and alteration of cell wall structural components is often detrimental to biomass production. However, the molecular mechanisms responsible for these negative effects are largely unknown. Arabidopsis (Arabidopsis thaliana) plants with altered pectin composition because of either the expression of the Aspergillus niger polygalacturonase II (AnPGII; 35S:AnPGII plants) or a mutation in the QUASIMODO2 (QUA2) gene that encodes a putative pectin methyltransferase (qua2-1 plants), display severe growth defects. Here, we show that expression of Arabidopsis PEROXIDASE71 (AtPRX71), encoding a class III peroxidase, strongly increases in 35S:AnPGII and qua2-1 plants as well as in response to treatments with the cellulose synthase inhibitor isoxaben, which also impairs cell wall integrity. Analysis of atprx71 loss-of-function mutants and plants overexpressing AtPRX71 indicates that this gene negatively influences Arabidopsis growth at different stages of development, likely limiting cell expansion. The atprx71-1 mutation partially suppresses the dwarf phenotype of qua2-1, suggesting that AtPRX71 contributes to the growth defects observed in plants undergoing cell wall damage. Furthermore, AtPRX71 seems to promote the production of reactive oxygen species in qua2-1 plants as well as plants treated with isoxaben. We propose that AtPRX71 contributes to strengthen cell walls, therefore restricting cell expansion, during normal growth and in response to cell wall damage.
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