Infection of plants by necrotizing pathogens or colonization of plant roots with certain beneficial microbes causes the induction of a unique physiological state called “ priming”. The primed state can also be induced by treatment of plants with various natural and synthetic compounds. Primed plants display either faster, stronger, or both activation of the various cellular defense responses that are induced following attack by either pathogens or insects or in response to abiotic stress. Although the phenomenon has been known for decades, most progress in our understanding of priming has been made over the past few years. Here, we summarize the current knowledge of priming in various induced-resistance phenomena in plants.

Summary: We have examined the role of the callose synthase PMR4 in basal resistance and β‐aminobutyric acid‐induced resistance (BABA‐IR) of Arabidopsis thaliana against the hemi‐biotrophic pathogen Pseudomonas syringae and the necrotrophic pathogen Alternaria brassicicola. Compared to wild‐type plants, the pmr4‐1 mutant displayed enhanced basal resistance against P. syringae, which correlated with constitutive expression of the PR‐1 gene. Treating the pmr4‐1 mutant with BABA boosted the already elevated levels of PR‐1 gene expression, and further increased the level of resistance. Hence, BABA‐IR against P. syringae does not require PMR4‐derived callose. Conversely, pmr4‐1 plants showed enhanced susceptibility to A. brassicicola, and failed to show BABA‐IR. Wild‐type plants showing BABA‐IR against A. brassicicola produced increased levels of JA. The pmr4‐1 mutant produced less JA upon A. brassicicola infection than the wild‐type. Blocking SA accumulation in pmr4‐1 restored basal resistance, but not BABA‐IR against A. brassicicola. This suggests that the mutant’s enhanced susceptibility to A. brassicicola is caused by SA‐mediated suppression of JA, whereas the lack of BABA‐IR is caused by its inability to produce callose. A. brassicicola infection suppressed ABA accumulation. Pre‐treatment with BABA antagonized this ABA accumulation, and concurrently potentiated expression of the ABA‐responsive ABI1 gene. Hence, BABA prevents pathogen‐induced suppression of ABA accumulation, and sensitizes the tissue to ABA, causing augmented deposition of PMR4‐derived callose.

In several plant species, oxidative stress has been shown to be one of the causes of damage produced by salinity. In order to assess the implication of oxidative stress in the reported sensitivity of the citrus rootstock Carrizo citrange to salt stress, 5-month-old seedlings were grown with increasing NaCl concentrations added to the watering solution. As an indicator of oxidative damage, malondialdehyde content was measured. The antioxidant capability of the plants was determined by measuring superoxide dismutase, ascorbate peroxidase, catalase and glutathione reductase activities together with the non-enzymatic antioxidant activity. As additional physiological responses to the stress, 1-aminocyclopropane-1-carboxilic acid and proline accumulation were assessed. Data indicate that Carrizo citrange responded to salt-induced oxidative stress by increasing enzymatic and non-enzymatic antioxidant defenses proportionally to the extent of the stress imposed, and that in all plants the malondialdehyde content remained at a moderate level. We suggest that the important deleterious effects reported in Carrizo citrange grown under high NaCl concentrations are mainly due to a cellular intoxication by Cl^– ions and not to the salt-induced oxidative stress.

The apoplast comprises the intercellular space, the cell walls, and the xylem. Important functions for the plant, such as nutrient and water transport, cellulose synthesis, and the synthesis of molecules involved in plant defense against both biotic and abiotic stresses, take place in it. The most important molecules are ROS, antioxidants, proteins, and hormones. Even though only a small quantity of ROS is localized within the apoplast, apoplastic ROS have an important role in plant development and plant responses to various stress conditions. In the apoplast, like in the intracellular cell compartments, a specific set of antioxidants can be found that can detoxify the different types of ROS produced in it. These scavenging ROS components confer stress tolerance and avoid cellular damage. Moreover, the production and accumulation of proteins and peptides in the apoplast take place in response to various stresses. Hormones are also present in the apoplast where they perform important functions. In addition, the apoplast is also the space where microbe-associated molecular Patterns (MAMPs) are secreted by pathogens. In summary, the diversity of molecules found in the apoplast highlights its importance in the survival of plant cells.

Plant 9-lipoxygenases (9-LOX) and α-dioxygenases (α-DOX) initiate the synthesis of oxylipins after bacterial infection. Here, the role of these enzymes in plants' defense was investigated using individual Arabidopsis thaliana lox1 and dox1 mutants and a double lox1 dox1 mutant. Studies with Pseudomonas syringae pv. tomato (Pst) revealed the enhanced susceptibility of lox1 to the virulent strain Pst DC3000 and the partial impairment of lox1 and dox1 mutants to activate systemic acquired resistance. Notably, both defects were enhanced in the lox1 dox1 plants as compared with individual mutants. We found that pre-treatment with 9-LOX- and α-DOX-generated oxylipins protected plant tissues against bacterial infection. The strongest effect in this respect was exerted by 9-ketooctadecatrienoic acid (9-KOT), which is produced from linolenic acid by 9-LOX. Quantification of 9-KOT revealed its accumulation after bacterial infection. The levels were reduced in lox1 and lox1 dox1 plants but strongly increased in the dox1 mutant due to metabolic interaction of the two pathways. Transcriptional analyses indicated that 9-KOT pre-treatment modifies hormone homeostasis during bacterial infection. The nature of the changes detected suggested that 9-KOT interferes with the hormonal changes caused by bacterial effectors. This notion was substantiated by the finding that 9-KOT failed to reduce the growth of PstDC3000hrpA, a mutant compromised in effector secretion, and of the avirulent strain Pst DC3000 avrRpm1. Further support for the action of the 9-LOX- and α-DOX-oxylipin pathways as modulators of hormone homeostasis was the observation that lox1 dox1 seedlings are hypersensitive to the growth-inhibitory effect of ABA and showed enhanced activation of ABA-inducible marker genes as compared with wild-type plants.

We have demonstrated that root treatment with hexanoic acid protects tomato plants against Botrytis cinerea. Hexanoic acid-induced resistance (Hx-IR) was blocked in the jasmonic acid (JA)-insensitive mutant jai1 (a coi1 homolog) and in the abscisic acid (ABA)-deficient mutant flacca (flc). Upon infection, the LoxD gene as well as the oxylipin 12-oxo-phytodienoic acid and the bioactive molecule JA-Ile were clearly induced in treated plants. However, the basal ABA levels were not altered. Hexanoic acid primed callose deposition against B. cinerea in a cultivar-dependent manner. Treated plants from Ailsa Craig, Moneymaker, and Rheinlands Ruhm showed increased callose deposition but not from Castlemart. Hexanoic acid did not prime callose accumulation in flc plants upon B. cinerea infection; therefore, ABA could act as a positive regulator of Hx-IR by enhancing callose deposition. Furthermore, although hexanoic acid protected the JA-deficient mutant defensless1 (def1), the priming for callose was higher than in the wild type. This suggests a link between JA and callose deposition in tomato. Hence, the obtained results support the idea that callose, oxylipins, and the JA-signaling pathway are involved in Hx-IR against B. cinerea. Moreover our data support the relevance of JA-signaling for basal defense against this necrotroph in tomato. Hexanoic acid also protected against Pseudomonas syringae, indicating a broad-spectrum effect for this new inducer.