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. 2012 Sep 4;14(1):58–70. doi: 10.1111/j.1364-3703.2012.00827.x

Figure 8.

figure

Hypothetical model illustrating β‐aminobutyric acid (BABA)‐induced resistance to Pectobacterium carotovorum ssp. carotovorum (Pcc). This model is based on the information provided in this study and references cited in the discussion. Thick bold black arrows represent priming, and thin arrows indicate no priming. Upon Pcc infection, BABA primes salicylic acid (SA)‐dependent signalling and the pattern‐triggered immunity (PTI) response. Priming leads to a potentiated expression of FLG22‐INDUCED RECEPTOR‐LIKE KINASE 1 (FRK1), ARABIDOPSIS NON‐RACE SPECIFIC DISEASE RESISTANCE GENE (NDR1)/HAIRPIN‐INDUCED GENE (HIN1)‐LIKE 10 (NHL10), CYTOCHROME P450, FAMILY 81 (CYP81F2) and PATHOGENESIS RELATED 1 (PR1), increased callose deposition and blockage of reopening of stomata. Even when the SA defence signalling cascade is disrupted in SA‐defective SA induction deficient 2‐1 (sid2‐1) and phytoalexin deficient 4‐1 (pad4‐1), priming of other PTI‐dependent defence responses may be sufficient for a functional BABA‐induced resistance. coi1, coronatine‐insensitive 1; ein2, ethylene‐insensitive 2.