Figure 1. Different modes of pathogen recognition. (a) Recognition of microbe-associated molecular patterns (MAMPs) by extracellular receptor-like kinases (RLKs) triggers basal immunity mediated via MAP kinase signalling and activation of WRKY transcription factors. (b) Direct recognition can occur between pathogen effectors and an NB-LRR encoded R gene. (c) NB-LRRs can indirectly recognize pathogens through the N-terminal domain via a host protein (guardee), alternatively (d) the guardee component can first be associated with the pathogen effector and subsequently become recognized by the N-terminal of a NB-LRR encoding gene. (e) The most recently found interaction is based on recognition of a pathogen effector that mimics a transcription factor and binds directly to a non-NB-LRR R protein. (f) Explanation of the symbols used.

Figure 2. Priming is a nonacute plant pathogen response, which renders the plant more resistant to future attack. In ISR priming models, a role for NPR1 in JA responses has been established, whereas this role is not apparent during infection with necrotrophs – where the detrimental role of NPR1-mediated antagonism by SA is more important. The chemical agent -aminobutyric acid (BABA) induces priming of callose deposition via interference of ABA signalling, resulting in BABA-induced resistance (BABA-IR). BABA-IR can act independently of SAR and ISR against some pathogens and via the SAR pathway against others.

Figure 3. Through observations of disease outcome in various mutants, the mutual antagonism between defences against necrotrophs and biotrophs was observed. Most classical models have focused on the two main pathways with SA-dependent resistance against biotrophs and JA and/or ET-dependent responses versus necrotrophs. As more mutants in other hormone pathways have been studied, a complex web of interactions has become more and more apparent. Some pathogens where the three main plant biotic defence hormones SA, JA and ET play no or a minor role in resistance, mutants in other hormone pathways have rendered susceptibility – indicating that there are yet undiscovered pathogen response pathways that need to be delineated and characterized in relation to the more well-established models. Each interaction is also more complex than indicated by simplified model drawings, since the combination of signals can cause some subsets of the responses to be antagonistic whereas others are synergistic or unaffected. The models are thus not representative for every response gene, but rather for the final disease outcome in those plant–pathogen systems hitherto studied.