SBT3.3 loss of function increases disease susceptibility to <i>P.</i><i>syringae</i> DC3000 and <i>H. arabidopsidis</i>.

<p>(<b>A</b>) Five-week-old plants were inoculated with <i>Ps</i>DC3000. Zero (white bars), three (grey bars) and five (black bars) days after inoculation, the bacterial growth was measured. Error bars represent standard deviation (n = 12). Asterisks indicate statistical differences to Col-0 (P<0.05) using Student's <i>t</i> test. Below are representatives of inoculated leaves of the indicated genotypes. (<b>B</b>) Quantification of <i>H. arabidopsidis</i> conidia development on Col-0, and <i>sbt3.3-1</i> and <i>sbt3.3-2</i> mutants. Asterisks indicate statistically different distributions of disease severity classes compared with Col-0 plants (χ² test; α = 0.05). (<b>C</b>) Western blots with anti-PR1 antibodies reveals inhibition of PR1 induced accumulation in <i>nrp1</i>, <i>sbt3.3-1</i> and <i>sbt3.3-2</i> mutant plants, compared to Col-0, following inoculation with <i>Ps</i>DC3000. The experiments were repeated three times with similar results. (<b>D–E</b>) Time-course RT-qPCR analysis showing <i>PR-1</i> (D) and <i>SBT3.3</i> (E) gene expression in Col-0, <i>sbt3.3-1</i>, and <i>npr1-1</i> plants after infection with <i>Ps</i>DC3000. Data represent the mean ± SD; n = 3 replicates and gene expression given as in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003445#ppat-1003445-g001" target="_blank">Fig. 1</a>.