Nevertheless, many biotrophic and hemibiotrophic pathogens pattern their in planta cytokinin secreting capability to increase uptake of nutrients and host cell cycle regulation for self-establishment (Walters and McRoberts, 2006; Pertry et al., 2009). However, the combination of kinetin and NAA manifested low GUS activity compared with kinetin alone. Logical operators OR (∨), AND (∧), and NOT (¬) in the SQUAD algorithm cumulate the effect of edges: either only activating or only inhibiting or both activating and/or inhibiting (see Methods and Supplemental Methods 1 online). Induction of medium alkalinization in Arabidopsis cell culture due to flagellin does not change with the addition of 1 μM t-zeatin (see Methods). wrote the paper.

These results demonstrate the behavior of the components of plant immunity and their innate properties and quantify their mutual interactions across the hormone disease networks. We used cytokinin as the activating input node in combination with Pst in the presence (+SA; to mimic overaccumulation of SA) and absence (−SA; to mimic deficiency in SA accumulation) of SA, while activation of PR-1 over time was used as the output marker node for the immune response (Figure 5C). In most cases, we observed only lack of activation (e.g., mitigated pathogen for most system nodes modeled). conceived and planned the project. We defined PR-1 as marker node for the output as it reflects (Mukhtar et al., 2011) the resulting immunological response of the host plant to the invading pathogen (Pst). Our dynamic model for Pst showed activation for nodes of SA, JA, ET, ABA, and auxin, while demonstrating lack of activation for GA and cytokinin (Figure 2A; see Supplemental Figure 4A online). These are shown as a heat map in terms of activity over time (early time points above and corresponding later time points follow in each heat map). Whether guarding the cell surface or being used for surveillance inside the plant cell, receptors are instrumental in the recognition of pathogenic PAMPs and effectors (Figure 1B, red). In contrast with wild-type infection, infection with the mutant Pst strain caused either repression of these genes or left them unchanged. Plant pathogenic bacteria (Pst) have evolved strategies to keep the host susceptible (Nishimura and Dangl, 2010).

In addition, according to our results, the system response differs according to pathogen load. Kinetin-treated PR1:GUS leaves showed higher GUS activity, while NAA treatment alone did not induce any GUS activity (Figure 8B). Was I wrong! Next, we investigated whether SlPIF4 directly regulated the transcription of SlCBF1.